Session 2 Lecture Notes Flashcards
(45 cards)
What is the definition of acute inflammation?
Response of living tissue to injury
- it is innate, immediate and imitated to limit the tissue damage
What do vascular and cellular reactions to acute inflammation result in?
Accumulation of fluid exudate (mass of cells and fluid from vessels and/or organs) and neutrophils in tissues
Suggest some causes of acute inflammation
- Microbial infections
- Physical agents such as heat, light or radiation
- Chemicals
- Tissue necrosis
What are the 5 clinical signs of acute inflammation?
Redness Swelling Heat Pain Loss of function
What is the first immediate vascular phase reaction in acute inflammation?
Vasoconstriction of arterioles for a few seconds
After vasconstriction of arterioles what are the following steps in the vascular stage of acute inflammation?
- Vasodilation of arterioles and capillaries (increase in blood flow leads to increased heat and redness)
- Increased permeability of blood vessels (leads of excursion of protein rich fluid into tissues and slowing of circulation as blood has become more viscous)
- Increased concentration of RBCs and more viscous blood leads to stasis
What is stasis?
Slow blood flow
Occurs when blood is more viscous after fluid exudate
What is the first chemical mediator in acute inflammation?
Where is it released from?
Histamine
Released from mast cells, basophils and platelets
Can also be released from C3a, C5a and interleukin 1
What happens to blood vessels in acute inflammation and how does this lead to oedema?
- Arterioles dilate = increased blood flow to capillaries
- Increased blood flow = increased hydrostatic pressure and fluid movement into interstitium
- Blood vessels become more permeable so proteins move out into interstitium also increasing movement of fluid
What is the difference between exudate and transudate interstitial fluid?
Exudate = only occurs in inflammation - the protein level is higher in interstitial fluid than in plasma Transudate = protein level is equal to plasma
If a patient has an oedema of plural cavity - how can measuring protein levels help diagnose the cause?
If protein levels are high = oedema is due to pneumonia (inflammation of lungs)
If protein levels are low = oedema is due to heart failure (pulmonary oedema)
When would fluid loss be exudate and when would it be transudate?
Exudate = when the fluid loss is due to inflammation and oedema has high protein content Transudate = when the fluid loss is due to heart failure and hydrostatic pressure imbalance and oedema will have lower protein content
State 5 ways in which vascular leakage occurs - state whether the fluid moves between the cells or through the cells
- Endothelial contraction
- Cytoskeletal reorganisation
- Direct injury eg sunburn
- Leukocyte dependent injury (products of WBCs can injure cells)
- these are all ways in which fluid moves BETWEEN cells - Transcytosis - blood movements THROUGH cells
What is transcytosis?
The movement of macromolecules from fluid across/through a cell via endocytosis
During inflammation when fluid leaks into the interstitium - what plasma protein is key and what does it do?
Fibrin - it is involved in blood clotting cascade and creates a meshwork to localise the inflammation
What is the primary white blood cell involved in inflammation?
Neutrophil
What is another term used for neutrophil?
Polymorph
or Polymorphonuclear leukocyte
Describe the appearance of a polymorph
They come in multiple shapes and have multi lobed nuclei
What happens to the blood when it slows down and why does it slow down?
You get sludging of RBCs in the centre of the vessel
This is due to increased blood viscosity (as inflammation has caused exudation of fluid)
In stasis describe the 4 movements of the neutrophils in/out the blood vessels
- Margination = they line up along endothelium
- Rolling = they roll along endothelium sticking to it intermittently
- Adhesion = they stick more stronger to endothelium
- Emigration = they move across blood vessel wall
What is chemotaxis?
Cells move in response to a chemical signal down concentration gradient eg emigration of neutrophils across endothelium in response to infection
How do neutrophils move across endothelium?
Relaxation of cell junctions and partial digestion of basement membrane
What are chemotaxins and how do they work?
Give 3 examples
Chemotaxins attract neutrophils
They act as ligands and bind to a receptor on the neutrophil which activates them - making them move towards more chemotaxins (at site of severe inflammation)
Examples: C5a, leukotriene B4 and bacterial peptides (only for bacterial infections)
Describe the 3 stages in which neutrophils are able to phagocyte
- Contact - get the polymorphs where they need to be using chemotaxins
- Recognition - get the polymorph to recognise the antigen by opsonisation
- Internalisation - the antigen is internalised to become a phagosome which is then fused with lysosomes which break down antigen
