Pathology - Inflammation 1 Flashcards
What is the response to injury in the body?
Vascular changes, cellular changes, chemical mediators and morphologic patterns. Slide 8
What are the vascular changes in response to injury?
Changes in flow and vasodilation. Slide 9
Where does vascular changes first occur?
In arterioles and then capillary beds. Slide 9
What mediates vascular changes in response to injury?
Histamine and nitric oxide. Slide 9
What does vascular changes in response to injury result in?
Increased heat (calor) and redness/erythema (rubor). Slide 9
What does calor mean?
Heat. Slide 9
What does rubor mean?
Redness. Slide 9
What are the cellular changes in response to injury?
Stasis, WBC margination, rolling, adhesions and migration. Slide 12
What happens during WBC margination?
When the blood vessels dilate the blood flow slows down and this means the WBC marginate over to the sides of the blood vessels instead of being in the centre. Slide 12
What are vessel walls normally like and what happens in response to injury?
They are usually slippy and the blood cells won’t stick, however in response to injury the vessels express various proteins on the lumenal surface which match WBC surfaces. Slide 15
What proteins are expressed on the lumenal surface?
Integrins, VCAM and ICAM. Slide 16
Where are the selectins situated?
On WBC and bind to cell adhesion molecules. Slide 16
What does ICAM stand for?
Intercellular adhesion molecules. Slide 16
What does it mean when rolling occurs with the WBC?
They form the integrin/selectin interaction with their ligands which is of low affinity and the bind and break and rebind to another, hence ‘rolling’ along the endothelial cells. Slide 17
What increases selectin expression?
Histamine and Thrombin. Slide 18
What does TNF and IL-1 do?
Increase endothelial cell expression of VCAM and ICAM. Slide 18
What do chemokines from the site of injury do?
Bind to proteoglycans on endothelial cell surface which increase affinity of VCAMS and ICAMS for integrins. Slide 19
What happens to the vascular permeability in response to injury?
Vessels become leaky so there is a loss of protein and a change in osmotic pressure as water follows protein causing swelling. Slide 21
What does tumour mean?
Swelling. Slide 21
How can vessels become leaky?
The endothelial cells contract, there has been a direct injury, WBC self harm, transocytosis (VEGF) or there are new vessels forming. Slide 22
What is chemotaxis?
When the cells follow a chemical gradient and move along it, it consists of bacterial components. Slide 24
What are the 3 phases of phagocytosis?
Recognition and attachment, engulfment and killing. Slide 26
What do mannose receptors do?
They alert the WBC that its a bacteria and it attacks it. Slide 27
What carries mannose receptors?
Bacterial surface glycoproteins and glycolipids. Slide 27
What are opsonins?
They are the ‘flags’ on bacteria which make them stand out from the crowd. Slide 29
What happens during engulfment?
Pseudopods wrap around the bacteria and form a vesicle called a phagosome inside the phagocyte. It then joins with a lysosome forming a phagolysosome where the bacteria is broken down. Slide 31
What happens during killing and degradation of the bacteria?
There are reactive oxygen species through NADPH oxidase causes oxygen to gain an electron from NADPH to form superoxide. There are also reactive nitrogen species where NO combines with super oxide to produce ONOO. Slide 38
What does dolor mean?
Pain. Slide 39
What are the clinical features of rubor?
Redness as there is increased perfusion due to increased permeability of vessels. Slide 41
What are the clinical features of calor?
Heat as increased perfusion and increased vascular permeability. Slide 42
What are the clinical features of tumour?
Swelling due to vascular changes. Slide 43
What are the clinical features of dolor?
Painful and is mediated by prostaglandins and bradykinin. Slide 44
What does functiono laesa mean?
Loss of function. Slide 45
What imflammatory cell characterises acute inflammation?
Neutrophil. Slide 46
