MCB Lecture 58 Inflammation I Flashcards Preview

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Flashcards in MCB Lecture 58 Inflammation I Deck (30)
0

What are the stages of inflammation?

Stimulus
Recognition
Recruitment
Removal
Regulation
Resolution

1

Differentiate between acute and chronic inflammation

Cells, duration

Acute: short duration, neutrophils
Chronic: long lasting, macrophages and lymphocytes

2

What are the aims of inflammation?

Dilute
Destroy
Neutralise
Initiate resolution

3

Which cells are involved with inflammation?

Neutrophils, aka PMN
Mast cells
Eosinophils
Basophils
Macrophages
Lymphocytes
NK cells
Dendritic cells

4

What is PMN?

Polymorphonuclear cell

5

What are the stimuli for inflammation?

Physical trauma
Necrosis
Chemical trauma
Foreign bodies
Infection

6

Describe the recognition phase of inflammation

Which things are recognised?
Which cells recognise?

PAMPs
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

7

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

8

Describe the stages of vascular change

i. Transient vasoconstriction
ii. Arteriolar vasodilation
iii. Stasis

9

Describe broadly how vascular change is mediated

Chemical mediators

10

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

11

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.

12

What is transudate?
When does it occur?

Net flow out of the blood vessels of a protein poor fluid

Due to:
High hydrostatic pressure
Decrease colloid osmotic pressure

13

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

14

What are the two types of vasoactive mediators?

Fast and transient

Slow and prolonged

15

What are the immediate and transient vasoactive mediators?

Histamine, Brady Kinins, leukotrienes

16

What are the slow and prolonged vasoactive mediators?

Cytokines

IL-1 and TNF

17

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

18

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

19

What happens to the lymphatics during inflammation?

There is increased drainage, and thus the lymphatics and lymphoid organs can become inflamed

20

What are the stages of leukocyte recruitment?

1. Marginisation
2. Rolling
3. Adhesion
4. Transmigration

21

Which molecules form the transient adhesion of leukocyte to the endothelial cells during rolling?

Selectins:
ICAM-1
VCAM-1 + integrins

Sialyl Lewis + L, P and E selectins

22

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

23

Leukocyte adhesion is:

When the leukocyte and the endothelial cells form transient adhesion interactions.

24

What regulates leukocyte adhesion?

Cytokine signalling causes the integrins to cluster together and form higher affinity interactions

25

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

26

Which molecule mediates diapedesis?

PECAM-1

27

What does PMN release to help it move through the ECM?

Collagenase

28

Describe chemotaxis of PMN during recruitment

1. Chemokines bind to cell surface receptors
2. Cytoskeletal changes
3. Extension of pseudopods

29

Describe how each of the cardinal signs of inflammation are caused by inflammation

Calor: increased blood from core, which is warm
Dolor: bradykinin, prostoglandin activate nocireceptors, and there is swelling which puts pressure on the tissue
Rubor: increased blood flow and RBCs
Tumor: exudate formation due to increase in vascular permeability

Loss of function: swollen area, reduced mobility, pain

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