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Miscellaneous > MCB Lecture 58 Inflammation I > Flashcards

MCB Lecture 58 Inflammation I Flashcards

0
Q

Differentiate between acute and chronic inflammation

Cells, duration

A

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

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1
Q

What are the stages of inflammation?

A 
Stimulus
Recognition
Recruitment
Removal
Regulation
Resolution
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2
Q

What are the aims of inflammation?

A

Dilute
Destroy
Neutralise
Initiate resolution

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3
Q

Which cells are involved with inflammation?

A 
Neutrophils, aka PMN
Mast cells
Eosinophils
Basophils
Macrophages
Lymphocytes
NK cells
Dendritic cells
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4
Q

What is PMN?

A

Polymorphonuclear cell

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5
Q

What are the stimuli for inflammation?

A 
Physical trauma
Necrosis
Chemical trauma
Foreign bodies
Infection
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6
Q

Describe the recognition phase of inflammation

Which things are recognised?
Which cells recognise?

A

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

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7
Q

Describe broadly what vascular change is

A

Vasodilation and increase in vascular permeability to deliver more plasma protein and cells to areas of injury or infection

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8
Q

Describe the stages of vascular change

A

i. Transient vasoconstriction
ii. Arteriolar vasodilation
iii. Stasis

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9
Q

Describe broadly how vascular change is mediated

A

Chemical mediators

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10
Q

What is occuring during stasis?

A

There is congestion and very slow flow of blood. As a result, neutrophils are pushed to the margins of the lumen

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11
Q

Compare extravasation under normal and inflammatory conditions

A

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.

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12
Q

What is transudate?

When does it occur?

A

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

Due to:
High hydrostatic pressure
Decrease colloid osmotic pressure

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13
Q

What is exudate?

What is it due to?

A

Net flow out of the vascularisation of a protein and cell rich fluid

It is due to an increase in permeability, mediated by chemicals

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14
Q

What are the two types of vasoactive mediators?

A

Fast and transient

Slow and prolonged

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15
Q

What are the immediate and transient vasoactive mediators?

A

Histamine, Brady Kinins, leukotrienes

16
Q

What are the slow and prolonged vasoactive mediators?

A

Cytokines

IL-1 and TNF

17
Q

Describe what is going on physically when vascular permeability is changed

A

The endothelial cells contract and separate from each other so that there is space between them for stuff to leak out

18
Q

Describe how endothelial injury can lead to an increase in vascular permeability

A

Injury can lead to a direct change in permeability by making the endothelium leaky

19
Q

What happens to the lymphatics during inflammation?

A

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

20
Q

What are the stages of leukocyte recruitment?

A
  1. Marginisation
  2. Rolling
  3. Adhesion
  4. Transmigration
21
Q

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

A

Selectins:
ICAM-1
VCAM-1 + integrins

Sialyl Lewis + L, P and E selectins

22
Q

Describe the presence of the selectins under normal and inflammatory conditions

A

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
Q

Leukocyte adhesion is:

A

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

24
Q

What regulates leukocyte adhesion?

A

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

25
Q

What is diapedesis?

What are the two types?

A

Para cellular and intracellular diapedesis.

This is the leukocyte moving across the endothelium of the blood vessel into the injured tissue

26
Q

Which molecule mediates diapedesis?

A

PECAM-1

27
Q

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

A

Collagenase

28
Q

Describe chemotaxis of PMN during recruitment

A
  1. Chemokines bind to cell surface receptors
  2. Cytoskeletal changes
  3. Extension of pseudopods
29
Q

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

A

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

Miscellaneous (109 decks)

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