Pathology 3 - Acute Inflammation Flashcards Preview

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Flashcards in Pathology 3 - Acute Inflammation Deck (48)
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1

What is the definition of acute inflammation?

"The response of living tissue to injury".

- innate, immediate, early, stereotyped
- short duration
- initiated to limit the tissue damage

2

What is acute inflammation generally controlled by?

A variety of chemical mediators derived from plasma or cells

3

Give some causes of acute inflammation

- microbial infections eg. pyogenic organism
- hypersensitivity reactions
- physical agent (heat, light etc)
- chemicals
- tissue necrosis

4

What are the main clinical signs of acute inflammation?

Rubor, tumor, calor, dolor, loss of function

5

What is the general pattern of acute inflammation?

1) changes in blood flow
2) exudation of fluid into tissues
3) infiltration of inflammatory cells

6

What are the 4 stages of changes in the blood flow during the inflammory response?

- transient vasoconstriction of arterioles
- vasodilatation of arterioles then capillaries, leading to increase in blood flow to area
- increased permeability of blood vessels, leading to exudation of protein-rich fluid into tissues and slowing of circulation
- concentration of RBCs in small vessels and increased viscosity of blood ('stasis')

7

What is histamine released from?

Mast cells, basophils and platelets

8

What does histamine cause?

Vascular dilatation, transient increase in vascular permeability, pain

9

True or false - histamine mediates the persistent response?

False - histamine lasts for around half an hour, and is therefore the 'immediate early response'. The persistent response is controlled by other mediators eg leukotrienes, bradykinin

10

What does Starling's Law state?

Fluid flow across vessel walls is determined by the balance of hydrostatic and colloid osmotic pressure, comparing plasma and interstitial fluid.

11

How does acute inflammation lead to oedema?

- Arteriolar dilatation leads to increase in hydrostatic pressure
- increased permeability of vessel walls leads to loss of protein into interstitium
- net flow of fluid out of vessel leads to oedema

12

Define 'oedema'

Excess of fluid in the interstitium

13

What is the difference between transudate and exudate?

Fluid loss due to inflammation will have a high protein content and is referred to as an EXUDATE, while fluid loss due to hydrostatic pressure imbalance will have low protein content and is a TRANSUDATE

14

Give some examples of mechanisms of vascular leakage

- endothelial contraction
- cytoskeletal reorganisation
- direct injury, eg toxic burns, chemicals
- leukocyte dependent injury
- increased transcytosis

15

Why does plasma contain fibrin?

It produces a meshwork which localises the inflammation and prevents it from spreading to the entire serosa cavity

16

What is the main cell involved with the cellular phase of acute inflammation?

Neutrophil leukocyte (aka 'polymorph')

17

Outline the four stages of infiltration of neutrophils into tissue

1) Stasis causes neutrophils to line up at the edge of blood vessels along the endothelium ('margination')
2) neutrophils roll along endothelium, sticking intermittently ('rolling')
3) they then stick more effectively ('adhesion')
4) neutrophils move through blood vessel wall ('emigration')

18

How do cell adhere in neutrophil migration?

They use proteins called selectins and integrins to adhere to the cell wall

19

How do neutrophils manage to get through the blood vessels?

- relaxation of inter-endothelial cell junctions
- digestion of vascular basement membrane
- movement

20

Define 'chemotaxis'

Movement of chemoattractants along concentration gradients

21

How do neutrophils 'move'?

Chemotaxins eg. C5a, LTB4, bacterial peptides bind to receptors on the neutrophils. When the receptor is activated, the neutrophil moves towards the chemotaxin by rearranging its cytoskeleton and producing a pseudopod

22

What do neutrophils do once they reach the tissues?

They phagocytose substances in three stages - contact, recognition and internalisation. Opsonins (Fc and C3b) facilitate this. They then fuse with lysosomes to produces secondary lysosomes.

23

What are the two methods of killing cells?

O2 dependent and O2 independent

24

Why may neutrophils sometimes cause inflammation to tissue?

They release toxic metabolites

25

Which chemical mediators are responsible for increased blood flow?

Histamine and prostaglandins

26

Which chemical mediators are responsible for vascular permeability?

Histamine and leukotrienes

27

Which chemical mediators are responsible for neutrophil chemotaxis?

C5a, LTB4, bacterial peptides

28

Which chemical mediators are responsible for phagocytosis?

C3b

29

What are proteases?

Plasma proteins synthesised in liver. Three large families - kinins, complement system (C3a, C5a), coagulation/fibrinolytic system

30

What are the two hallmarks of acute inflammation?

Exudate of oedema fluid, and infiltrate of inflammatory cells

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