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Flashcards in MoD S3 - Acute inflammation Deck (42)
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1

What is 'Acute inflammation'?

The response of living tissue to injury, initiated to limit the tissue damage

The mechanisms of acute inflammation are innate, immediate and of short duration (minutes to a few days)

2

What are some of the causes of acute inflammation?

Microbial infections (E.g. Pyogenic organisms)
Hypersensitivity reactions (acute phase)
Physical agents
Chemicals
Tissue necrosis

3

What are the macroscopic features of acute inflammation?

What are the microscopic hallmarks of acute inflammation?

Rubor - erytherma (redness)
Tumor - oedema (swelling)
Calor - heat
Dolor - pain
Loss of function

Exudate of fluid
Infiltrate of inflammatory cells

4

What are the major tissue changes present in acute inflammation and how are they controlled?

Changes in blood flow
Exudation of fluid into tissues
Infiltration of inflammatory cells

Inflammatory mediators control each step

5

Give description of how blood flow changes during acute inflammation

Mention how these changes result in a macroscopic clinical feature of acute inflammation

Transient vasoconstriction of arterioles (only lasts a few seconds)

Then vasodilation of arterioles then capillaries, leading to an increase in blood flow (erythrema)

High concentration of RBCs in small vessels and increased viscosity of blood leads to stasis (serious slowing or cessation of blood flow)

6

Describe how exudation of fluid into tissues comes about

What macroscopic feature of acute inflammation does this cause?

Increased permeability of blood vessels caused by histamine release in the tissue

Histamine causes endothelial cells to swell and retract, leaving gaps in the endothelium

This, along with arteriolar dilatation leads to exudation of protein rich fluid into tissues (oedema) and a slowing of the circulation

Macroscopically, this causes swelling

7

What determines fluid flow across a vessel wall?

How does this relate to acute inflammation?

Fluid flow across the vessel wall determined by the balance between hydrostatic and colloid osmotic pressures (Starling's Law)

Increased hydrostatic pressure = increase fluid flow out of the vessel
Increased colloid osmotic pressure = increased fluid flow into the vessel

In acute inflammation:

Arteriolar dilatation leads to increased hydrostatic pressure, fluid moves into the interstitium

Increased permeability of vessels leads to protein loss into interstitium

This leads to protein rich exudate in the tissues (oedema/excess fluid in interstitium)

8

What is the difference between exudate and transudate?

Which of these leads to oedema?

Exudate is protein rich fluid loss in inflammation

Transudate is fluid loss due to hydrostatic pressure only and is therefore low in protein

Oedema can result from both

9

Name a major consequence of oedema

Increased lymphatic drainage

10

What are some other mechanisms of vascular leakage seen in acute inflammation?

Include some of the possible causes for each mechanism

Cytoskeletal reorganisation leading to gaps in the endothelium:
- Cytokines, IL-1 and TNF

Direct injury:
- Toxic burns
- Chemicals

Leukocyte dependent injury:
-ROS damage
- Enzymes from leukocytes

Increased transcytosis across endothelial cells:
- VEGF

11

what is the most common cell type seen infiltrating into the tissues during acute inflammation?

What other types of cells infiltrate into acutely inflamed tissues?

Neutrophils

Macrophages, Lymphocytes

12

Describe in basic terms how neutrophils infiltrate into tissues

Hint: 4 stages

Margination:
Stasis causes neutrophils to line up along the endothelium

Rolling:
Neutrophils roll along the endothelium, sticking intermittently

Adhesion:
Then stick more avidly

Emigration:
Neutrophils move through the cell wall

13

How is it that once neutrophils have adhered to the vessel walls they are able to move into tissues?

Relaxation of endothelial cell junctions

Digestion of the vascular basement membrane

14

What is a neutrophil? (TOB)

A white blood cell involved in inflammation

Polymorphonuclear leukocyte

15

List the actions of a neutrophil

Migrate to and infiltrate tissues by chemotaxis

Phagocytose microorganisms

May release toxic metabolites and enzymes that damage the host tissue

16

What is chemotaxis?

How do neutrophils perform chemotaxis?

Movement along a concentration gradient of chemoattractants

Neutrophils have cell surface receptors that bind to these chemoattractants and allow the neutrophil to direct its migration

Examples of neutrophil chemoattractants include:
- C5a (complement)
- Bacterial peptides
- IL-8

17

How do neutrophils perform phagocytosis?

Neutrophil must make contact with a cell coated in opsonins (C3b, Antibodies) that it then recognises with cell surface receptors

Cytoskeletal changes allow the neutrophil to internalise the cell forming a phagosome

A lysosome is fused with the phagosome to form a secondary lysosome and digest the internalised cell

18

By what mechanisms might neutrophils kill internalised cells?

Hint: 2 types of mechanism

O2 dependent mechanisms:
- Produces superoxide and H2O2
- H2O2-myeloperoxidase-halide system (produces HOCl)

O2 independent mechanisms:
- Lysozyme and hydrolases
- Bactericidal permeability increasing protein (BPI)
- Cationic proteins (Defensins)

19

List some of the chemical mediators of inflammation according to the process they mediate

Vasodilation:
Histamine
Prostaglandins
C3a
C5a

Increased vascular permeability:
Histamine
Prostaglandins
Kinins

Chemotaxis:
Bacterial peptides
C5a
IL-8
Leukotrienes (leukocytes)

Phagocytosis:
C3b

20

How does exudation of fluid into tissue combat injury?

Delivers plasma proteins to area of injury
For example:
Ig
Fibrinogen
Inflammatory mediators

Dilutes toxins

Increases lymphatic drainage delivers microorganisms to phagocytes and antigens in the immune system

21

How does infiltration of inflammatory cells help combat injury?

Removes pathogenic organisms and necrotic debris

22

How does vasodilatation help combat injury?

Increases delivery of blood to the area and increases temperature

23

How does pain and loss of function help combat injury?

Enforces rest
Reduces chance of further traumatic damage

24

What are the possible local complications of acute inflammation?

Swelling can cause the blockage of tubes, for example in the bile duct or intestine

Exudate into tissues can cause compression (as in cardiac tamponade) and serositis

Can lead to loss of fluid (E.g. In burns)

Can lead to pain and loss of function, especially when prolonged

25

List the systemic effects of acute inflammation

Fever
Leukocytosis
Acute phase response
Spread of microorganisms and toxins that can lead to shock

26

Why does acute inflammation lead to fever?

What can be done to reduce the fever?

Endogenous pyrogens produced:
IL-1
TNF-alpha

Note: Pyrogens are compounds that cause fever

Prostaglandins also produced, therefore aspirin reduces fever

27

What is leukocytosis?

Why does acute inflammation lead to leukocytosis?

Leukocytosis is a white blood cell count of above normal range, a sign of inflammatory response

IL-1 and TNF-alpha produce an accelerated release of WBCs from the marrow

Macrophages produced as T-lymphocytes produce M-CSF (Macrophage colony stimulating factor)

In bacterial infections, neutrophils are produced

In viral infections, lymphocytes are produced

28

What is the acute phase response and what does it cause?

A class of proteins whose concentrations increase or decrease in response to inflammation

Causes:
Decreased appetite
Raised pulse rate
Altered sleep patterns
Changes in plasma protein concentrations

29

List some proteins involved with the acute phase response

C-reactive protein (CRP)
Alpha-1 antitrypsin
Haptoglobin
Fibrinogen
Serum amyloid A protein

30

List the possible consequences of acute inflammation

Complete resolution

Continued acute inflammation with chronic inflammation = abscess

Chronic inflammation and fibrous repair, probably with tissue regeneration

Death