Acute Inflammation 1- Lecture 7

Question 0

What are some features of acute inflammation?

Ie what is it characterised by?

Answer 0

-Immediate response to tissue damage
-primarily an innate response
-cells and molecules of the innate immune system: non specific
-local response to limit tissue damage
Characterised by:
- leakage of blood proteins (fibrinogen➡ fibrin)
-recruitment of leukocytes from the blood
Inflammatory exudate
-hallmark features of Al

Why acute: 
Acute inflammation: 
-starts in seconds, lasts up to 2 or 3 days 
sub acute Inflammation 
-2-3 days up to about 2 weeks 
Chronic inflammation: 
-weeks to months 

Slide 4

Question 1

What are the cardinal signs of acute inflammation

Answer 1

1. Heat (calor)
2. Pain (Dolar)
3. Redness (rubor)
4. Swelling (tumor)
5. Loss of function (functio laesa)
   Slide 3

Question 2

What is acute inflammation good for?

Answer 2

-aids the delivery of mediators of host defence (leukocytes, antibodies) to the site of injury.
-removes the cause of injury and initiates tissue repair
-but sometimes it can do more tissue damage than the injury
6

Question 3

How can acute inflammation become the enemy within?

Answer 3

Vasculitis- note neutrophil infiltration, arterial wall necrosis (arrow) and thrombus formation.
-inflammatory cells in wall of BV so there’s a loss of elasticity ➡ can lead to thrombosis
-neutrophil trying to remove debris but breaks down walls
7

Question 4

What are the 4 components of an acute inflammation

Answer 4

Vascular response- changes to blood flow and vessel permeability
Cellular Response- recruitment of leukocytes
Soluble mediators- co-ordinations of the tissue response
Molecular “sensors”- control the type of inflammation
8

Question 5

Understand the acute inflammation cycle on slide 9

Answer 5

Tissue damage causes start of response ➡triggers inducers➡ the sensors are (mast cells, macrophages, epithelial cells, dentritic cells)
-soluble mediators- coordinates cell type and tells them were to go and what to do
➡Response targeted at damaged tissue ➡blood vessel changes
➡Tissue inducers are eliminated ➡inflammation goes away

Question 6

What are some inducers of acute inflammation?

Answer 6

-infections
-trauma (+/- sterile)
-physical an chemical agents
-foreign bodies
-tissue necrosis (“bad death”)
-hypersensitivity reactions
10

Question 7

What are the vascular changes in Acute inflammation?

Answer 7

-first reaction to tissue injury
-fundamentals to initiating an acute inflammatory reaction
-involve changes in:
-blood flow to tissue
-vascular permeability to BV in tissue
-cell migration- allowing cells out of blood into tissue
13

Question 8

What are the key processes in a vascular response

Answer 8

1. Transient vasoconstriction -neurogenic-occurs within seconds (limits the blood flow out of infected site)
2. Arteriolar dilation
   - axon reflex arc➡ capillary beds open: red and hot
   - histamine, nitric oxide ➡this is to increase blood to a site (redness and heat)
3. Increased blood viscosity- thicker = ⬇flow rate
   - blood stasis-slowing = ⬆ blood accumulation
   - impedes blood outflow
4. Increased vascular permeability
   -fluid enters interstitial space (transudate)
   -hallmark features of Acute I
   -the BV wall increase permeability so fluid flows out which is followed by the inflammatory cells,
   14

Question 9

Increased vascular permeability

The difference between transudate, exudate and oedema

Answer 9

Slide 17

Question 10

What are the plasma proteins found in Exudates?

Answer 10

Albumin- transports Ca, Cu, Zn as well as many therapeutic drugs
Transferrin- transports Fe and may have antibacterial p/ antiviral properties
Haptoglobin- binds free haemoglobin
Ceruloplasmin- iron metabolism
Immunoglobulins- varied roles including binding to antigen, fixing complements and opsonisation.
18

Question 11

What are the mechanisms of increased vascular permeability Ie how does it come about?

Answer 11

1. Gaps between endothelial cells
   - vasoactive mediators (histamine, Leukotrienes)
   - VEGF-induced channels
2. Direct endothelial injury
   - toxins, burns, chemicals
3. Leukocyte-mediated injury to endothelium
   - leukocyte products (ROS, enzymes)
4. Angiogenesis- leakage from new vessels
5. Radiation damage
   - sunburn, X-rays, UV radiation damage to endothelial cells

Question 12

Increased vascular permeability:Leukocyte Extravasation
Extravasation 
Margination 
Transmigration
Migration

Answer 12

Extravasation:

• movement of leukocytes from the blood to site of tissue injury
• ingest offending agents
• kill microbes
• remove necrotic tissue and foreign substances

Marination:
-leukocytes to adhere to endothelial cells

Transmigration:
-leukocytes move across the endothelium

Migration:
-movement of leukocytes into interstitial fluid

Slide 20

Question 13

Review questions:
Why are vascular changes important in Acute inflammation?
What major processes mediate vascular changes and what are the mechanisms?
What are clinical signs of vascular changes in Al?
(Clue: what happens in the triple response?)
-how can you tell a transudate from an exudate and what do they mean?
-what are the sequences of events and key molecules involved in leukocyte extravasation?

Answer 13

Should know this by now mate or your in deep do do