Acute Inflammation

Question 1

Inflammation

Answer 1

The reaction of living vascularised tissue to injury

Question 2

Purpose of injury

Answer 2

Start repair of tissue, eliminate the cause of injury, eliminate infection

Question 3

How to recognise infection

Answer 3

Red (erythema), warm, tender, swollen, infiltration of white blood cells, loss of function

Question 4

Exudate

Answer 4

Concentrated,activated materials of the immune system (phagocytes, plasma proteins - opsonising and complement) in fluid

Question 5

Danger signals

Answer 5

trigger inflammation by activating the innate immune system

Question 6

Inflammation is accelerated by active changes in small blood vessels

Answer 6

1. Initial trigger 2. Dilation of arteriolar 3. Increased blood flow 4. Capillary bed opens fully 5. Skin redness, heat 6. Fluid leak from vessels, slows blood flow causing stasis, congestion and purple skin

Question 7

Local tissue swelling is due to

Answer 7

Fluid leaving vessels

Question 8

Leaks in vessels are caused by

Answer 8

Active structural changes to endothelium in response to vasoactive mediators

• > endothelial contraction opens gaps
• > transcytosis channels

Question 9

Passive leaks of vessels can occur at

Answer 9

Sites of endothelial injury

During angiogenesis

Question 10

Tissue swelling is limited by

Answer 10

Skin (consequence of heat redness and pain)

Brain;skull (consequence as brain sweeps and is pushed out of foremena can cause necrosis)

Joint spaces (consequence synovial joint fluid can be squeezed out by exudate

Soft tissue compartment (e.g nasal polyp - uncomfortable but not life threatening)

Question 11

Serous exudate

Answer 11

Few cells, serum like, little fibrinogen or platelets

Question 12

Haemorrhagic

Answer 12

Vascular destruction, result of cancer or serious bacterial infection

Question 13

Pus

Answer 13

neutrophil and enzyme rich, green/yellow colour

Question 14

Fibrinous

Answer 14

Few cells, contains fibrinogen, greyish, sticky fibrin coating

Question 15

Circulating neutrophils get to an injury site by

Answer 15

Leukocytes passively marginating (accumulating and adhering to epithelial cells of blood vessel walls at the site fo an injury) on venues, pushed by the greater number of red blood cells in normal blood flow
Slower blood flow during inflammation means more neutrophils contact the endothelium
Cytokines increase endothelial surface adhesion molecules that firmly bind neutrophils, which spread and crawl
When crawling neutrophils encounter platelets bound to endothelium, they move to the endothelial junction to exit

Question 16

Transmigration

Answer 16

Pericyte guiding molecules lead transmigrating neutrophils out of the endothelium

Extravasated neutrophils have transcriptional energy burst, releasing cytokines, chemokines, growth factors, modified by what they detect as they emerge and screen the perivascular tissue

Question 17

Chemotaxis

Answer 17

Movement of an organism in response to chemical stimulus

Neutrophils use fibrin scaffold to crawl over

Question 18

Agents which cause chemotaxis in neutrophils

Answer 18

IL-8, coagulation products, bacterial endotoxins (lipopolysaccharides), complement c5a and c3a, f-met-leu-phe peptides (amino acid tag)

Question 19

Resident macrophages shield trivial injury

Answer 19

Don’t want to trigger inflammation for normal wear and tear as can be damaging
Macrophages can cover small, sporadic, sparse injuries - preventing neutrophils from detecting it so no inflammation is triggered
Big injuries cannot be hidden and so is detected by neutrophils and inflammation is triggered9

Question 20

Systemic effects of inflammation

Answer 20

Cytokine induced depression
Fever - prostaglandin synthesis in hypothalamus raises body temp
Sickness behaviour - fatigue, irritability, social withdrawal, listlessness
Leukocytosis- accelerated release of leukocytes from bone marrow
Acute phase proteins - mostly from liver; fibrinogen and C-reactive protein, serum amyloid A