Acute Inflammation

Question 1

Why is there A.I?

Answer 1

• removal of injurious agents/stimulus (eg. Pathogens, necrotic tissue)
• initiate repair

Question 2

What cause A.I?

Answer 2

• tissue necrosis (ischaemic infarction)
• infections by microbes
• hypersensitivity reactions
• physical harmful agents (trauma, heat, cold)
• chemicals (acids, alkalis)

Question 3

How does A.I occur?

3 events

Answer 3

1. vascular changes
2. Cellular events
3. Release of chem mediators

Question 4

Outcome of A.I?

5 cardinal signs

Answer 4

1. Heat
   - increased blood flow (vascular)
   - fever due to pyrogens which are almost all the cytokines (pyrogen initiate the release of prostaglandins from hypothalamus) (cellular event)
2. Redness
   - dilation of blood vessels (vascular)
3. Swelling
   - increased leakiness of vessels causing fluid retention (vascular)
   - localised increase of inflammatory cells (cellular)
4. Pain
   - stretching of eodema/pus
   - chem mediators (bradykinin, prostaglandin, serotonin) induce pain
5. Loss/limited of fx
   - due to swelling
   - due to pain

Question 5

Vascular changes:

Microscopically

Answer 5

1. Vasodilation
   - comes after TRANSIENT VASOCONSTRICTION
   - due to release of vasodilators (histamine from mast cell, prostaglandin from leukocytes, nitric oxide from leuko)
   - vasodilate to increase leakiness/permeability and adhesion&attraction
2. Vascular permeability
   - recruitment of neutrophils (phagocyte) and go out via margination
   - lymph flow increases to drain cellular exudates, neutrophils and debris

Question 6

Cellular events:

Microscopically

Answer 6

• chemotaxis of polymorphonuclear leuko (neutrophil, basophil, eosinophil)
• chemotaxis driven by: chemokines (IL-8 released by macrophages), bacterial products, C5a from complement system, leukotrienes
• leuko activated to undergo phagocytosis
• extravasation of neutrophil etc: margination, rolling, adhesion, transmigration/diapedesis, chemotaxis

Question 7

Types of A.I:

Answer 7

1. Serous inflammation (skin blisters)
2. Fibrinous inflammation (
3. Purulent inflammation (brain abscess)
4. Haemorrhagic inflammation (exudates containing red blood cells eg. viral pneumonia)
5. Gangrenous inflammation (perforation of appendix)

Question 8

Fx of complement system:

Answer 8

1. opsonisation
2. Chemotaxis
3. Cell lysis
4. Clumping

Question 9

Outcomes of A.I:

Answer 9

1. Complete resolution
2. Resolution by fibrosis (replaced by fibrous tissue)
3. Abscess formation (will heal)
4. Progression into chronic inflammation (when body cant get rid of the injurious agent)

Question 10

Harmful effects of A.I:

Answer 10

• digestion of normal tissue (collagenase & protease)
• swelling (airway obstruction, raised intracranial pressure etc)
• inappropriate (hypersensitivity)