A4 Case Study: Acute Inflammation

Question 1

How do blood vessels respond to injury?

Answer 1

Vasoconstriction and Vasodilation.
- Vasoconstriction: Blood vessel constricts by smooth muscle cells for a second

• Vasodilation: Vessel dilates allowing blood to flow into site of injury

Question 2

What are the different types of exudates?

Answer 2

• Serous exudate
• Fibrinous exudate
• Serosanguinous exudate
• Purulent exudate

Question 3

How do the changes in the vessels relate to the visible signs of inflammation?

Answer 3

Increased blood flow (vasodilation) to affect area causes:
- Heat (calor)
- Redness (rubor)

Due to increased blood flow and inflammation:

Question 4

What cells are involved in inflammation?

Answer 4

Leukocytes (WBC):
- Neutrophils
- Basophils
- Eosinophils
- Monocyte

Question 5

How do circulating cells get from inside the blood vessels to the injury site?

Answer 5

Cellular Events:
- Margination, rolling and adhesion
- Emigration and chemotaxis
- Opsonisation and phagocytosis

Question 6

Difference between transudate and exudate?

Answer 6

• Transudate: Leaked low protein fluid (oedema) out of blood vessels (ultrafiltrate of blood plasma) due to high-pressure in vessel
• Exudate: High protein (Oedema) fluid leaks due to inflammation or increased vascular permeability

Question 7

How are the 4 exudate different from each other?

Answer 7

• Serous exudate: Blisters, clear and watery fluid
• Fibrinous exudate: Wounds like burns, little blood, Large fibrin content,
• Serosanguinous exudate: Serous exudate (blister) combined with blood
• Purulent exudate: Pus (yellow cellular content)

Question 8

Difference between vasoconstriction and vasodilation?

Answer 8

• Vasoconstriction: blood vessels constricting
• Vasodilation: Blood vessels dilating

Question 9

What is the role of the main chemical mediators of inflammation - how do they influence the vessels, cells, and cardinal signs of inflammation?

Answer 9

Role: Certain chemicals mediate (trigger) events in acute inflammation.
- e.g. such as vasodilation, vascular permeability etc.

• Histamine: In early stages of inflammation mast cells release histamine. Role of histamines include mediating vasodilation of blood vessels, induce pain, increase vascular permeability and endothelial activation.
• Serotonin: When platelets aggregate (blood clotting) it triggers release of serotonin. Role of serotonin includes mediating increase vascular permeability and vasodilation
• Bradykinin: Bradykinin is from activation of the Hageman factor. Role of Bradykinin includes mediating vasodilation and increase vascular permeability and pain (dolor)
• Complement 3a:
• Complement 3b:
• Complement 5a:
• Prostaglandins:
• Leukotrienes:
• Coagulation Cascade (Clotting system): Is from activation of the Hageman factor. Role of Coagulation cascade includes mediating fibrin formation. fibrin holds down RBC creating = blood clot

Question 10

Explain the process of Cellular events (from cell in vessel to the injury site)?

Answer 10

• Margination: Leukocytes move to the margins of the endothelium (vessel walls)
• Rolling: leukocyte rolls on the vessel wall to adhere to endothelial cells
• Adhesion: leukocyte adheres to the adhesion molecules on the endothelial cells.
• Emigrations: Leukocyte changes shape (cytoskeleton) and squeezes through between endothelial cells exiting the vessel
• Chemotaxis: Leukocyte travels to the site of injury with chemotactic/chemical gradient as guidance.
• Opsonisation: Serum factor called opsonin coat pathogens to be destroyed (undergo phagocytosis) Detects and tags pathogens to undergo phagocytosis
• Phagocytosis: Eats away the tagged pathogens to prevent bacterial infections of injury

Question 11

Where do chemical mediators come from?

Answer 11

• Blood plasma or
• From cells

Question 12

What actions of this chemical mediator of inflammation is histamine, serotonin and bradykin?

Answer 12

Histamine: Vasodilation, increased vascular permeability and pain
Serotonin: Vasodilation and increased vascular permeability
Bradykinin: Vasodilation, increased vascular permeability and Pain

Question 13

What actions of this chemical mediator of inflammation is C3a, C3b and C5a?

Answer 13

Complement 3a (C3a): Vasodilation, increased vascular permeability and chemotaxis
Complement 3b (C3b): Opsonisation
Complement 5a (C5a): Vasodilation, increased vascular permeability and chemotaxis

Question 14

What actions of this chemical mediator of inflammation is Inflammation Prostaglandins, Inflammation Leukotrienes and Inflammation Coagulation cascade?

Answer 14

Inflammation Prostaglandins: Vasodilation and pain
Inflammation Leukotrienes: Increase vascular permeability and chemotaxis.
Inflammation coagulation cascade: Fibrin formation