A4 Case Study: Acute Inflammation Flashcards
How do blood vessels respond to injury?
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
What are the different types of exudates?
- Serous exudate
- Fibrinous exudate
- Serosanguinous exudate
- Purulent exudate
How do the changes in the vessels relate to the visible signs of inflammation?
Increased blood flow (vasodilation) to affect area causes:
- Heat (calor)
- Redness (rubor)
Due to increased blood flow and inflammation:
What cells are involved in inflammation?
Leukocytes (WBC):
- Neutrophils
- Basophils
- Eosinophils
- Monocyte
How do circulating cells get from inside the blood vessels to the injury site?
Cellular Events:
- Margination, rolling and adhesion
- Emigration and chemotaxis
- Opsonisation and phagocytosis
Difference between transudate and exudate?
- 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
How are the 4 exudate different from each other?
- 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)
Difference between vasoconstriction and vasodilation?
- Vasoconstriction: blood vessels constricting
- Vasodilation: Blood vessels dilating
What is the role of the main chemical mediators of inflammation - how do they influence the vessels, cells, and cardinal signs of inflammation?
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
Explain the process of Cellular events (from cell in vessel to the injury site)?
- 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
Where do chemical mediators come from?
- Blood plasma or
- From cells
What actions of this chemical mediator of inflammation is histamine, serotonin and bradykin?
Histamine: Vasodilation, increased vascular permeability and pain
Serotonin: Vasodilation and increased vascular permeability
Bradykinin: Vasodilation, increased vascular permeability and Pain
What actions of this chemical mediator of inflammation is C3a, C3b and C5a?
Complement 3a (C3a): Vasodilation, increased vascular permeability and chemotaxis
Complement 3b (C3b): Opsonisation
Complement 5a (C5a): Vasodilation, increased vascular permeability and chemotaxis
What actions of this chemical mediator of inflammation is Inflammation Prostaglandins, Inflammation Leukotrienes and Inflammation Coagulation cascade?
Inflammation Prostaglandins: Vasodilation and pain
Inflammation Leukotrienes: Increase vascular permeability and chemotaxis.
Inflammation coagulation cascade: Fibrin formation