2. Inflammation And Repair - BP Flashcards
Why is incr. vascular permeability necessary in inflammation?
These changes allow edema of the interstitial tissue to be formed.
What are the 5 mechanisms for increasing vascular permeability?
- Endothelial contraction
- Endothelial cell retraction
- Direct endothelial injury
- Delayed prolonged response
- Leukocyte mediated damage
What are the mediators, the time course, and the mechanism of endothelial cell retraction?
Mediators –> TNF + IL-1.
How –> Structural rearrangement of cytoskeleton.
Time course –> 4-6hrs (delayed response, long lived).
What is the mechanism of action of endogenous chemotactic agents?
Most via activation of GTPases, which cause polymerization of actin.
How do the WBCs recognize foreign material?
Via the mannose and scavenger receptors.
Where do we see serous inflammation?
Viral infections and burns.
Where do we see fibrinous inflammation?
Uremic and post myocardial infarct pericarditis.
Where do we see purulent inflammation?
In bacterial and fungal infections.
What are the 6 outcomes of acute inflammation?
- Resolution
- Abscess formation
- Ulcers
- Fistula formation
- Chronic inflammation
- Scar formation
What are the requirements for abscess formation?
The body cannot get rid itself of the inciting agent, or the process of repair and scarring is occurring more rapidly in the tissue around the site of abscess.
Mention 4 complications of abscess.
- Pain
- Fever
- Rupture
- Swelling
What is the definition of the ulcer?
Loss of mucosa and deeper tissues.
If ONLY the mucosa is lost, the correct term is erosion.
What are the requirements for ulcer formation?
The body cannot rid itself of the inciting agent.
What is the microscopic morphology of an ulcer?
4 layers, which recapitulate steps from acute inflammation to repair
- Fibrin
- Neutrophils
- Granulation
- Fibrosis
Mention some complications of an ulcer?
- Pain
- Hemorrhage (if it involves a vessel)
- Perforation –> hemorrhage within a cavity/lumen of the GI tract.