Acute inflammation Flashcards
What are exonogous triggers of acute inflammation?
molecules from microbes
What are endogenous triggers of acute inflammation?
molecules from dead or damaged cells
What are DAMPs?
host biomolecules which can initiate and perpetuate a inflammatory response
What are PAMPs?
small molecular motifs produced by microbes
Why does apoptosis not cause a immune response?
cytoplasmic budding preventing molecules like DAMPs from being released
Outline the stages of the vascular phase of acute inflammation?
- mast cells produce vasoactive amines (histamine)
- bradykinin and other mediators are also released
- vasodilation and slow down blood flow - also facilitates cell margination
- Increased permeability of the engorged bed causing an increase of outflow fluid and possibly proteins and RBCs
What is exudate?
fluid that leaks out of blood vessels into nearby tissues
What are the features of the 3 types of exudate?
serous,
fibrinous
neutrophils
What occurs in the cellular phase of acute inflammation
Phagocytic cells release enzyme and mediators
- NLs leave capillaries and veniules via a leukocyte adhesion cascade
- NLs congregate in the inflammatory exudate and they follow a gradient of chemotactic molecules to the site of initiation
What happens in the leukocyte adhesion cascade?
- Cells marginate and neutrophils roll along the endothelium.
- Cytokine activation of the NLs and endothelium switches to a integren expression and the NLs move to the cell junctions - firm adhesion
- NLs transmigrate through the junctions due to leukocyte adhesion molecules - PECAM-1 found on endomembranes
What does histamine cause?
vasodilation, increased permeability, itching and pain
What does cyclooxygenase produce?
pro inflammatory prostaglandins and thromboxanes
anti-inflammatory lipoxin
What are the 5 families of cytokines and there features?
- Haematopoietins: growth factors for cell colonies
- Interferons: antiviral, cell growth, immune activation
- Chemokines:‘chemo-attractants’
- Tumour Necrosis Factors: activate signalling pathways for cell survival, death, differentiation
- Interleukins: Promote leukocyte development and differentiation
What are the 5 classifications of acute inflammation, according to the fluid & cellular components of the exudate?
- Serous
-fluid in the site of inflammation is essentially transudate
-fluid appears watery & clear / slightly yellow - Catarrhal (mucoid)
-mucus secreted at the site mixes with the inflammatory fluid making it appear thick (mucinous)
-this type of inflammation is typically seen at sites of normal mucous production, such as the respiratory tract / some parts of the GI tract - Fibrinous
-the fluid at the site of the inflammation is exudate
-often associated with endothelial injury, which allows leakage of large plasma proteins, such as fibrinogen
-fibrinogen then polymerises to form fibrin (gelatinous protein)
-most commonly seen where there are serous membranes (serosae), such as pericardium, pleura, peritoneum & synovial membranes in joints - Suppurative (purulent)
-accumulation of thick opaque fluid (pus) which has high numbers of leukocytes (which may include alive and/or dead cells), tissue cells (alive and/or dead) & high concentrations of plasma proteins
-pus will often contain bacteria (live and/or dead), as it is often produced when the original damaging stimulus was a bacterial infection of the site - Others, eg haemorrhagic
-when the inflammation causes significant haemorrhage (usually damage of blood vessels, which will also have become congested when the inflammatory process starts - vascular phase of inflammation)
How is acute inflammation resolved?
- Stimulus is removed
- Degradation of pro-inflammatory mediators
- Down-regulation of receptors
- Dephosphorylation of signalling molecules
- Death of inflammatory cells
- Progresses to chronic inflammation or tissue repair
