CP1: Acute inflammation Flashcards
What is acute inflammation
response of the microcirculation to injury and it is an all purpose defence mechanism to contain and isolate the injury to achieve healing and repair
Where do these inflammatory processes occur;
- Hepatitis
- Endocarditis
- Cystitis
- Dermatitis
- Pleuritis (pleurisy)
- Pneumonitis (pneumonia)
- liver
- heart
- bladder
- skin
- lungs
- lungs
Give examples of exogenous causes of inflammation
Trauma, infection, chemicals, temperature, radiation
Give examples of endogenous causes of inflammation
anoxia (caused by hypoxia), antigen-antibody complexes, body chemicals, metabolic products
What are the macroscopic changes seen (cardinal signs)
- redness
- swelling
- heat
- pain
- loss of function
What are the microscopic changes occuring
- Initial constriction followed by immediate dilation of vessels thus causing redness
- Increased blood flow to site
- Increased permeability of vessels due to endothelial cells pulling together creating leaky vessels allowing WBCs to flow out and stimulate an immune response
- Migration of leucocytes through wall causes oedema
Why is there protein deposition in inflamation
This stops bleeding by creating a mechanical barrier (fibrin clot)
What is extravasation
This is the movement of WBCs out of capillaries into the surrounding tissue
How does extravasation occur
- Margination = where WBCs gather at endothelial wall and there is rolling as the WBCs aren’t firmly attached
- Pavementing is where there is stable adhesion and firm attachment to the endothelium
- Transmigration (diapedesis) ; to the site of injury through the endothelium
What is the first cell to arrive at the site of injury
Neutrophil polymorphs (6-24 hours)
- mobile, phagocytic, responds to chemotaxis
- segmented nucleus, granular cytoplasm
What is the second cells to arrive at the site of injury
Eosinophils
- especially in allergy and helminth infections
- these are bilobed red granules larger than RBCs
Basophils/mast cells
- blue/purple cytoplasm
- degranulates with release of vasoactive amines
What is the third cell to arrive at the site of injury
Monocytes/macrophages (after 24 hours)
- these circulate/ are in the tissue and are the second main cell of acute inflammation
- mobile, phagocytic, responds to chemotaxis
- bean shaped nucleus and copious cytoplasm
What is chemotaxis
The movement of organisms in response to chemical changes this occurs in the presence of
- bacteria, fungi, immune complexes, toxins
- complement components, lipoxygenase products
- WBC breakdown products
What are the two ways in which phagocytosis can be initiated in acute inflammation
- Mechanical contact = immediate response
- Opsonisation = opsinosins coat microbes that go unrecognised and this triggers phagocytes; opsinosins are non-specific to the foreign body
What is a pseudopod
The cytoplasm of phagocytes that will extend around the pathogen to form a phagosome
- killing and degradation of the contents occurs via lysosomal activity
What are the roles of mediators in the acute inflammatory response
To recognise when a threat is gone or to amplify the response by directing WBCs to the site of injury
Where are mediators
These direct the WBCs to the site of injury and are released from the damaged tissues
- Circulating in the plasma (made in liver)
- Intracellularly (either preformed or synthesised once tissue damage has occurred)
What are the clinical features of acute inflammation
- pyrexia
- drowsiness
- lethargy
(all three are because much energy is used) - leukocytosis (increased WBCs)
- decreased appetite (not enough energy for digestion)
- acute phase proteins
How does acute inflammation result in resolution
- by clearance of injury
- clearance of inflammatory cells and mediators
- replacement of injured cells
- normal functioning resumed (this may require use of antibiotics)
How does acute inflammation result in repair
some tissue lost may not be able to regenerate and so it is replaced by granulation tissue and fibrosis meaning it has less than ideal functioning
How does acute inflammation result in chronic inflammation
This is when the injury cannot be dealt with and there has been repeated episodes
How does acute inflammation result in suppurative inflammation
This is where an exudate is formed by WBC leakage
If the neutrophils, dead cells, bacteria and debris are walled off and surrounded by a fibrous rim, it will become an abscess (well defined radiolucent area) this will stop the spread of infection
How does acute inflammation result in septicaemia
This is the worse outcome and could occur if someone is immunocompromised
= When organism gains access to lymphatics then the blood - this has high mortality and a heightened response
What are the 5 fates of acute inflammation
- resolution
- repair
- chronic inflammation
- suppurative inflammation
- septicaemia
What is the purpose of acute inflammation
- all purpose defence mechanism
- produced to contain and isolate injury
- to destroy/neutralise injury
- ideally resolves injury
- achieves healing and repair
- can become chronic
What results from permeable vessels (a microscopic change in acute inflammation)
This enhances the migration of cells and dilution of toxins: it stimulates lymphatics/immune response and the deposition of proteins (e.g. fibrin to form a mechanical barrier and stop bleeding)
