MoD 2 Acute Inflammation Flashcards
Describe the length of time involved in acute and chronic inflammation.
Acute - arises from seconds to minutes of injury.
Chronic - arises from days to weeks and years.
Why do leukocytes take longer to get to the site of the infection, whereas fluid (containing plasma proteins) get there very rapidly?
Leukocytes can’t just pour out of the blood the way fluid can, therefore it takes longer.
Name and describe the symptoms of acute inflammation.
Rubor - redness. Due to increase vascularity and more blood flow.
Dolor - pain. Due to stimulation of specialised nerve endings.
Color - heat. Due to increased blood flow some higher temp. (Max 37)
Tumour - swelling. Accumulation of fluid/leukocytes in tissue spaces = swelling.
LoF - protective to prevent another injury and to allow healing to occur.
What are the 3 tissue changes in acute inflammation?
Vascularity, neutrophils and formation of tissue exudate.
Describe the 3 tissue changes seen in acute inflammation.
Vascularity
- histamine causes dilation of arterioles and more blood flows through.
- pressure in capillary bed increases and fluid escapes through gaps in the endothelial cells of venules (histamine also causes endothelial cells to contract which forms the gaps between them).
- dilation causing blood to flow slower, the haematocrit (% of Rbc in blood) increases which causes stasis.
Formation of tissue exudate.
- arterioles dilate + endothelial contraction = increase to fluid permeability.
- increase hydrostatic pressure = fluid leak out of vessel.
- increase colloid osmotic pressure = fluid leak out of vessel.
Neutrophils.
These are a type of leukocyte that live for around 12-20 hours.
They are not normally present in tissue, and their presence in tissue usually means there is an infection, or there recently was one.
They are end cells - they do not replicate (cf macrophages, which can).
They contain ~ 2,000 granules of bactericidal substance.
What are the two types of oedema and what is the difference? In which scenario do you expect to see which?
Transudate is oedema with low protein content. Eg, in heart failure.
Exudate is oedema with high protein content. Eg inflammation.
What is lymphadenitis? What is the link to oedema?
Lymphadenitis is the inflammation of the lymph nodes. This can often become quite painful.
Oedema can often drain to the lymph nodes and cause them to inflame. If the oedema contains microorganisms, then the drainage to the lymph nodes will also present these to the immune system and make it aware of the presence of microorganism.
Describe the process by which neutrophils migrate into tissue from a blood vessel.
Margination - stasis causes them to line up on the edge of the vessel.
Rolling - they roll along the vessel, occasionally binding to adhesion molecules such as SELECTIN
Adhesion - they stick more avidly when their receptors bind to adhesion molecules such as ICAM-1
Emigration - they then migrate out of the vessel.
Why which process do neutrophils move towards their target? Briefly describe this.
Chemotaxis.
This is the process of movement towards a chemical attractant (chemotaxin, eg endotoxins from bacterial cell wall). It is the movement along a concentration gradient of chemoattractants.
Roughly 2mm/hr.
Why is fresh blood not chemoattractant but clotted blood is?
The thrombin and fibrin degradation products are chemoattractant in respect to clotted blood. In fresh blood, because you don’t have these, there is no chemotaxis of neutrophils.
What is diapedesis and how does this differ to the way fluid escapes blood, in relation to inflammation?
Diapedesis is the process by which neutrophils escape the venules and into the tissue.
They do not escape through the gaps in endothelial cells (the way fluid does) but they secrete collagenases which then destroy the basement membrane. They then find their target by using the collagen framework of the tissue structure to get them where they need to be.
What is degranulation and how does this process affect healthy tissue and cause local tissue injury?
Phagocytes enclose the particle to be destroyed, slowly wrapping around it before it is enclosed in a vacuole. Bactericidal substances are then released which destroy it.
The process of degranulation occurs before the phagocyte has completely wrapped around the particle and therefore this is known as early degranulation. Some of the killing substances seep out and then can damage host cells. Hence this is local tissue damage.
Killing is either O2 dependent or independent. Give example of what is used in either pathway.
Independent - enzymes
Dependent - Free radicals - oxidative burst.
What are the local complications of acute inflammation?
Obstruction of tubes - eg Fallopian. (Due to swelling)
Local tissue damage - early degranulation.
Loss of fluid.
Pain and LoF.
What are the systemic effects of acute inflammation,
Inflammatory mediators can enter the blood and cause systemic effects.
Fever - thermostat is reset at a higher setting due to PGE2. (NSAIDs!)
Leukocytosis - increase in the number of leukocytes.
Shock- wide spread vasodilation together with increased permeability to fluid can result in shock.
Acute phase response - due to cytokines. Increased synthesis of complement etc and decreased synthesis of other proteins (in the liver).
