5 Acute inflammation Flashcards
What is an acute inflammatory response?
It is the most common response of the body tissues to an area of nearby damage
What are the 4 cardinal signs of inflammation?
- Calor (Heat)
- Dolor (Pain)
- Rubor (Redness)
- Tumor (Mass)
What stimulates the acute inflammatory response?
- Microorganisms (bacteria)
- Trauma (surgical incision)
- Ischaemic necrosis (infarction)
- Radiation damage (sunburn)
- Chemical damage (acids, alkali)
What is the purpose of acute inflammatory response?
- To destroy or neutralise the damaging agent
- To liquefy and remove dead tissue
- To prepare the damaged area for healing
How does acute inflammatory response occur?
- By the production of an acute inflammatory exudate derived from blood components from capillaries adjacent to damaged mass
- Acute inflammatory exudate compromises:
> Fluid
> Fibrin
> Neutrophils, but also a few macrophages and lymphocytes
How does exudate work?
- Fluid dilutes any toxins
- Fluid carries nutrients, mediators, and antibodies
- FIbrin - function is speculative
- NEUTROPHILS
Describe the formation of exudate (steps)
- Blood vessels near damaged tissues become dilated
- Blood flow becomes turbulent
- Endothelial cells swell + retract; vessels leak
- Neutrophils marginate and emigrate
Describe the events in the first step of exudate formation (blood vessel dilation + loss of axial flow pattern of blood)
- Blood vessels near to damaged tissue become dilated
- Blood flow initially increases (Rubor is a result of this, and calor), then slows down (due to changes in osmotic pressure - blood spends longer in this area)
- Axial flow pattern of blood is lost (turbulent blood flow - cells in the middle of bloodstream are being - on outside of the wall as well)
Why does this stage of exudate formation occur? (blood vessel dilation
- Release of inflammatory mediators from damaged tissue
- Area of damaged tissue > mediators released into surrounding tissue - act on blood vessel
- Vessels dilate (histamine affects)
Describe the next stage of exudate formation
endothelial cells swell + retract; vessels leak
- Inflammatory mediators affect endothelial cells - they swell
- They now separate, junctions are less robust - increased permeability
- Blood vessels become leaky
- Fluid (exudate) can now exit from the vessel into surrounding tissue
> smaller molecules first (water, salt)
> larger molecules follow with more fenestrations (proteins; fibrinogen becomes cross-linked - becomes degraded by enzymes - products of this stimulate other products to move out of vessel too [chemotaxic effect] - This results in swelling [tumor]
Describe the next stage of exudate formation
neutrophils marginate and emigrate
- Exiting of neutrophils from blood vessels into the area of tissue damage
- Turbulence in blood flow -allows neutrophils to move from the middle of vessels to edges, and allows it to leave vessels
- Inflammatory mediators > make endothelial cells express different receptors on the surface - once they meet neutrophils - they make the neutrophils adhere to them on the side of the blood vessels (margination)
- Once they marginate, inflammatory mediators send signals causing chemotaxis - polymorphs (neutrophils) are now induced by chemical signals to exit blood vessels and enter the area of tissue damage
- In this time, fibrin is polymerised (from fibrinogen) and released
List the clinical types of exudate
- Serous: excess fluid accumulation - in the pericardial sac
- Purulent: (lots of neutrophils) can be found in meninges
- Fibrinous (lots of fibrin)
- Fibrino-purulent (lots of fibrin and cross-linked fibrin - and pus
Describe the mediators of inflammation
They can cause vascular and cellular changes
- Mediated by a series of mediators of acute inflammation
e.g. o Complement system o Coagulation system o Fibrinolytic system o Kinin system o Platelet-activating factor o Histamine o Serotonin o Nitric oxide o Endotoxin
What are selectins and integrins?
- Selectins and integrins are adhesive molecules on the surface of endothelial cells
- These allow polymorphs to enter cells to enter cells
- These also have chemotactic effects - attracting cells to leave vessels