Acute inflammation Flashcards
What are the five clinical signs of acute inflammation?
Redness, swelling, heat, pain and loss of function.
What can cause acute inflammation?
Foreign bodies, tissue necrosis, physical or chemical agents, trauma, infections and immune reactions.
What happens to blood vessels in acute inflammation?
Initially they constrict, but then they dilate so that there is increased perfusion to the tissue.
What vascular changes occur in acute inflammation?
The blood vessels increase in permeability, and so there is exudate on of fluid.
What are the consequences of swelling and exudate on of fluid?
Leads to slowing of the circulation, increased RBC concentration and increased blood viscosity.
What chemical is a key player at the beginning of acute inflammation? What does it cause?
Histamine. It causes pain, arteriolar dilation and venular leakage.
In what cells is histamine found?
Mast cells, basophils and platelets
What stimuli can lead to histamine release?
Physical damage, immune reactions and complement components.
What is the difference between serotonin and histamine?
They have similar properties but serotonin also stimulates fibroblasts.
What are prostaglandins? What drug can block their production?
These are produced by membrane phospholipids and cause vasodilation. Aspirin blocks their production, reducing pain and swelling.
In normal conditions, what molecules leave capillaries?
Water and electrolytes
What is the main driving force of fluid back into the blood?
Colloidal osmotic pressure of plasma proteins.
What three factors cause the main flow of fluid to be out of vessels in acute inflammation?
The semi-permeable membranes have become leaky, the capillary pressure driving fluid out increases and the force driving fluid back into capillaries is reduced as proteins escape through tissue spaces.
State the three consequences of increased fluid moving out of blood vessels
Oedema, increased lymphatic drainage (presents antigens to immune system), delivery of plasma proteins such as fibrin
What is the difference between transudate and exudate?
Transudate has a low protein content whilst exudate has a high protein content.
What can cause to transudate oedema?
Heart failure.
What do bradykinin and complement components induce?
Vascular leakage.
What defensive proteins are found in exudate?
Opsonins, complement and antibodies
What is inflammation?
It is the response of living, vascularised tissue to injury.
What is the primary cell type associated with acute inflammation?
Neutrophils
What is chemotaxis?
It is directional movement towards a chemical attractant.
What can be a chemotaxin?
Leucocytes, clotted blood, bacterial products, injured cells.
What happens to a neutrophil when a chemotaxin binds?
Na and Ca flow into the cell, it swells and points towards stimulus. It switches to a higher metabolic rate and is activated.
What is a Pseudopodia?
A projection of a neutrophil which occurs in a acute inflammation.
In acute inflammation, once a neutrophil has been activated - what happens next?
Margination - move to the edges of blood vessels
Rolling - roll along the wall and bind to selections
Adhesion - bind to integrins
What do neutrophils bind to when rolling?
Selectins
What increases selectin/ integrins activation?
Inflammatory mediators and chemotaxins
What is diapedesis?
This is the movement of leucocytes which move by pulling along collagen fibres of other tissue structures.
Name two opsonins which can be recognised by neutrophils.
IgG antibody - if not the first encounter
C3b fragment of complement which is released on activation.
What is degranulation?
This is the process of cell granules combining with the phagosome and injecting bactericidal substances into it.
When in acute inflammation can local tissue injury occur?
Early degranulation before the particle is completely enclosed within the phagosome.
Name the two mechanisms by which phagocytose do articles are killed.
Oxygen dependant - free radicals (oxygen/respiratory burst)
Oxygen independent - enzymes e.g. Proteases
Name a vasoactive peptide.
Histamine and seratonin.
What is the inhibitor of bradykinin?
It is cleaved by kallikrein in the blood.
What is the function of complement?
These form tubes in membranes and so lead to death of bacteria. In the blood this circulates as diassembled proteins.
Name some biproducts of complement components.
Inflammatory mediators C3a/c5a and opsonins c3b
What is the precursor for prostaglandins?
Arachadonic acid
What is the difference between a cytokine and a chemokine?
Cytokines are chemical messengers between cells whilst chemokines are involved in chemotaxis.
Give an example of an endogenous mediator
endotoxins which causes inflammation in tissue.
What are four common complications of acute inflammation?
Fluid loss, obstruction of tubes/ compression, normal tissue damage and pain and loss of function.
Why does acute inflammation cause fever?
Exogenous pyrogens (endotoxins) stimulate macrophages to produce pyrogenic cytokines. These increase prostaglandin production in anterior hypothalamus and therefore increase the body thermostat.
Why is fever advantageous in acute inflammation?
Inflammatory response is more effective at higher temperatures.
What substance produces an increase in neutrophils in acute inflammation?
Colony stimulating factor from macrophages and endothelial cells. This stimulates the bone marrow to produce more neutrophils.
What is acute phase response?
This is a response produced by cytokines where there is a change in plasma proteins as a result of altered synthesis by liver
What is shock?
This is when inflammatory mediators/ bacterial products enter the blood stream and leads to whole body inflammation. Vasodilation and massive exudate of fluid leads to a drop in blood pressure.
What stops the acute inflammation response?
Mediators only have short half lives and so they are degraded. Also inflammation triggers are reduced and so there is no emigration of neutrophils.
What happens in the tissues after acute inflammation?
Neutrophils are phagocytose do, fluid is reabsorbed and fibrin is degraded. If the tissue has parenchymal cells then it regenerates. Otherwise an extensive fibrous scar will remain.
What is pus?
It is an exudate that is creamy white due to its high neutrophil content.
When do haemorrhagic exudates occur?
This is seen I don’t extractive infection or when there is extensive vascular damage. Exudate contains RBC and so appears bloody.
Where might you see a serous exudate?
Blisters - no colour and no neutrophils.
What is a seroma?
This is a fluid filled pocket with sterile fluid. This usually occurs post op.
When can we clinically identify a fibrinous exudate?
If there is deposition of fibrin in the pericardium or pleural sacs then the surfaces cannot move over each other smoothly and so a rubbing sound is heard.
What causes hereditary angio-oedema?
C1 esterase inhibitor deficiency. Sufferers have attacks of angio-oedema and abdominal pain.
What problems are associated with a1- anti trypsin deficiency?
Neutrophils act unchecked and so this can lead to damage to the lungs - emphysema.
Also causes liver problems as ER secretes an incorrectly folded protein which cannot leave ER.
What is chronic granulomatous disease?
This is where phagocytes are unable to produce superoxide and so no oxygen burst is created.
Name the microorganism which causes lobar pneumona.
Streptococcus pneumoniae
Name a microorganism which can cause Appendicitis
Escherichia coli
What condition can Neisseria meningitidis cause?
Bacterial meningitis
What can cause liver abscess?
Escherichia coli
