Acute Inflammation (Session 2) Flashcards
What is inflammation?
Inflammation is a rapid response to injury of vascularised living tissue.
1) What is the purpose of inflammation?
2) What does inflammation aim to do?
1) To deliver defensive materials (white blood cells and fluid containing plasma proteins) to a site of injury.
2) to protect the body against infection, particularly bacterial infection, and to clear damaged tissue and initiate tissue repair.
1) How long does acute inflammation take to evolve?
2) Give 2 words to describe acute inflammation
1) Over hours or days
2) Innate and stereotyped.
How long does chronic inflammation take to evolve?
Over weeks, months or even years;
What suffix is used to indicate inflammation of an organ or tissue, and give an example
–itis
e.g., appendicitis = inflammation of the appendix.
In inflammation, why do defensive cells, fluid and proteins need to be delivered?
as local defences are not adequate to protect against infection
1) How do the defensive agents circulate in the blood?
2) What happens when they are needed?
3) Where do defensive agents leave the blood vessels?
4) How must this be accomplished?
1) Most, but not all, of the defensive agents circulate in the blood in inactive form.
2) they are delivered and activated.
3) at the site of the injury.
4) without interrupting the blood flow which must continue on to other tissues.
1) Describe the process of the passage of leucocytes and fluids (which contains plasma proteins) out of the blood
2) What is it controlled by?
3) How long does it take to deliver fluids to the site of injury?
4) How long does it take to deliver leukocytes to the site of injury?
1)complex process
2) chemical messages which are called chemical mediators or mediators of inflammation.
3) delivered to the site of injury first in seconds
4) leucocytes take longer (minutes) because they can’t just pour out of the vessels.
Give 6 causes of acute inflammation
- Foreign bodies (splinters, dirt, sutures)
- Immune reactions
- Infections (bacterial, viral, parasitic) and microbial toxins
- Tissue necrosis (any cause)
- Trauma (blunt and penetrating)
- Physical and chemical agents (e.g., thermal injury, e.g., burns or frostbite, irradiation,
environmental chemicals).
Give 6 clinical signs of inflammation
- Rubor = redness
- Calor = heat
- Tumour = swelling
- Dolor = pain
- Loss of function – this enforces rest and reduces the chance of further damage (this sign was
added more recently by Virchow).
1) What is the first thing that happens when inflammation occurs?
a brief moment of vasoconstriction which is swiftly followed by vasodilatation of the arterioles (small arteries).
What brings about vasodilation of the arterioles in inflammation?
Vasoactive mediators such as histamine (many other mediators that also cause vasodilatation).
1) What happens during arteriole dilation?
2) Why does vasodilation in arterioles occur in inflammation?
- Flow accelerates in the capillaries and capillary
pressure rises.
2) These changes increase the delivery of fluid and leucocytes to the area of injury.
1) What is the second step that occurs in inflammation? (following the dilation of arterioles)
2) What does this cause ?
1) Walls of the venules become leaky and plasma can escape through tiny gaps between endothelial cells
2)
- An increased haematocrit within the venules and increased resistance to blood flow within them.
- This stops blood outflow from the area of injury and there is increased pressure upstream.
- The lumens of the upstream vessels thus dilate and blood flow slows down.
- The increased pressure within the vessels results in greater exudation of fluid into the tissue spaces thus delivering plasma proteins to the site of injury.
What is a really important substance in the early changes in inflammation?
Histamine
1) What group does histamine belong to?
2) Name another substance than belongs to this group
1) a group of chemical mediators called vasoactive amines
2) Serotonin
What are usually the first mediators to appear during inflammation?
Vasoactiveamines
Many mediators are not available immediately from performed supplies during inflammation.
Name some mediators that are already present within cells in the tissues and platelets
Histamine and serotonin
1) Where is histamine stored before release?
2) Where is serotonin stored before release?
1) in the granules of mast cells, basophils and platelets
2) In the granules of platelets
Name some stimuli that can warrant the release of histamine (3)
- Physical damage
- Immune reactions
- Complement components
What does histamine cause in acute inflammation?
What does serotonin cause?
1)
- Produces pain
- Arteriolar dilatation
- Venular leakage (increased permeability).
2) The vascular effects are similar to those of histamine
Why does fluid leakage occur in acute inflammation?
- The fluid leakage occurs as histamine causes endothelial cells to contract and pull apart.
- This creates gaps through which plasma proteins can pass.
What are prostaglandins?
substances produced in inflammation from cell membrane phospholipids
What do prostaglandins do? (3)
- Cause vasodilation
- Make the skin more sensitive to pain
- Cause fever
1) How can the production of prostaglandins be blocked?
2) How does this work?
1) By aspirin and NSAIDs
2) They inhibit cyclo-oxygenase, the enzyme that produces prostaglandins from arachidonic acid).
What effect to aspirin and NSAIDs have on the body?
How?
Reduce pain and swelling by blocking the production of prostaglandins
Name 2 other substances that have vasoactive properties
leukotrienes and bradykinin
What are the effects of bradykinin?
produces pain and increased vascular permeability.
1) How does acute inflammation throw off the equilibrium of fluid exchange in the microcirculation?
2) Which law describes the forces involved in this equilibrium?
1)
- In acute inflammation, arterioles, under the direction of chemical mediators, dilate and venules, also under the direction of chemical mediators, become leaky as the endothelial cells contract and create gaps.
2) Starling’s law
What forces are involved in the equilibrium of fluid exchange?
- Capillary pressure
- Interstitial free fluid pressure
- Plasma colloid osmotic pressure
- Interstitial fluid colloid osmotic pressure.
1) Describe the usual way that capillaries and venues act and the force involved
2) In the usual case, what is the main force driving fluid out of the vessels?
3) What is the main force driving fluid back into the blood?
4) Describe how this changes in acute inflammation
- In the usual state, endothelium of the capillaries and venules acts as a semipermeable membrane, allowing escape of water and electrolytes but retaining plasma proteins hence the exchanges between the blood and tissue spaces depends on the four forces listed above.
2) The hydrostatic pressure of the blood
3) The colloidal osmotic pressure of the plasma proteins.
4) In acute inflammation:
- The semipermeable membrane becomes leaky
- The main force driving the fluid out of the vessels is increased (arterioles dilate increasing
capillary pressure) - The main force driving fluid back into the blood is reduced as plasma proteins escape into the
tissue spaces raising the osmotic pressure there so that it roughly equals that of blood.
In acute inflammation, the balance of starling’s forces is altered. Describe what this results in
- The net flow of fluid (with its plasma proteins) out of the vessels into the tissue spaces.
Describe 2 main functions of (the abundant) tissue fluid/exudate
- Delivering plasma proteins to the site of injury
- Excess tissue fluid drains from the tissues in the lymphatics taking with it micro-organisms and antigens which are thus presented to the immune system within the lymph nodes.
Name and describe the 3 defensive proteins found in tissue fluid (exudate)
- Opsonins – which coat foreign materials and make them easy to phagocytose.
- Complement – a group of proteins that are assembled locally to produce a bacteria- perforating structure (see below).
- Antibodies – bind to the surface of micro-organisms and also act as opsonins.
1) Name and describe the 2 types of tissue fluid
2) What kind of tissue fluid develops in inflammation?
1)
- Exudate (protein rich)
- Transudate (protein poor)
2) Exudate
1) What is a transudate?
2) What does it occur with?
3) Give an example of a condition that it is seen in
1) an ultrafiltrate of plasma
2) occurs with normal vessels (i.e., there are no gaps caused by endothelial cell contraction).
3) conditions such as heart failure when there is increased capillary hydrostatic pressure.
List some chemical mediators that induce vascular leakage and state where they are found (4)
- Histamine (found in mast cells and platelets)
- Serotonin (found in mast cells and platelets)
- Bradykinin (formed from a plasma precursor)
- The complement components C3a, C4a and C5a (also formed from plasma precursors).
What is the primary type of leucocyte involved in acute inflammation?
Neutophil
1) Where are neutrophils only found, normally?
2) What does their presence in tissue indicate?
1) only found in the blood and bone marrow
2) their presence in the tissue indicates invasion by bacteria or some other parasite and/or tissue injury.
1) What is the lifespan of neutrophils?
2) What kind of cells are they?
1) 12- 20 hours and
2) an end cell - they cannot multiply.
What does each neutrophil contain?
about 2,000 granules and these contain bactericidal substances.
How do neutrophils act?
Neutrophils escape from blood vessels into tissue spaces in response to chemical ‘calls’ originating from bacteria, injured cells or other inflammatory cells.
