MOD - Lecture 3 Flashcards
Name 3 facts of acute inflammation
Evolves over hours or days
Innate
Stereotyped
How long does chronic inflammation take to evolve?
Weeks, months or years
What suffix is used to indicate inflammation of tissue or organ?
Itis e.g. Appendicitis
Describe acute inflammation
Rapid response that aims to deliver mediators of host defence
Most defensive agents circulate in the blood in active form
When needed, delivered and activated
Leave the blood at site of injury
Why is fluid delivered to site of injury before leucocytes?
Fluid - within seconds
Leuocytes - minutes
As leucocytes can’t just pour out of vessels
What causes acute inflammation? (6)
Foreign bodies Immune reactions Infections Tissue necrosis Trauma Physical/chemical agents e.g burns, irritation
What are the clinical signs of acute inflammation? (5)
Rubor = redness Calor = heat Tumour = swelling Dollar = pain Loss of function - enforces rest and reduces chance of further damage
When does pain occur in acute inflammation?
When the specialised nerve endings are stimulated by mediators especially bradykinin
Why does swelling occur in inflammation?
Fluid and leucocytes take up space within the tissue
What forces are involved in Starlings Law equilibrium?
Capillary pressure
Interstitial free fluid pressure
Plasma colloid osmotic pressure
Interstitial fluid colloid osmotic pressure
Where is histamine stored?
Granules for mast cells, basophils and platelets
Histamine and serotonin are available immediately from preformed supplies
What does histamine produce in acute inflammation?
Pain
Arteriolar dilation
Venular leakage
How does histamine cause fluid leakage?
Causes endothelial cells to contract and pull apart.
This creates gaps through which plasma proteins can pass
How can you reduce pain and swelling?
Describe the mechanism.
What drugs are taken?
Block the production of prostaglandins
By inhibiting the enzyme (cyclo-oxygenase) that produces prostaglandins from arachadonic acid.
Aspirin
NSAIDs
What is the effect of bradykinin?
Pain
Increased vascular permeability
How does serotonin differ from histamine?
Serotonin produces fibroblasts
In relation to Starlings law, what is the main force driving fluid out of the vessels?
and back into the blood?
Hydrostatic pressure of the blood
Colloidal osmotic pressure of plasma proteins
How does excess fluid drain from the tissues?
Lympathics - excess fluid drawings from the tissues taking with it microorganisms and antigens which are presented to the immune system in the lymph nodes.
Lymph nodes draining a focus of inflammation can themselves become inflamed, swollen and painful. (Lympahedenitis)
What are the three defensive proteins in the exudate?
How do they work?
Opsonins - coat foreign material and make them easy to phagocytose.
Complement - proteins assembled locally to produce bacteria-perforating structure
Antibodies - bind to surface of microorganisms, also act as opsonins.
What is the protein rich and protein poor tissue fluid that develops in inflammation called?
Exudate - protein rich
Transudate - protein poor
Name the chemical mediators that induce vascular leakage?
Histamine & Serotonin (mast cells and platelets)
Bradykinin (formed from plasma precursor)
Complement components - C3a, C4a, C5a (formed form plasma precursors)
What is the primary type of leucocyte found in acute inflammation?
Where are they normally found?
What does their presence in the tissue indicate?
What type of cell are they?
Neutrophil
Blood or bone marrow
Invasion by bacteria or some other parasite or tissue injury
End cell - cannot multiply
What is chemotaxis?
Directional movement towards a chemical attractant
E.g. Clotting blood (fresh blood isn’t)
Activation of complement fragments C3a, C4a, C5a. All chemotactic - especially C5a.
Leukotriene produced by leucocytes