Week 2 - Acute inflammation Flashcards
(37 cards)
What is inflammation? What is its function?
response to injury of vascularised living tissue to deliver defensive material- leucocytes and plasma proteins to the site of injury protecting the body against infection and to clear damaged tissue initiating repairesponse to injury of vascularised living tissue to deliver defensive material- leucocytes and plasma proteins to the site of injury protecting the body against infection and to clear damaged tissue initiating repair.
Give three properties of acute inflammation
Innate, stereotyped and rapid
When is acute inflammation needed?
When local defenses are no longer adequate.
How do most defensive agents circulate?
In the blood in inactive form and are delivered/ activated when needed.
What must defensive agents be able to do?
leave blood vessel at the site without interrupting blood flow as this is needed at further sites
Give 6 causes of acute inflammation
Foreign bodies Immune reactions Infections and microbial toxins Tissue necrosis Trauma ( blunt and penetrating) Physical and chemical agents( thermal injury, environmental chemicals)
Give the 5 signs of acute inflammation and explain why
Rubor – redness caused by dilation of blood vessels
Color- heat caused by dilation of blood vessels
Tumour – swelling caused by fluid and leucocytes in tissue
Dolor – pain caused by specialised nerve endings stimulated by mediators - bradykinin
Loss of function which enforces rest and decreases chance of further damage
Give the first stage of formation of exudate
Vasoconstriction
Give the second step in the formation of exudate and what brings this about?
- Vasodilation of arterioles- brought about by vasoactive mediators histamine from mast cells and platelets, nitric oxide from macrophages and endothelium
What changes about the venule walls during exudate formation? What does this allow?
They become leaky allowing plasma to escape through
Loss of fluid from the venules leads to what?
Increased haemocrit within the venules and increased resistance to blood flow reducing it to further along venules and increased pressure upstream. This causes their lumens to dilate and reducing the blood flow speed.
The increased pressure in the venules leads to what?
Increased fluid into the tissues and therefore increased proteins to the site of injury.
What is generally the first mediator in acute inflammation?
Histamine
Where is histamine found usually?
Cells in the tissue and platelets. It is also stored in the granules of Mast cells and basophils.
What is histamine used as in the brain?
Neurotransmitter
What effects does histamine induce in acute inflammation?
Produces pain.
Causes arteriolar dilation
Venular leaking by causing endothelial cells to contract and pull apart allowing proteins to pass
What other mediator is similar to histamine in terms of the effects exerted? What other effect does it cause ?
Serotonin
Stimulates fibroblasts
What chemical mediator is made from cell membrane phospholipids?
Prostaglandins
What effects do prostaglandins have?
Vasodilation
Makes skin increase sensitive
Cause fever
What drugs block the production of prostaglandins? How?
Steriods - inhibit the phopholipases therefore cannot go from phospholipids to arachondonic acid
Aspirin and NSAIDs inhibit cyclo-oxygenases therefore cannot go from arachadonic acid to prostaglandin
What defensive proteins are found in the exudate? What are their functions?
Opsonins – coat foreign material and make them easy to phagocytose
Complement – group of proteins assembled locally to produce bacteria perforating structure
Antibodies – bind to surface of microorganisms – act as opsonins
Explain how lymphadenitis occurs
Excessive fluid drains from tissue in lymphatic taking with it microorganisms and antigens therefore presenting them to the immune system within lymph nodes – can become inflamed, swollen and painful – LYMPHADENITIS
Explain the difference between exudate and transudate
Rich in proteins - exudate
Low in proteins - transudate
When does transudate occur?
secondary to osmotic or hydrostatic imbalance across a vessel wall without increase in permeability
