MOD 2 Acute Inflammation Flashcards
(35 cards)
Define ACUTE INFLAMMATION
The innate and stereotyped rapid response to cell injury, with the aim of delivering mediators of host defence (leukocytes & plasma proteins) to the site of injury.
What can cause acute inflammation?
Infection Foreign Bodies (e.g. splinters, dirt, sutures) Immune reactions Tissue necrosis Trauma Physical and chemical agents
What are the clinical signs of acute inflammation?
Rubor (red), Calor (hot), Tumour (swelling), Dolor (pain) & loss of function
What local mediator causes the pain associated with acute inflammation? What else causes pain?
Bradykinin. Histamine also causes pain.
Why does the site of acute inflammation swell?
Accumulation of leukocytes & fluid at the site.
What 3 steps can acute inflammation be broken down into?
- Change in blood flow
- Exudation of fluid
- Infiltration of inflammatory cells
What changes in blood flow are associated with acute inflammation?
HISTAMINE released from mast cells, basophils & platelets prompts VASODILATION of the arterioles leading to the site, causing an INCREASE IN BLOOD FLOW (rubber & calor)
What class of chemicals do serotonin (5HT) & histamine belong to?
Vasoactive amines
What are the effects of histamine?
Pain, vasodilatation and venular leakage
Describe how the changes in blood flow brought about by local mediators e.g. histamine cause an exudation of fluid
Increased capillary hydrostatic pressure because of arteriolar dilation. Venule walls become leaky due to gaps widening in the endothelium.
Thus resistance before the capillaries is decreased and after the capillaries is increased, causing greater exudation of fluid.
In the long term, the mediators responsible for the vasodilation switch from histamine to two others. What are they?
Bradykinin & Prostaglandins.
Prostaglandins are made in the cyclooxygenase pathway and thus their production can be reduced by prescribing aspirin.
What are the three main proteins present in the exudate?
Opsonins, complement and antibodies
What is the difference between an exudate and a transudate?
An exudate is rich in plasma proteins.
A transudate is largely fluid and plasma protein deprived This occurs when the vessel permeability has not been increased.
What is the role of Leukotrienes and how are they made?
Made from arachidonic acid, a product of phospholipid when acted upon by phospholipase.
The reaction requires the enzyme lipoxygenase.
Leukotrienes are PERMEABILITY INCREASERS
From which vessels does the exudate move out from in acute inflammation?
Venues & capillaries
What is the predominant immune cell type in acute inflammation?
Neutrophils
What are the key steps in a neutrophil arriving at the correct site and performing its function?
- Chemotaxis
- Activation
- Margination
- Rolling
- Adhesion
- Diapedesis
- Recognition-attachment
- Phagocytosis
- Killing
Describe CHEMOTAXIS
The movement of a neutrophil towards a chemical attractant (CHEMOTAXIN) e.g. a bacterial endotoxin.
Thrombin
Describe the appearance and function of neutrophils.
Phagocytosis
Trilobular nucleus
Finite number of granules, once used the cell dies
Cannot divide
Describe activation
Metabolic rate is increased
Begins on chemotaxin binding
Neutrophil becomes wedge shaped pointing in the direction of the stimulus
List some chemotaxins
FDPs Bacterial endotoxins clotted blood thrombin C3a, C4a, C5a
Define margination, rolling and adhesion
When the neutrophils adopt positions around the edge of the blood vessel cross section.
The neutrophils then ROLL along the wall, bound to SELECTINS
They then ADHERE to INTEGRINS (e.g. ICAM-1)
How do neutrophils leave the venule?
They don’t use endothelial gaps, they use COLLAGENASES to digest the basement membrane of the endothelium.
This process is called DIAPEDESIS & takes 3-9 minutes
Describe the process of recognition-attachment
The bacterium may have been OPSONISED by IgG antibody or C3b or the neutrophil will recognise antigens
