Inflammatory Response Flashcards
Inflammation
Destroy infectious and injurious organisms
Block site of infection to limit damage
Stimulates the immune response (3-4 days)
Stimulates tissue healing
Inflammationcharacteristics of IR
Occurs in vascular tissues Immediate anywhere between minutes to a few hours Nonspecific No memory Self limitating
Cytokines and mediators
INflammatory chemicals that can affect anything, host and non-host
Cells of IR
WBC’s
Endothelial cells
And platelets
Chemicals of IR
Cytokines, vasoactive inflammatory mediators, and anti-inflammatory mediators
Use them to communicate between WBC’s
Plasma protein systems IR
Complement, clotting, and kinin systems
Activation of IR
Trauma to cell membrane
Ex.) hypoxic injury, chemical injury, thermal injury, radiation, infection, immmune injury
*****Mast cells
Cells of IR
Most important activator Of the local IR
Location: tissue not blood
Activation of mast cells
Local cellular injury
Bacterial endotoxin
Complement proteins
Immunologic factors
Function of mast cells
Degranulation
Release of preformed chemicals such as: histamine
Synthesis of mediators: arachadonic acid
Histamine:
Major chemical
Vasodilation
Increased capillary permeability
Non-vascular smooth muscle contraction
Vasodilation
Increases blood flow
Quick and temporary vasoconstriction
Caused by relaxing of vascular smooth muscle cells in blood vessels
Increased capillary permeability
Plasma, proteins, etc… leave capillaries to go to the sight of infection
Non-vascular smooth muscle contraction
When they are not in the blood vessels GI tract (cramping from an infection in stomach causing you to throw up) Bronchi constriction
Synthesis of mediators
AA metabolites
- leukotrienes
- prostaglandins
Leukotrienes
Same as a histamine actions
Synthesized in mast cells
Released near capillaries would cause increase of cap permeability
Released in lungs would cause vasoconstriction due to it not being a blood vessel
Benadryl
Prostaglandins
Histamine and pain
Synthesized in mast cells
Chemical that causes pain
Counteracted by aspirin, ibuprofen, and Tylenol
Basophils
Similar to mast cells and they release histamine and leukotrienes into the blood stream
Also releases heparin(blood thinner)
Neutrophils/bands
Arrive during acute phases of inflammation (6-12 hours)
One of the first WBC’s to the sight
Phagocytosis of debris and infection
Eosinophils
Release chemicals that control inflammation
Histamine is inactivated by histaminase
Phagocytosis of parasites
Involved in allergic responses
High eosinophil countr
High count then that might mean that there is a parasitic infection or and allergic reaction happening
Monocytes/macrophages
Released into bloodstream by the bone marrow as a monocytes
Once it has reached the infected tissue then it matures to a macrophage
They don’t side right away can stay for long periods of time to fight the next infection
Phagocytosis of bacteria and debris
Complement system
10% of proteins Vasodilation Opsonizatin Chemotaxis Cell lysis
Opsonization
Bound onto outside of bacteria so that it is attractive to the phagocyte. Without it there will be no recognition
Chemotaxis
The release of chemicals that attract other histamine circling, chemical road map
Clotting system
Produces fibrin
Fibrin
Forms a meshwork to stop bleeding
Limits infection
Forms framework for scar tissue formation
Heat and redness
The blood flow (vasodilation) is causing the heat and redness
How close it is to the surface will determine the heat and redness