Inflammation (Week 1) Flashcards
Inflammation designed to:
Break down and remove dead cells
Inactivate the injurious agent
Initiate healing of tissues
Inflammation involves responses from what systems?
Vascular
Humoral
Neurologic
Cell
Humeral
Chemical components from cellular reactions carried in the blood by plasma and/or tissue fluid
Acute inflammation
Lasts hours to a few days
Rapid in onset
Stops when harmful stimulus is removed
Can become chronic if inflammatory stimulus is not removed
How can acute inflammation become chronic?
Poor rehab/tx can lead to alteration of joint structure and lead to more inflammation
Goal of acute inflammation
Deliver white blood cells and plasma proteins (antibodies) to the area of injury or infection
Why is chronic inflammation bad?
Inflammation can damage healthy tissue (leakage of hypochlorite & peroxynitrite)
How are WBCs delivered to injury/infection site
- Vasodilation
- Increased permeability of capillary walls
- Chemotaxis
How does vasodilation help get WBCs to injury/infection site?
- Allows increased blood flow to area
- Reduces speed at which blood travels
- Sets up hemodynamic change that causes WBCs to collect along endothelium
- Gives WBCs more time to move thru capillary wall, resulting in more WBCs getting to site
Chemotaxis
Chemically mediated movement of WBCs
- along chemical gradient
- bacteria: produce peptides that are chemoattractants
- injured tissue: produces compounds (cytokines, IL-8, and leukotriene B4) that attach to WBCs and stimulate their migration
Inappropriate or poorly controlled inflammation is thought to contribute to:
Rheumatoid arthritis Atherosclerosis Type II diabetes Some types of cancer Lung fibrosis Emphysema Allergic reactions
What to white blood cells do?
Destroy foreign and dead tissues
What are Toll-like receptors and where are they found
Detect presence of infection
Found on surface of WBCs
What stimulates acute inflammation?
infection
tissue necrosis/injury
foreign bodies
immune reactions
What initiates vasodilation
histamine and nitric oxide acting upon vascular smooth muscle
How is vascular permeability increased?
histamine (primarily) causes endothelial cells contract, increasing the size of pores
how is edema drained from area
lymphatics; results in swelling of lymph nodes
what is an indication of infection
red streaks near a wound typically moving proximally; these red streaks will follow the course of lymph vessels
what do some WBCs that encounter microbes/dead tissue release?
tumor necrosis factor (TNF)
interleukin-1 (IL-1)
chemokines
what do TNF and IL-1 do?
enhance immune response to a microbea
what do chemokines do?
attract more WBCs to area
what are DMARDs
Disease Modifying Anti-Rheumatic Drugs (drug class)
- Slows, stops, and may reverse immunologic attack on healthy tissue
- 2 Classes: biologic & classic
how do biologic DMARDs work?
inhibit TNF or some interleukins
How do WBCs recognize dead tissue?
receptors on WBCs recognize components released by injured/dead tissue: platelet activating factor, prostaglandins, leukotrienes
immune complex
antibody attached to something that does not belong
opsonization
signal for the WBCs that the item the antibody is attatched to should be phagocytosed
Process of WBC attaching to and phagocytosing object
- immune complex formed (antibody attached to something that does not belong)
- immune complex attaches to receptor on WBC
- attachment activates WBC
- Phagocytosis occurs
- chemokines released to attract more WBCs
- chemotaxis
what is the phagocytosed particle exposed to?
hydrogen peroxide + myeloperoxidase (enzyme) –> hypochlorite (active ingredient in bleach)
nitric acid–> peroxynitrite (highly corrosive)
2 types of mediators of inflammatory response
cell derived (humeral compounds) plasma protein derived (from immune system & clotting cascade system)
cell derived mediators of inflammatory response
histamine serotonin phosphatidyl inositol arachidonic acid prostaglandins
histamine
released by mast cells when they undergo degranulation
cause vasodilation
cause increased capillary wall permeability
serotonin
released from platelets when they aggregate
cause vasodilation
cause increased capillary permeability
phosphatidyl inositol
part of every cell membrane
released into tissue fluid
acted upon by phospolipase –> arachidonic acid
arachidonic acid
can be converted into prostglandins, leukotrienes, and lipoxins
prostaglandins
converted from arachidonic acid by COX enzymes
COX1=good prostaglandins (necessary for normal tissue fxn)
COX2=bad prostaglandins (stimulation of pain, increased dilation and permeability of vessels)
COX3=not fully understood
how do steroids reduce inflammation?
inhibit phospholipase (converts phosphatidyl inositol –> arachidonic acid)
