2/5/13- inflammation Flashcards
hypersensitivity type I
- what cells are involved?
- what is the first thing that happens? what does this do?
- what happens after that? what does this cause?
- mast cells
- vasoconstriction: reduces blood flow giving the cells time to work locally
- vasodilation: establishes blood flow in order to provide nutrient to damaged tissue
what happens after vasodilation (or actually d/t vasodilation)?
- exudative stage occurs from excess fluid causes edema which flushes out debris, toxins etc.
- what activates the mast cell?
2. what happens to cause the mast cell to degranulate (regarding FC receptor)?
- the “arming” of the mast cell with IgE (antibody)
- anything that binds to the IgE causes the IgE to change shape; this causes the FC receptor to change shape which signals a second messenger which causes the mast cell to “degranulate”
what else (besides antigen-antibody complex) can activate the mast cell?
- any stage of complement cascade
- chemical activation: when O2 radicals, toxins, hydrogen peroxides etc. are released; tissue damage releases K+ which can also activate mast cells
- physical activation: pressure or jarring of mast cells (getting hit) can cause degranulation
what can cause toxic shock?
chemicals in the body such qas O2 radicals, toxins, hydrogen peroxides
- what is the key chemical released with mast cell degranulation
- how many histhamine receptors are there?
- histhamine
2. 2; H1 & H2
what stabilizes the mast cell membrane to keep it from degranulationg?
antihisthamine
- what does histhamine (H1 receptor) do?
- what is this process (when wbcs come thru) called?
- which receptor initiates this process?
- increases capillary permeability by causing endothelial cells to contract inwardly (leaving spaces between cells) and opening up the paracellular space that fluid, exudate, and blood cells can come in.
- DIAPEDEIS
- H1 (positive feedback)
what other chemicals (besides histhamine) are released from mast cell degranulation?
- neutrophil chemotactic factor (d/t positive feedback mechanism of histhamine H1 receptor)
- eosinophil chemotactic factor (not d/t histhamine)
how does vasoconstriction help diapedesis?
slows blood flow and keeps WBCs from whipping by the site where they are needed
- what kind of “crine” feedback is neutrophil chemotactic factor
- what does this mean
- autocrine
- (self regulating), the release of neutrophil chemotactic factor from the mast cell causes the mast to secrete more neutrophil chemotactic factor
what happens to someone who is prone to inflammatory asthma?
- allergen binds to IgE and activates the 2nd messenger system
- mast cell releases eosinophil chemotactic factor
- eosinophils migrate to site and are pulled into airway, stimulating inflammation
H1 will also stimulate what other inflammatory hormones?
- Prostaglandin E
2. Leukotrienes
what does the negative feedback of H2 cause (4 things)
- suppression of immune cells (lymphocytes and eosinophils),
- decrease production of neutrophil chemotactic factor,
- stabilize mast cell and
- decrease degranulation
- what do leukotrienes do?
2. what do leukotrienes mimic?
- do what histhamine does, vasodilation and mast cell activation
- leukotrienes mimic histhamine (reactions), but at a slower pace (and last longer)
what does prostaglandin E do?
- (the same as histhamine) increases capillary permiability BUT ALSO causes vasoconstriction of venule
- this causes backpressure on capillaries (increases hydrostatic pressure and filtering=increases exudate; edema)
what do leucotrienes and prostaglandin E contribute to?
pain (but they dont cause it, they accentuate it)
Hageman factor;
- what factor is it?
- what does it become when activated
- an extrinsic activator called _____ changes it to ____
- it(_____) activates ____, which turns ___ into _____
- XII
- hageman XII becomes XIIa when activated
- extrinsic activator called Lipoprotein Thromboplastin turns XIIa to Stuart factor
- Stuart Factor activates Prothrombin Activator which turns Prothrombin it into Thrombin
Thrombin activates _____ which becomes ____ and starts the clotting process
____ is the mortar; ____ are the bricks
fibrinogen; fibrin
fibrin is the mortar, platelets are the bricks
Hageman activates another cascade, what is it called?
- hageman turns ___ ______ to ______ which is an____
- _____ converts ____ to _______
- -kallecrien-kininogen-bradykinin pathway
1. hageman turns pre kallicrien to kallicrien(an enzyme)
2. Kallicrien converts Kininogen to bradykinin
Bradykinin has multiple functions:what does Bradykinin do?
causes vasodilation, increase capillary permeability, actually causes pain
1,2,3. what 3 factors work with plasminogen activator to keep clotting in check (to help it in turning plasminogen to plasmin)?
4. why do you need 3 factors to prevent excess clotting?
- Hageman’s factor helps plasminogen activator
- thrombin helpss plasminogen activator
- kallikrien helps plasminogen activator
- preventing excess clotting is of utmost importance and clotting is a positive feedback that wont stop itself-it has to BE stopped
- what activates complement (5 things)
2. why can so many things activate compliment?
- plasmin, hageman, kallikrien, gram negative bacteria & antigen antibody complex
- because there are alot of pathogens and “mimics” trying to get into our cells
what is the order of the CLASSIC complement cascade?
- starte with antibody then goes to- C1; then C4,C2,C3; then C5-C9
what is the order of ALTERNATE complement cascade?
gram negative gets bound by C3; then C5-C9 come and attack
- what are the attack proteins?
- where are they made?
- what does liver disease do?
- C5-C9
- made in liver
- liver disease causes for less attack proteins to be made
what is the cellular component of inflammation?
1.endothelial cells undergo contraction and cause spaces
when you get a cut, what causes the vessel to vasoconstrict?
thromboxane from the platelets
what causes white blood cells to migrate thru the space created by contracted epithelial cells?
WBCs are recruited by chemotactic factors (complement, eosinophil and neutrophil chemotactic factors)
cytotoxic Ts do “drive by shootings” with what chemical?
perforin
- what is ICAM?
- what is its function?
- what does surface of endothelium look like after ICAM?
- intracellular adhesion molecules that sit on endothelial cells
- ICAM is like velcro that allows WBCs to marginate and stick to the surface of the endothelium
- coblestone road
what cells are responsible for healing; neutrophils or macrophages?
macrophages
what do the marginated cells do next?
slip thru the gaps (diapedesis) and start phagocytocyze
what do neutrophils have that they release?
proteolytic enzymes, o2 radicals, peroxides and hypochlorite (chlorox bleach)
what do monocytes become?
macrophages
- what do eosinophils do?
2. who calls them in?
- they are the clean up crew, kill worms with major basic protein (cuts thru worm cuticle)
- mast cells
