2/5/13- inflammation

Question 1

hypersensitivity type I

1. what cells are involved?
2. what is the first thing that happens? what does this do?
3. what happens after that? what does this cause?

Answer 1

1. mast cells
2. vasoconstriction: reduces blood flow giving the cells time to work locally
3. vasodilation: establishes blood flow in order to provide nutrient to damaged tissue

Question 1

what happens after vasodilation (or actually d/t vasodilation)?

Answer 1

1. exudative stage occurs from excess fluid causes edema which flushes out debris, toxins etc.

Question 2

1. what activates the mast cell?

2. what happens to cause the mast cell to degranulate (regarding FC receptor)?

Answer 2

1. the “arming” of the mast cell with IgE (antibody)
2. 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”

Question 3

what else (besides antigen-antibody complex) can activate the mast cell?

Answer 3

1. any stage of complement cascade
2. chemical activation: when O2 radicals, toxins, hydrogen peroxides etc. are released; tissue damage releases K+ which can also activate mast cells
3. physical activation: pressure or jarring of mast cells (getting hit) can cause degranulation

Question 4

what can cause toxic shock?

Answer 4

chemicals in the body such qas O2 radicals, toxins, hydrogen peroxides

Question 5

1. what is the key chemical released with mast cell degranulation
2. how many histhamine receptors are there?

Answer 5

1. histhamine

2. 2; H1 & H2

Question 6

what stabilizes the mast cell membrane to keep it from degranulationg?

Answer 6

antihisthamine

Question 7

1. what does histhamine (H1 receptor) do?
2. what is this process (when wbcs come thru) called?
3. which receptor initiates this process?

Answer 7

1. 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.
2. DIAPEDEIS
3. H1 (positive feedback)

Question 8

what other chemicals (besides histhamine) are released from mast cell degranulation?

Answer 8

1. neutrophil chemotactic factor (d/t positive feedback mechanism of histhamine H1 receptor)
2. eosinophil chemotactic factor (not d/t histhamine)

Question 9

how does vasoconstriction help diapedesis?

Answer 9

slows blood flow and keeps WBCs from whipping by the site where they are needed

Question 10

1. what kind of “crine” feedback is neutrophil chemotactic factor
2. what does this mean

Answer 10

1. autocrine
2. (self regulating), the release of neutrophil chemotactic factor from the mast cell causes the mast to secrete more neutrophil chemotactic factor

Question 11

what happens to someone who is prone to inflammatory asthma?

Answer 11

1. allergen binds to IgE and activates the 2nd messenger system
2. mast cell releases eosinophil chemotactic factor
3. eosinophils migrate to site and are pulled into airway, stimulating inflammation

Question 12

H1 will also stimulate what other inflammatory hormones?

Answer 12

1. Prostaglandin E

2. Leukotrienes

Question 13

what does the negative feedback of H2 cause (4 things)

Answer 13

• suppression of immune cells (lymphocytes and eosinophils),
• decrease production of neutrophil chemotactic factor,
• stabilize mast cell and
• decrease degranulation

Question 14

1. what do leukotrienes do?

2. what do leukotrienes mimic?

Answer 14

1. do what histhamine does, vasodilation and mast cell activation
2. leukotrienes mimic histhamine (reactions), but at a slower pace (and last longer)

Question 15

what does prostaglandin E do?

Answer 15

1. (the same as histhamine) increases capillary permiability BUT ALSO causes vasoconstriction of venule
2. this causes backpressure on capillaries (increases hydrostatic pressure and filtering=increases exudate; edema)

Question 16

what do leucotrienes and prostaglandin E contribute to?

Answer 16

pain (but they dont cause it, they accentuate it)

Question 17

Hageman factor;

1. what factor is it?
2. what does it become when activated
3. an extrinsic activator called _____ changes it to ____
4. it(_____) activates ____, which turns ___ into _____

Answer 17

1. XII
2. hageman XII becomes XIIa when activated
3. extrinsic activator called Lipoprotein Thromboplastin turns XIIa to Stuart factor
4. Stuart Factor activates Prothrombin Activator which turns Prothrombin it into Thrombin

Question 18

Thrombin activates _____ which becomes ____ and starts the clotting process
____ is the mortar; ____ are the bricks

Answer 18

fibrinogen; fibrin

fibrin is the mortar, platelets are the bricks

Question 19

Hageman activates another cascade, what is it called?

1. hageman turns ___ ______ to ______ which is an____
2. _____ converts ____ to _______

Answer 19

• -kallecrien-kininogen-bradykinin pathway
  1. hageman turns pre kallicrien to kallicrien(an enzyme)
  2. Kallicrien converts Kininogen to bradykinin

Question 20

Bradykinin has multiple functions:what does Bradykinin do?

Answer 20

causes vasodilation, increase capillary permeability, actually causes pain

Question 21

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?

Answer 21

1. Hageman’s factor helps plasminogen activator
2. thrombin helpss plasminogen activator
3. kallikrien helps plasminogen activator
4. preventing excess clotting is of utmost importance and clotting is a positive feedback that wont stop itself-it has to BE stopped

Question 22

1. what activates complement (5 things)

2. why can so many things activate compliment?

Answer 22

1. plasmin, hageman, kallikrien, gram negative bacteria & antigen antibody complex
2. because there are alot of pathogens and “mimics” trying to get into our cells

Question 23

what is the order of the CLASSIC complement cascade?

Answer 23

1. starte with antibody then goes to- C1; then C4,C2,C3; then C5-C9

Question 24

what is the order of ALTERNATE complement cascade?

Answer 24

gram negative gets bound by C3; then C5-C9 come and attack

Question 25

1. what are the attack proteins?
2. where are they made?
3. what does liver disease do?

Answer 25

1. C5-C9
2. made in liver
3. liver disease causes for less attack proteins to be made

Question 26

what is the cellular component of inflammation?

Answer 26

1.endothelial cells undergo contraction and cause spaces

Question 27

when you get a cut, what causes the vessel to vasoconstrict?

Answer 27

thromboxane from the platelets

Question 28

what causes white blood cells to migrate thru the space created by contracted epithelial cells?

Answer 28

WBCs are recruited by chemotactic factors (complement, eosinophil and neutrophil chemotactic factors)

Question 29

cytotoxic Ts do “drive by shootings” with what chemical?

Answer 29

perforin

Question 30

1. what is ICAM?
2. what is its function?
3. what does surface of endothelium look like after ICAM?

Answer 30

1. intracellular adhesion molecules that sit on endothelial cells
2. ICAM is like velcro that allows WBCs to marginate and stick to the surface of the endothelium
3. coblestone road

Question 31

what cells are responsible for healing; neutrophils or macrophages?

Answer 31

macrophages

Question 32

what do the marginated cells do next?

Answer 32

slip thru the gaps (diapedesis) and start phagocytocyze

Question 33

what do neutrophils have that they release?

Answer 33

proteolytic enzymes, o2 radicals, peroxides and hypochlorite (chlorox bleach)

Question 34

what do monocytes become?

Answer 34

macrophages

Question 35

1. what do eosinophils do?

2. who calls them in?

Answer 35

1. they are the clean up crew, kill worms with major basic protein (cuts thru worm cuticle)
2. mast cells