2.5 Inflammation and adhesion Flashcards Preview

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Flashcards in 2.5 Inflammation and adhesion Deck (87)
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31

exudate

fluid accumulation in body cavity with high protei/ specific gravity

32

edema

interstitial fluid accumulation (may be transudate or exudate)

33

purulent

pus

34

exudate in lungs

pneumonia

35

transudate in lungs

heart failure

36

duet to normal laminar flow and arterial and venou pressure

hydrostatic pressure forces fluid out and osmotic pressure draws fluid back in but only 80%. The other 20% goes to lymphatics

37

with increased flow during vasodialation you get

increased hydrostatic pressure and transudate

38

when endothelial cells get "leaky" you get

exudate - endothelial cells have increased permeability for proteins increasing the osmotic pressure

39

hemoconcentration and stasis

loss of lamnar flow, rolling, attachment, transmigration

40

factors affecting vascular permeability (leakage)

endothelial gap formation,
endothelial retraction,
increasaed trancytosis,
direct injury,
delayed prolonged leakage (like sunburn),
leukocyte-mediated damage,
leakage from new blood vessels

41

Endothelial gap formation

most common mechnaism of non damage active vascular leakage

42

endothelia gap formation is the major effecto of mediators such as

histamine, bradykinin, leukotrienes, substance P

43

where does endothelial gap formation occur

exclusively in post capillary venules of 20 to 60 um in diameter (receptor density)

44

how long does endothelia gap formation last

rapid and short lived - immediate transient response

45

cytoskeletal reorganization/endothelial retraction

cytoskeleton changes and endothelial cells retract from one another

46

how is endothelial retraction induced

by cytokines such as Il1 and TNF alpha or hypoxia and sublethal injury

47

how long does cytoskeletal reorganization take

endothelial retraction is delayed 4-6 hrs and lasts longer up to 24 hrs

48

is endothelial retraction localized

not perfectly localized bc injury can induce it

49

increased trancytosis

movement of fluid and material across endothelial cytoplasm, occurs through clusters of uncoated vesicles and vacuoles called the vesiculovacular organelle

50

how is trancytosis induced

vascular endothelial growht factor (VEGF) - also may be induced by histamine

51

Direct endothelial injury resulting in necrosis results in

leakage from damaged vessels, immediate and long lasting (immediate sustained response), happens in small and large vessels, and is associated with platelet aggregation and thrombosis

52

Delayed prolonged leakaged

2-12 hours lasting for hours to dayes, occurs at venules and capilaries

53

how is delayed prolonged leakage induced

by mild thermal burns, ionizing and UV radiation (sunburn--get pain not just on skin but all over, chills..)

54

delayed prolonged leakage mechanism

maybe apoptosis from DNA damage

55

leukocyte mediated damage

leukocytes adhere to activated or damaged endothelium, secrete reactive and toxic products that damage self as well as microbes, location dependent on why and where leukocytes bind

56

leakage from new blood vessels

during repair angiongenesis occurs and new vess are nleaky before new endothelial cells fully differentiate and form gap junctions, VEGF induces increased vascular permeability, new endothelium has an increased density of receptors for vasoactive signals

57

what allows for pure collection of white exudate (pus)

mediators allowing collection of neutrophoils - so don't need vessel trauma for inflammation

58

Margination

a hemodynamic effect where lamina flow of leukocytes changes to peripheral and contacto vascular wall duing stasis

59

rolling-adhesion-extravasation occurs by

modulating various adhesion molecules on the surface of endothelial cells and leukocytes

60

rolling-adhesion-extravasation is mediated by

secreated or formed inflammatory mediators