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Flashcards in Inflammation Deck (67):
1

This is a protective response to rid the body of the cause of cell injury and the resultant necrotic cells that cell injury produces

Inflammation

2

name the 4 cells/molecules involved in inflammation

1) leukocytes
2) endothelial cells
3) cells & extracellular matrix of the surrounding tissue
4) plasma cells/proteins

3

these are mediators released by platelets,inflammatory cells, endothelial cells

plasma cells/proteins

4

what releases plasma cells/proteins

1) platelets
2) inflammatory cells
3) endothelial cells

5

types of inflammation

acute inflammation
chronic inflammation

6

rapid onset & short duration (hours to few days)

acute inflammation

7

characterized by:
1) exudation of of fluid & plasma proteins (edema) &
2) the emigration of leukocytes, predominantly neutrophils (PMN)

acute inflammation

8

longer time course (days to years)

chronic inflammation

9

involves different cell types compared to acute inflammation

chronic inflammation

10

cell types involved in chronic inflammation

lymphocytes
macrophages

11

cell types involved in acute inflammation

plasma cells/proteins
leukocytes (neutrophils/PMN)

12

when tissue repair coexists with tissue destruction

chronic inflammation

13

cardinal signs of acute inflammation

-calor (heat)
-rubor (redness)
-tumor (swelling)
-dolor(pain)
-loss of motion

14

causes of acute inflammation

-infection
-trauma
-physical & chemical agents
- necrosis (Myocardial Infarction)
- foreign bodies
- immune reaction (2ndary to allergic rxn; endogenous & exogenous)

15

stages of acute inflammation

1) vasodilation
2) increased vascular permeability
3) movement of WBCs from blood vessels into soft tissue at the site of inflammation

16

occurs through a release of mediators

vasodilation

17

happens after a transient vasoconstriction

vasodilation

18

mediators released during vasodilation

1) histamine
2) prostaglandin i2 (resp. for fever)
3) nitric oxide

19

what mediator is responsible for fever

prostaglandin

20

vasodilation first involves the?

arterioles

21

vasodilation= arterioles --> leading to ______

opening of new capillary beds in the area

22

increased blood flow caused by __-

heat

23

increased blood flow caused by heat results to?

erythema/redness

24

vasodilation increases the ___?

hydrostatic pressure

25

increase in hydrostatic pressure due to vasodilation causes what?

slowing/sludging of blood flow

26

slowing of blood flow causes ?

migration of leukocytes along the wall of blood vessels

27

increased leakiness of blood vessels

stage 2= increased vascular permeabilty

28

outpouring of protein-rich fluid into the extravascular tissues (edema)

increased vascular permeability

29

the hallmark of acute inflammation

increased vascular permeability

30

allows fluid to cross into the interstitial tissue

increased vascular permeability

31

fluid crossing into the interstitial tissue due to increased vascular permeability causes

increased protein levels in the interstitial tissue

32

increased interstitial protein levels in interstitial tissue, causes an ______ osmotic pressure in the interstitial tissue

decreased!!!

33

this causes fluid to flow out of the vessel resulting to edema to interstitial fluid

increased vascular permeability

34

mediators of increased vascular permeability

1)histamine
2)bradykinn
3)leukotrienes (C4, D4, E4)

35

name the 4 mechanisms of increased vascular permeability

1) endothelial cell contraction
2) endothelial cell retraction
3) direct endothelial injury
4) delayed prolonged response

36

these are physiologic mechanisms and are due to mediators
(referring to the type of mechanism of increased vascular permeability)

endothelial contraction & retraction

37

these are pathologic mechanisms due to damaging agents not under the body's control
(referring to the type of mechanism of increased vascular permeability)

direct endothelial injury

38

contraction of endothelial cells result to

increase in ___? spaces

39

mediators of endothelial cell contraction

1) histamine
2) bradykinin
3) leukotrienes

40

time course of endothelial cell contraction

immediate;short (30 minutes)

41

mediators of endothelial cell retraction

1) TNF
2) interleukins

42

occurs due to structural rearrangement of cytoskeleton

endothelial cell retraction

43

time course of endothelial cell retraction

4-6 hours; delayed response

44

mediators of direct endothelial injury

bacterial enzyme

45

occurs due to endothelial cell necrosis

direct endothelial injury

46

time course of direct endothelial injury

immediate; immediate sustained response

47

occurs due to UV light, xray, and mild termal injury

delayed prolonged response

48

uncertain mechanism

delayed prolonged response

49

pushes fluid from vessel to tissue

HP

50

attract fluid back to blood vessels

albumin

51

takes care of remaining fluid in interstitium

lymphatics

52

fluid only

filtrate

53

components of protein-rich fluid

fluid + albumin

54

what is the fist stage of acute inflammation

vasodilation

55

what is the 2nd stage of acute inflammation

increased vascular permeability

56

what is the 3rd stage of acute inflammation

movement of WBCs from blood vessels into soft tissue @ site of inflammation

57

steps in the 3rd stage of acute inflammation

"RPT"
1) rolling
2) pavementing
3) transmigration

58

the process by which WBCs are drawn to the site of acute inflammation

CHEMOTAXIS

59

loose, intermittent contact of WBCs with endothelium

rolling

60

partially due to margination of WBC from stages? of blood

rolling

61

tight, constant contact of WBC with endothelium

pavementing

62

WBC crossing through the endothelial layer

transmigration

63

particles that bind to foreign materials & signals leukocytes to remove it

opsonin

64

types of opsonins

1) IgG
2) C3b
3) Collectins

65

type of opsonin that is recognized by Fc receptor of WBC

IgG

66

type of opsonin that is recognized by Cr 1, 2 &3 of leukocyte

C3b

67

type of opsonin that is recognized by C2q on leukocyte

collectins