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Histopathology > Inflammation > Flashcards

Inflammation Flashcards

1
Q

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

A

Inflammation

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2
Q

name the 4 cells/molecules involved in inflammation

A

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

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3
Q

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

A

plasma cells/proteins

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4
Q

what releases plasma cells/proteins

A

1) platelets
2) inflammatory cells
3) endothelial cells

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5
Q

types of inflammation

A

acute inflammation

chronic inflammation

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6
Q

rapid onset & short duration (hours to few days)

A

acute inflammation

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7
Q

characterized by:

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

A

acute inflammation

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8
Q

longer time course (days to years)

A

chronic inflammation

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9
Q

involves different cell types compared to acute inflammation

A

chronic inflammation

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10
Q

cell types involved in chronic inflammation

A

lymphocytes

macrophages

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11
Q

cell types involved in acute inflammation

A

plasma cells/proteins

leukocytes (neutrophils/PMN)

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12
Q

when tissue repair coexists with tissue destruction

A

chronic inflammation

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13
Q

cardinal signs of acute inflammation

A
  • calor (heat)
  • rubor (redness)
  • tumor (swelling)
  • dolor(pain)
  • loss of motion
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14
Q

causes of acute inflammation

A
  • infection
  • trauma
  • physical & chemical agents
  • necrosis (Myocardial Infarction)
  • foreign bodies
  • immune reaction (2ndary to allergic rxn; endogenous & exogenous)
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15
Q

stages of acute inflammation

A

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

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16
Q

occurs through a release of mediators

A

vasodilation

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17
Q

happens after a transient vasoconstriction

A

vasodilation

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18
Q

mediators released during vasodilation

A

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

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19
Q

what mediator is responsible for fever

A

prostaglandin

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20
Q

vasodilation first involves the?

A

arterioles

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21
Q

vasodilation= arterioles –> leading to ______

A

opening of new capillary beds in the area

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22
Q

increased blood flow caused by __-

A

heat

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23
Q

increased blood flow caused by heat results to?

A

erythema/redness

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24
Q

vasodilation increases the ___?

A

hydrostatic pressure

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25
Q

increase in hydrostatic pressure due to vasodilation causes what?

A

slowing/sludging of blood flow

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26
Q

slowing of blood flow causes ?

A

migration of leukocytes along the wall of blood vessels

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27
Q

increased leakiness of blood vessels

A

stage 2= increased vascular permeabilty

28
Q

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

A

increased vascular permeability

29
Q

the hallmark of acute inflammation

A

increased vascular permeability

30
Q

allows fluid to cross into the interstitial tissue

A

increased vascular permeability

31
Q

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

A

increased protein levels in the interstitial tissue

32
Q

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

A

decreased!!!

33
Q

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

A

increased vascular permeability

34
Q

mediators of increased vascular permeability

A

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

35
Q

name the 4 mechanisms of increased vascular permeability

A

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

36
Q

these are physiologic mechanisms and are due to mediators

referring to the type of mechanism of increased vascular permeability

A

endothelial contraction & retraction

37
Q

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

A

direct endothelial injury

38
Q

contraction of endothelial cells result to

A

increase in ___? spaces

39
Q

mediators of endothelial cell contraction

A

1) histamine
2) bradykinin
3) leukotrienes

40
Q

time course of endothelial cell contraction

A

immediate;short (30 minutes)

41
Q

mediators of endothelial cell retraction

A

1) TNF

2) interleukins

42
Q

occurs due to structural rearrangement of cytoskeleton

A

endothelial cell retraction

43
Q

time course of endothelial cell retraction

A

4-6 hours; delayed response

44
Q

mediators of direct endothelial injury

A

bacterial enzyme

45
Q

occurs due to endothelial cell necrosis

A

direct endothelial injury

46
Q

time course of direct endothelial injury

A

immediate; immediate sustained response

47
Q

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

A

delayed prolonged response

48
Q

uncertain mechanism

A

delayed prolonged response

49
Q

pushes fluid from vessel to tissue

A

HP

50
Q

attract fluid back to blood vessels

A

albumin

51
Q

takes care of remaining fluid in interstitium

A

lymphatics

52
Q

fluid only

A

filtrate

53
Q

components of protein-rich fluid

A

fluid + albumin

54
Q

what is the fist stage of acute inflammation

A

vasodilation

55
Q

what is the 2nd stage of acute inflammation

A

increased vascular permeability

56
Q

what is the 3rd stage of acute inflammation

A

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

57
Q

steps in the 3rd stage of acute inflammation

A

“RPT”

1) rolling
2) pavementing
3) transmigration

58
Q

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

A

CHEMOTAXIS

59
Q

loose, intermittent contact of WBCs with endothelium

A

rolling

60
Q

partially due to margination of WBC from stages? of blood

A

rolling

61
Q

tight, constant contact of WBC with endothelium

A

pavementing

62
Q

WBC crossing through the endothelial layer

A

transmigration

63
Q

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

A

opsonin

64
Q

types of opsonins

A

1) IgG
2) C3b
3) Collectins

65
Q

type of opsonin that is recognized by Fc receptor of WBC

A

IgG

66
Q

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

A

C3b

67
Q

type of opsonin that is recognized by C2q on leukocyte

A

collectins

Histopathology (4 decks)

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