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Histopathology > Inflammation > Flashcards

Inflammation Flashcards

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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
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

Histopathology (4 decks)

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