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Pathobio and host defense > Inflammation and repair > Flashcards

Inflammation and repair Flashcards

1
Q

what is the purpose of inflammation

A

protective response intended to eliminate cause of cell injury

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2
Q

Inflammation is part of what type of immunity

A

innate immunity

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3
Q

characteristics of acute inflammation

A

sudden and short term

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4
Q

characteristics of chronic immunity

A

gradual and prolonged

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5
Q

inflammation is induced by ______ produced by _____

A

chemical mediators; injured host cells

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6
Q

when a tissue is injured, different cells secrete _____ that _____ and ____ inflammatory response

A

chemokines; induce and regulate

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7
Q

what are the main components of inflammation

A
  • vascular changes (vasodilation and increased vascular permeability)
  • cellular events (cellular recruitment and activation)
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8
Q

what are the Five Rs of inflammatory response

A
  1. recognition of injurious agent
  2. recruitment of WBCs
  3. removal of agent
  4. regulation of the response
  5. repair (resolution)
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9
Q

what are the cardinal signs of inflammation

A

Heat, redness, swelling, pain, and loss of function

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10
Q

what causes redness

A

dilation of arterioles and increase blood flow

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11
Q

what causes heat

A

increased chemical activity and increase blood flow to surface

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12
Q

what causes swelling

A

accumulation of blood and damaged tissue cells

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13
Q

what causes pain

A

direct injury of nerve fibers, pressure

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14
Q

what causes loss of function

A

increased pain/swelling

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15
Q

the primary cause of redness, heat, swelling/edema is

A

histamine which increases fluid into tissue

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16
Q

the primary cause of pain is

A

bradykinin and PGE2

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17
Q

major local manifestations of acute inflammation are

A
  1. vascular dilation and increased blood flow (erythema and heat)
  2. extravasation of plasma fluid and proteins (edema)
  3. leukocyte emigration and accumulation
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18
Q

how do cell recognize presence of potentially harmful agents

A

immune cells have pattern recognition receptors designed to sense presence of pathogens (toll like receptors and inflammasome)

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19
Q

what are toll like receptors

A

microbial sensors on plasma membrane or endosomes that recognize extraceullar and ingested microbes

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20
Q

what are the functions of toll like receptors

A

activates transcriptions factors that stimulate production of secreted and membrane proteins that promote lymphocyte activation

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21
Q

what are inflammasome

A

multiprotein cytoplasmic complex that recognize products of dead cells

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22
Q

what is the function of inflammasome

A

activates caspase-1 resulting in WBC recruitment

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23
Q

interstitial fluid accumulation is caused by

A

increased hydrostatic pressure

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24
Q

protein rich fluid accumulation is typical in

A

inflammation

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25
what are the mechanisms involved in increased vascular permeability
- endothelial cell contraction leading to gaps in post capillary venules - endothelial injury - increased transcytosis of proteins - leaking from new blood vessels
26
what role do lymphatic response have in inflammation
increase lymph flow and help remove excess water, WBC, debris from extravascular space
27
lymphangitis is
inflamed lymphatics
28
lymphadenitis is
inflamed lymph nodes
29
leukocyte work to
ingest agents, kill bacteria, and eliminate necrotic tissue
30
the steps for leukocyte recruitment are
1. margination and rolling 2. adhesion 3. transmigration 4. migration
31
define what occurs at margination
when leukocytes accumulate at periphery of vessels
32
what occurs during rolling
cytokines activate endothelial cells, express adhesion molecules to which WBCs attach loosely
33
what occurs during adhesion
mediated by integrins expressed on WBC interacting with their ligand on endothelial cells
34
in diapedesis,
WBCs migrate through vessel wall
35
WBC move towards site of injury by what
chemotaxis
36
how are leukocytes activated
by microbes products of necrotic cells and chemical mediators
37
leukocyte activation promotes:
- phagocytosis - release substances to destroy microbes - produce chemical mediators
38
what are the phagocytosis steps
1. recognition and attachment 2. engulfment and formation of phagocytic vacuole 3. killing and degradation of ingested material
39
what causes injury to normal cells and tissues
- defense against difficult infections - autoimmune reactions - XS host reaction
40
what are the possible outcomes to acute inflammation
- resolution - chronic inflammation - scarring (fibrosis)
41
characteristics of serous inflammation
skin blister from burn or viral infection
42
characteristics of fibrinous inflammation
due to see injuries that result in exudate of fibrinogen leading to fibrin
43
characteristics of ulcerative inflammation
ulcer on surface of organ
44
characteristics of supurative (purulent) inflammation
presence of large amounts of purulent exudate (pus) and edema fluid
45
cell derived mediators
- vasoactive amines - arachidonic acid metabolites - platelet activating factor - cytokines - reactive oxygen species - nitric oxide - lysosomal enzymes of WBC - neuropeptides
46
plasma protein derived mediators include
- complement proteins - coagulation protein - kinins
47
complement proteins are responsible for
leukocyte chemotaxis, opsonization, and phagocytosis of microbes and cell kiling
48
coagulation proteins are activated by
factor XII that will active the fibrinolytic system (triggers clotting, kinin and complement cascade)
49
kinins are produced by
proteolytic; mediates vascular reaction and pain
50
chronic inflammation is characterized by
inflation with mononuclear cells, tissue destruction induced by byproduct of inflammatory cells, and repair involving anigogenesis and fibrosis
51
what cells is most dominant in chronic inflammation
macrophages
52
how are macrophages activated
- by microbial products - induced by cytokines
53
role of lymphocytes in chronic inflammation
migrate to injury sites
54
B cells develop to what in tissues
plasma cells and CD4+ lymphocytes
55
eosinophils are found in
parasitics inflammatory response mediated by IgE (allergies)
56
Mast cells are ...
sentinel cells in connective tissue. produce cytokines (TNF, chemokines)
57
granulomatous inflammation known as
- clusters of T cell activated macrophages to engulf foreign bodies
58
what are the most important mediators of acute phase reaction
TNF, IL-1, and IL-6
59
system effects of acute phase response
- fever - plasma levels of acute phase proteins - leukocytosis
60
repair occurs by
- regeneration of injured tissue (proliferation of uninjured cells) - scar formation (if tissue not capable of regeneration)
61
what are the methods that macrophages are activated
- induced by microbial products, T-cell signals, and foreign substances (classical) - induced by cytokines produced by T-cells, eosinophils and mast cells (alternative)
62
what cell types proliferate during tissue repair
-remnants of injured tissue - vascular endothelial cells - fibroblasts
63
body tissue can be divided into what kinds of tissues
- labile tissue - stable tissue - permeant tissue
64
describe labile tissues
continuously lost and replaced by stem cells (bone marrow hematopoietic cells, epithelial cells)
65
describe stable tissues
quiescent with minimal proliferative capacity (parenchyma of solid tissues, endothelial cells, smooth muscle fibers, fibroblasts)
66
describe permanet tissues
postnatally terminally differentiated and non proliferative (cardiac muscle)
67
what is extracellular matrix made up of
collagen, glycoproteins, basement membranes underlying epithelia and surrounding vessels
68
what function does ECM serve
- provide mechanical support to tissues (collagen and elastin) - acts as substrate for cell growth - regulates cell proliferation and differentiation
69
steps in scar formation are
- angiogenesis - activation of fibroblasts - remodeling
70
angiogenesis is
process of new blood vessels development from existing vessels
71
angiogenesis is critical in
- healing injury - development of collateral circulation at sites of ischemia - allowing tumors to growth
72
activation of fibroblasts and deposition of connective tissue occurs in two steps:
- migration and proliferation of fibroblasts into injury site - deposition of ECM protein
73
what growth factors are involved in activation of fibroblasts
TGF-Beta, PDGF, FGF

Pathobio and host defense (7 decks)

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