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inflammation Flashcards

1
Q

____, ____, and _____ are due to vascular changes; ____ and _____ are due to chemical mediators and infiltration of leukocytes

A

heat (calor); redness (rubor); swelling (tumor)

pain (dolor); loss of function

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2
Q

acute inflammation is characterized by ____ and ____

A

exudation (emitting fluid); neutrophil infiltration

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3
Q

chronic inflammation is characterized by _____ with _____ and _____ in later stages

A

mononuclear inflammatory cell infiltration (lymphocytes, macrophages, plasma cells); vascular proliferation; fibrosis

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4
Q

fever is mediated by:

A

IL-1, TNF, and PGE2

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5
Q

vascular changes in acute inflammation include _____ and ______

A

vasodilation; increased vascular permeability

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6
Q

vasodilation is mediated by endothelial cell release of ____ which induces vascular smooth muscle relaxation and _____ release of ____; vasodilation is maintained by ______

A

NO; mast cell; histamine; prostaglandins (PGI2, PGD2, PGE2, and PGF2)

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7
Q

vasodilation beings in the _____ and results in engorgement of ______

A

pre-capillary arterioles; capillary beds

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8
Q

movement of inflammatory cells out of the vessels (bc of increased vascular permeability), called ____, occurs at the level of _____

A

diapedesis; post-capillary venules

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9
Q

transudate usually accumulates due to _____ (due to ______) and/or _____

A

increased hydrostatic pressure (usually due to reduced venous return); decreased serum oncotic pressure

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10
Q

exudate is indicative of ____ and _____ damage

A

tissue; endothelial cell

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11
Q

increased vascular permeability may be due to _____ or ____ to the endothelial cells

A

inflammatory mediators; direct injury

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12
Q

endothelial cell contraction forms _____ (mainly in ______) due to reversible contraction; occurs rapidly and lasts for 15-30 min

A

intercellular gaps; post-capillary venules

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13
Q

endothelial cell contraction is mediated by ____ and ____ early, and later on by ____ and _____; ____ and ____ induce vasoactive amine release which leads to edema

A

histamine; bradykinin; leukotrienes; PAF; C3a and C5a

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14
Q

endothelial cell retraction due to ____ of _____ is mediated by _____; takes 4 to 6 hours to develop and lasts for 24 hours or more

A

restructuring; cytoskeletal proteins; IL-1, TNF, and IFNgamma

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15
Q

direct venule endothelial cell injury may occur from _____ of _____ and ______ during the inflammatory response

A

neutrophilic release of ROS and lysosomal enzymes (proteases)

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16
Q

3 cellular changes during inflammation

A
  • endothelial cell activation
  • leukocyte extravasation
  • leukocyte activation/phagocytosis
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17
Q

factors that will activate endothelial cells

A

histamine, thrombin, complement factors, cytokines (IL-1, TNF), bacterial products, hypoxia, viruses, PAF

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18
Q

activated ECs are characterized by production of ___ and ___ that induce vasodilation, ____, rearrangement of cytoskeletal proteins leading to ____, increased expression and affinity of _____, and synthesis and release of ____

A 
PGI2; NO
contraction/retraction
retraction
surface cell adhesion molecules
inflammatory mediators: IL-1, IL-6, PGI2, PAF, chemokines
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19
Q

sequence of leukocyte extravasation

A
  1. leukocyte margination
  2. leukocyte rolling
  3. leukocyte adhesion
  4. emigration or transmigration
  5. chemotaxis
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20
Q

_____ mediate the processes involved in the movement of leukocytes from the blood stream into the extravascular tissue

A

cell adhesion molecules (CAMs)

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21
Q

in rolling, _____ mediate a weak, transient sticking that slows the cells forward progression

A

selectins (adhesion molecules)

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22
Q

adhesion is mediated by _____

A

integrins (ICAM and VCAM on endothelial cells)

23
Q

emigration/transmigration of ECs through the vessel wall (diapedesis) mediated by _____; occurs mainly in the ____ of the systemic vasculature

A

PECAM-1; venules

24
Q

chemotactic factors involved in chemotaxis

A

PAF (potent)
LTB4- leukotriene B4 (potent)
C5a, chemokines, bacterial lipids and peptides, fibrin degradation products (FDP)

25
Q

factors that activate leukocytes during an inflammatory reaction

A

bacterial products, cellular debris, Ab-Ag complexes, cytokines and chemokines, chemotactic factors

26
Q

activation of leukocytes characterized by production of ____ and ____ from _____; degranulation and release of _____; production of ____; synthesis and secretion of ____; altered expression of _____

A 
leukotrienes and prostaglandins from arachidonic acid
lysosomal enzymes
ROS
cytokines
cell adhesion molecules
27
Q

4 steps of phagocytosis

A
  1. attachment
  2. engulfment
  3. lysosomal degranulation
  4. oxidative burst
28
Q

attachment mediated by ____ on targets and specific _____; engulfment into a _____; lysosomal degranulation by fusion with the ____; oxidative burst releasing ____

A

opsonins (IgG, C3b, collectins); specific leukocyte receptors (Fc receptor for IgG, complement receptors)
phagocytic vacuole
phagosome
ROS (superoxide, hydrogen peroxide, hypochlorous radical)

29
Q

other mechanisms of intracellular killing by leukocytes

A

lysozyme, major basic protein, defensins, bactericidal permeability-increasing protein

30
Q

cells of acute inflammation

A

neutrophils (morphologic hallmark of acute inflammation)

monocytes (macrophages/histiocytes)

31
Q

activated macrophages have several functions including ____ and ____ cellular debris and organisms; they also take up and metabolize ____ and present _____ to immunocompetent T cells

A

phagocytize; digest

antigens; membrane-bound Ag

32
Q

activated macrophages elaborate various factors including:

A

enzymes (proteases); complement and coagulation factors; cytokines (IL-1, TNF), ROS and NO, prostaglandins, growth factors

33
Q

other inflammatory cell types

A
  1. lymphocytes, plasma cells (immune functions)
  2. eosinophils (allergic rxns, parasitic infections)
  3. mast cells- surface IgE- release histamine
34
Q

while prostaglandins generally cause vasodilation, ____ causes vasoconstriction; another example of opposing effects: _____ promotes platelet aggregation and ____ inhibits platelet aggregation

A

thromboxane A2; thromboxane A2 ; prostacyclin

35
Q

cells of chronic inflammation

A

lymphocytes
macrophages
plasma cells
eosinophils

36
Q

role of growth factors and cytokines in wound healing

A 
epithelial proliferation
monocyte chemotaxis
fibroblast proliferation
angiogenesis
collagen synthesis
37
Q

3 types of exudate

A
  1. fibrinous- high protein (fibrin), few cells, cloudy
  2. purulent (pus)- contains cells (neutrophils); opaque
  3. sanguineous- pink/red fluid due to blood
38
Q

neutrophils infiltrate tissue in response to _____ and _____ infections

A

tissue necrosis; bacterial (some fungal) infections

39
Q

in acute inflammation, neutrophils begin to accumulate within ____ hours; neutrophils are replaced with monocytes/macrophages within ____ hours

A

4-6; 48

40
Q

diffuse, permeative infiltration of neutrophils with edema

A

cellulitis

41
Q

localized area of neutrophils or liquefactive necrosis (pus)

A

abscess

42
Q

erosion of an epithelial surface exposing underlying connective tissue

A

ulcer

43
Q

causes for chronic inflammation include:

A
  1. persistent infections
  2. prolonged exposure to a toxic agent
  3. immune-mediated inflammatory disease
44
Q

non-specific chronic inflammation often assoc with _____

A

tissue repair (granulation tissue/fibrosis)

45
Q

granulomatous inflammation linked to the _____

A

delayed type IV hypersensitivity immune reaction

46
Q

morphology of granulomatous inflammation includes:

A
  1. epithelioid (activated) histiocytes
  2. central caseous necrosis
  3. multinucleated giant cells (langhans)
  4. collar of mononuclear cells
  5. heal by fibrosis
47
Q

diseases characterized by granulomatous inflammation include:

A
  1. bacterial infection- M. tuberculosis
  2. parasitic infection
  3. fungal infection
  4. inorganic matter
  5. unknown etiology
48
Q

PGs and LTs are derived from arachidonic acid through the action of ____ or ____

A

cyclo-ocygenase (PGs) ; lipo-oxygenase (leukotrienes)

49
Q

aspirin and non-steroidal anti-inflam drugs reduce inflammation by ______; steroids inhibit release of ____ from _____

A

blocking cyclo-oxygenase activity; arachidonic acid; cell membrane phospholipids

50
Q

factors that affect wound healing

A
  1. infection
  2. nutrition
  3. steroids
  4. mechanical factors
  5. poor tissue perfusion
  6. DM, atherosclerosis
51
Q

increased vascular permeability- immediate transient- EC contraction mediated by:

A

histamine, BK, PAF, leukotrienes

52
Q

in direct EC injury, increased vascular perm med by _____ or _____

A

injurious agents; ROS/enzymes from PMNs

53
Q

EC retraction mediated by:

A

IL-1, TNF, IFN gamma

54
Q

pain mediated by:

A

BK and PGE2

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