Exam 1; Inflammation Flashcards

1
Q

What are the four clinical signs of inflammation

A

redness
swelling
heat
pain

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2
Q

What causes the redness, swelling, and heat associated with inflammation

A

vascular changes

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3
Q

What causes the pain and loss of function associated with inflammation

A

chemical mediators and leukocytes

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4
Q

What is acute inflammation characterized by

A

lasting from hours to days

characterized by exudation and neutrophil infiltration

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5
Q

What is chronic inflammation characterized by

A

spans days to years
characterized by mononuclear inflammatory cells (lymphocytes, macrophages, plasma cells) infiltration with vascular proliferation and fibrosis in later stages

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6
Q

What is fever mediated by

A

IL-1
TNF
PGE2

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7
Q

This accounts for redness and localized heat, beginning in the pre capillary arterioles and results in engorgement of capillary beds

A

vasodilation

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8
Q

What is vasodilation mediated by

A

endothelial cell derived NO that induces vascular smooth muscle relaxation, and mast cell release of histamine
it is maintained by prostaglandins

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9
Q

This results in movement of fluid out of the microvasculature, transudate, or exudate

A

increased vascular permeability

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10
Q

During increased vascular permeability, does the blood flow become more concentrated and flow slows down or speeds up

A

slows down

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11
Q

This occurs at the level of the post-capillary venules

A

movement of inflammatory cells out of the vessels (diapedesis)

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12
Q

This type of fluid accumulation has a low protein content, low specific gravity, and is clear and yellow

A

transudate

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13
Q

What occurs when there is a non-inflammatory transudate response

A

then endothelium is intact, fluid accumulates due to increased hydrostatic pressure and/or decrease in serum oncotic pressure

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14
Q

What occurs when there is an inflammatory transudate response

A

early endothelial cell contraction

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15
Q

This is indicative of tissue and endothelial cell damage, has a high protein content and a high specific gravity

A

exudate

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16
Q

This type of exudate is highly protein with few cells, cloudy

A

fibrinious

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17
Q

This type of exudate is highly protein with many cells (neutrophils), opaque

A

purulent

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18
Q

This type of exudate is highly protein with blood, may look pink to red

A

sanguineous

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19
Q

This mechanism of increasing vascular permeability forms intercellular gaps due to reversible contraction; occurs rapidly and lasts for 15-30 minutes

A

endothelial cell contraction

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20
Q

What is endothelial cell contraction mediated by

A

histamine and bradykinin early, then later, leukotrienes and PAF

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21
Q

These induce vasoactive amine release that leads to edema

A

C3a and C5a

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22
Q

This mechanism of increasing vascular permeability is due to the restructuring of cytoskeletal proteins and is mediated by IL-1, TNF, INF-ɣ; takes 4-6 hour to develop and lasts for 24 hours or more

A

endothelial cell retraction

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23
Q

Increased vascular permeability due to this may start immediately or be delayed and persist for hours to days

A

direct endothelial injury

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24
Q

direct venue endothelial injury may occur from the neutrophilic release of what

A

ROS and lysosomal enzymes during the inflammatory response

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25
What are some factors that activate endothelial cells
infectious agents hypoxia inflammatory mediators
26
Activated endothelial cells are characterized by what
production of PGI2 and NO that induce vasodilation contraction rearrangement of cytoskeletal proteins leading to retraction increased expression and affinity of surface cell adhesion molecules synthesis and release of inflammatory mediators
27
Leukocyte extravasation and accumulation at the site of injury proceeds in an orderly coordinated sequence of what events
``` margination rolling adhesion emigration or transmigration chemotaxis ```
28
These mediate the processes involved in the movement of leukocytes from the blood stream into the extravascular tissue
cell adhesion molecules
29
This is a mechanical process due to slowing of blood flow involving leukocyte extravasation
margination
30
This process involving leukocyte extravasation is when selectins mediate a weak, transient, sticking that slows the cells forward progression
rolling
31
This process involving leukocyte extravasation is mediated by interns (ICAM and VCAM)
adhesion
32
Transmigration of the leukocyte (cells) through the vessel wall (diapedesis) is mediated by what
PECAM-1
33
This is a non-random movement of leukocytes to the site of injury along a concentration gradient of chemotactic factors, these factors bind to the cell surface receptors. Chemotactic factors also stimulate leukocyte activation
chemotaxis
34
What are some chemotactic factors (2 potent)
``` PAF and LTB4 are potent C5a chemokines bacterial lipids and peptides fibrin degradation products ```
35
What are five different factors that activate leukocytes during an inflammatory response
``` bacterial products cellular debris Ab-Ag complexes cytokines and chemokines chemotactic factors ```
36
Activation of leukocytes is characterized by what five things
production of leukotrienes and prostaglandins from arachidonic acid degranulation and release of lysosomal enzymes production of reactive oxygen species synthesis and secretion of cytokines altered expression of cell adhesion molecules
37
In regards to phagocytosis attachment is mediated by this on targets and specific leukocyte receptors
opsonins
38
What are the steps of phagocytosis
attachment engulfment into a phagocytic vacuole lysosomal degranulation by fusion with the phagosome oxidative burst releasing ROS
39
What are other mechanisms besides phagocytosis on intracellular killing
lysozyme major basic protein defensins bactericidal permeability increasing protein
40
These cells are the morphologic hallmark of acute inflammation; beginning to accumulate within 6-24 hours
neutrophils
41
Neutrophils infiltrate tissues in response to what
tissue necrosis | bacteria and some fungal infections
42
What do the neutrophils release
ROS and lysosomal enzymes
43
Neutrophils undergo this, after phagocytosis and digestion
apoptosis
44
These replace the PMNs, usually beginning within 48 hours
monocytes (macrophages)
45
What are the functions of active macrophages
phagocytize and digest cellular debris and organisms take up and metabolize antigens and present membrane bound antigen to T cells elaborate various functions such as complement, ROS, etc.
46
What is the function of the other immune cells such as lymphocytes, eosinophils, and mast cells
lymphocytes - immune eosinophils - allergy and parasites mast cells - histamine
47
This inflammatory pattern involves a diffuse, permeative infiltration of neutrophils with edema
cellulitis
48
This inflammatory pattern involves a localized area of liquefactive necrosis
abscess
49
This inflammatory pattern involvers erosion of an epithelial surface exposing underlying connective tissue
ulcer
50
What differs regarding the duration of acute vs chronic inflammation
acute; 10 to 14 days | chronic; months to years
51
What differs regarding the location of acute vs chronic inflammation
acute; localized | chronic; maybe systemic
52
What differs regarding the immune response of acute vs chronic inflammation
acute; innate (no response) | chronic; specific, adaptive immune response
53
What differs regarding the reversibility of acute vs chronic inflammation
acute; often reversible | chronic; maybe reversible
54
What differs regarding the cells involved of acute vs chronic inflammation
actue; neutrophils | chronic; macrophages and lymphocytes
55
What are three causes for chronic inflammation
persistent infection prolonged exposure to a toxic agent immune-mediated inflammatory disease
56
Non-specific chronic inflammation is often associated with what
tissue repair (granulation/fibrosis)
57
This is linked to delayed-type IV hypersensitivity immune reaction
granulomatous inflammation
58
What is the morphology of granulomatous inflammation
epithelioid (activated) histiocytes - granular pink cytoplasm with indistinct cell borders central caseous necrosis often present epithelia histiocytes coalesce to form multinucleated giant cells a collar of mononuclear cells often surrounds the aggregated epithelia histiocytes; older granulomas develop a rim of fibroblasts and connective tissue heal by fibrosis
59
What are some diseases characterized by granulomatous inflammation
``` bacterial (tuberculosis) parasitic (toxo) funfal (histo) inorganic matter unknown (Crohn's) ```
60
What is the source and function of histamine
source; mast cells | function; vasodilation and increases vascular permeability
61
What is the source and function of bradykinin
source; plasma protein | function; increase vascular permeability, pain
62
What is the source and function of nitric oxide
source; endothelial and other cells | function; vasodilation, tissue damage
63
What is the source and function of prostaglandins
source; membrane phospholipids | function; vasodilation, pain, fever, potentiate other mediators
64
What is the source and function of leukotrienes C, D, E
source; membrane phospholipid | function; increase vascular permeability, vasoconstriction, bronchoconstriction
65
What is the source and function of leukotrienes B
source; leukocytes | function; leukocyte activation, chemotaxis
66
What is the source and function of PAF
source; leukocytes and endothelial cells | function; increase vascular permeability
67
What is the source and function of cytokines
source; macrophages and endothelial cells | function; endothelial cell and leukocyte activation, fever
68
What is the source and function of C5a and C3a
source; plasma protein | function; chemotaxis, phagocytosis, increases vascular premeability
69
What are the seven steps of wound healing by the first (primary) intention
blood clots (minutes) neutrophils early proliferation/migration of epithelial cells macrophages replace neutrophils; early granulation tissue peak neovascularization progressive collagen deposition increasing wound strength during the next four months
70
What are the two steps of wound healing by second intention
more inflammation; more granulation tissue | wound contraction due to myofibroblasts
71
What are six factors that affect wound healing
``` infection nutrition steroids mechanical factors poor perfusion diabetes mellitus ```
72
What are the three categories of the intrinsic capacity for proliferation regarding wound healing
labile (continuously dividing) stable permanent