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SP15 Pathology > Exam 1; Inflammation > Flashcards

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
Q

What are some factors that activate endothelial cells

A

infectious agents
hypoxia
inflammatory mediators

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26
Q

Activated endothelial cells are characterized by what

A

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

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27
Q

Leukocyte extravasation and accumulation at the site of injury proceeds in an orderly coordinated sequence of what events

A 
margination
rolling
adhesion
emigration or transmigration
chemotaxis
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28
Q

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

A

cell adhesion molecules

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29
Q

This is a mechanical process due to slowing of blood flow involving leukocyte extravasation

A

margination

30
Q

This process involving leukocyte extravasation is when selectins mediate a weak, transient, sticking that slows the cells forward progression

A

rolling

31
Q

This process involving leukocyte extravasation is mediated by interns (ICAM and VCAM)

A

adhesion

32
Q

Transmigration of the leukocyte (cells) through the vessel wall (diapedesis) is mediated by what

A

PECAM-1

33
Q

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

A

chemotaxis

34
Q

What are some chemotactic factors (2 potent)

A 
PAF and LTB4 are potent
C5a
chemokines
bacterial lipids and peptides
fibrin degradation products
35
Q

What are five different factors that activate leukocytes during an inflammatory response

A 
bacterial products
cellular debris
Ab-Ag complexes
cytokines and chemokines
chemotactic factors
36
Q

Activation of leukocytes is characterized by what five things

A

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
Q

In regards to phagocytosis attachment is mediated by this on targets and specific leukocyte receptors

A

opsonins

38
Q

What are the steps of phagocytosis

A

attachment
engulfment into a phagocytic vacuole
lysosomal degranulation by fusion with the phagosome
oxidative burst releasing ROS

39
Q

What are other mechanisms besides phagocytosis on intracellular killing

A

lysozyme
major basic protein
defensins
bactericidal permeability increasing protein

40
Q

These cells are the morphologic hallmark of acute inflammation; beginning to accumulate within 6-24 hours

A

neutrophils

41
Q

Neutrophils infiltrate tissues in response to what

A

tissue necrosis

bacteria and some fungal infections

42
Q

What do the neutrophils release

A

ROS and lysosomal enzymes

43
Q

Neutrophils undergo this, after phagocytosis and digestion

A

apoptosis

44
Q

These replace the PMNs, usually beginning within 48 hours

A

monocytes (macrophages)

45
Q

What are the functions of active macrophages

A

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
Q

What is the function of the other immune cells such as lymphocytes, eosinophils, and mast cells

A

lymphocytes - immune
eosinophils - allergy and parasites
mast cells - histamine

47
Q

This inflammatory pattern involves a diffuse, permeative infiltration of neutrophils with edema

A

cellulitis

48
Q

This inflammatory pattern involves a localized area of liquefactive necrosis

A

abscess

49
Q

This inflammatory pattern involvers erosion of an epithelial surface exposing underlying connective tissue

A

ulcer

50
Q

What differs regarding the duration of acute vs chronic inflammation

A

acute; 10 to 14 days

chronic; months to years

51
Q

What differs regarding the location of acute vs chronic inflammation

A

acute; localized

chronic; maybe systemic

52
Q

What differs regarding the immune response of acute vs chronic inflammation

A

acute; innate (no response)

chronic; specific, adaptive immune response

53
Q

What differs regarding the reversibility of acute vs chronic inflammation

A

acute; often reversible

chronic; maybe reversible

54
Q

What differs regarding the cells involved of acute vs chronic inflammation

A

actue; neutrophils

chronic; macrophages and lymphocytes

55
Q

What are three causes for chronic inflammation

A

persistent infection
prolonged exposure to a toxic agent
immune-mediated inflammatory disease

56
Q

Non-specific chronic inflammation is often associated with what

A

tissue repair (granulation/fibrosis)

57
Q

This is linked to delayed-type IV hypersensitivity immune reaction

A

granulomatous inflammation

58
Q

What is the morphology of granulomatous inflammation

A

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
Q

What are some diseases characterized by granulomatous inflammation

A 
bacterial (tuberculosis)
parasitic (toxo)
funfal (histo)
inorganic matter
unknown (Crohn's)
60
Q

What is the source and function of histamine

A

source; mast cells

function; vasodilation and increases vascular permeability

61
Q

What is the source and function of bradykinin

A

source; plasma protein

function; increase vascular permeability, pain

62
Q

What is the source and function of nitric oxide

A

source; endothelial and other cells

function; vasodilation, tissue damage

63
Q

What is the source and function of prostaglandins

A

source; membrane phospholipids

function; vasodilation, pain, fever, potentiate other mediators

64
Q

What is the source and function of leukotrienes C, D, E

A

source; membrane phospholipid

function; increase vascular permeability, vasoconstriction, bronchoconstriction

65
Q

What is the source and function of leukotrienes B

A

source; leukocytes

function; leukocyte activation, chemotaxis

66
Q

What is the source and function of PAF

A

source; leukocytes and endothelial cells

function; increase vascular permeability

67
Q

What is the source and function of cytokines

A

source; macrophages and endothelial cells

function; endothelial cell and leukocyte activation, fever

68
Q

What is the source and function of C5a and C3a

A

source; plasma protein

function; chemotaxis, phagocytosis, increases vascular premeability

69
Q

What are the seven steps of wound healing by the first (primary) intention

A

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
Q

What are the two steps of wound healing by second intention

A

more inflammation; more granulation tissue

wound contraction due to myofibroblasts

71
Q

What are six factors that affect wound healing

A 
infection
nutrition
steroids
mechanical factors
poor perfusion
diabetes mellitus
72
Q

What are the three categories of the intrinsic capacity for proliferation regarding wound healing

A

labile (continuously dividing)
stable
permanent

SP15 Pathology (17 decks)

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