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Pathology Exam 1 > Lecture 3 - Inflammation > Flashcards

Lecture 3 - Inflammation Flashcards

1
Q

what is the clinical evidence of inflammation in terms of vascular changes?

A

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

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2
Q

what is clinical evidence of inflammation in terms of chemical mediators and leukocytes?

A

pain (dolor) and loss of function

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3
Q

how long does acute inflammation last and how is it characterized?

A
  • from hours to days

- exudation and neutrophil infiltration

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4
Q

how long does chronic inflammation last and how is it charcterized?

A
  • spans days to years
  • mononuclear inflammatory cell (lymphocytes, macrophages, plasma cells) infiltration with vascular proliferation and fibrosis in later stages
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5
Q

does acute or chronic inflammation cause additional tissue injury

A

trick questionnnn

*BOTH acute and chronic inflammation may cause additional tissue injury

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6
Q

what factors is fever mediated by?

A

IL-1, TNF, PGE2

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7
Q

role of vasodilation

A
  • begins in the precapillary arterioles and results in engorgement of capillary beds
  • account for the redness and localized heat
  • mediated by endothelial cell derived NO that induces vascular smooth muscle relaxation, and mast cell release of histamine
  • it is maintained by prostaglandins (PGI2, PGD2, PGE2, and PGF2)
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8
Q

increased vascular permeability results in:

A
  • movement of fluid outside of the microvasculature, transudate or exudate
  • blood becomes more concentrated and flow slows (stasis)
  • movement of inflammatory cells out of the vessels (diapedesis) occurs at level of post- capillary venules
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9
Q

accumulation of fluid in the extravascular tissue leads to..

A

swelling (edema)

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10
Q

what are some characteristic of transudate?

A
  • low protein content
  • low specific gravity (<1.012)
  • clear and yellow
  • Noninflammatory - endothelium is intact, fluid accumulates due to increase hydrostatic pressure and/ or decreased serum oncotic pressure
  • Inflammatory - early endotheial cell contraction
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11
Q

what are some characteristics of exudate?

A
  • indicative of tissue and endothelial cell damage
  • high protein content
  • high specific gravity (> 1.020)
  • often contains inflammatory cells
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12
Q

what kind of exudate has the following characteristics: high protein (fibrin), few cells, cloudy?

A

fibrinous exudate

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13
Q

what kind of exudate has the following characteristics: contains cells (neutrophils), opaque

A

purulent exudate (pus)

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14
Q

what kind of exudate has the following characteristics: pink to red due to blood

A

sanguineous

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15
Q

increased vascular permeability may be due to..

A

inflammatory mediators or direct injury to the endothelial cells

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16
Q

what happens as a result of endothelial cell contraction

A

forms intracellular gaps (mainly in post capillary venules) due to reversible contraction

  • occurs rapidly and lasts for 15-30 mins
  • it is mediated by histamine and bradykinin early, and later by leukotrienes and PAF
  • C3a and C5a induce vasoactive amine release that leads to edema
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17
Q

what happens as a result of endothelial cell retraction?

A

due to restructuring of cytoskeletal proteins is mediated by IL-1, TNF, and IFN-gamma
- takes 4-6 hours to develop and lasts for 24 hours or more

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18
Q

increased vascular permeability due to direct endothelial injury may….

A

start immediately (immediate-sustained) or be delayed (delayed - prolonged) and persists for hours to days

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19
Q

direct venule endothelial injury may occur from what?

A

neutrophilic release of ROS and lysosomal enzymes (e.g. proteases) during the inflammatory response

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20
Q

various factors will activate endothelial cells, these include:

A 
histamine
thrombin
complement factors
cytokines (IL-1 and TNF)
bacterial products
hypoxia
viruses
PAF
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21
Q

activated endothelial cells are characterized by:

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 (PGI2, PAF, IL-1, IL-6, and chemokines)
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22
Q

leukocyte extravasation and accumulation at the site of injury proceeds in an orderly coordinated sequence of events, what are they?

A
  1. leukocyte migration
  2. leukocyte rolling
  3. leukocyte adhesion
  4. emigration
  5. chemotaxis
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23
Q

cell adhesion molecules mediate the processes involved in the movement of leukocytes from the blood stream to the

A

extravascular tissue

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24
Q

margination definition

A

mechanical process due to slowing of blood flow

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25
Q

rolling definition

A

selectins mediate a weak, transient, sticking that slows the cells forward progression

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26
Q

adhesion definition

A

mediate by integrins through the vessel wall (diapedesis) - mediated by PECAM-1

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27
Q

what is chemotaxis

A

it is a non-randomized movement of leukocytes to the site of injury along a concentration gradient of chemotactic factors

  • the factors bind to the cell surface receptors
  • chemotactic factors also stimulate leukocyte activation
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28
Q

what are examples of chemotactic factors? (6 of them)

A 
PAF (potent)
LTB4 (potent)
C5a
chemokines
bacterial lipids and peptides
fibrin degradation products
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29
Q

Several different factor activate leukocytes during an inflammatory response, these include:

A 
bacterial products
cellular debris
Ab-Ag complexes
cytokines and chemokines
chemotactic factors
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30
Q

activation of leukocytes is characterized by:

A
  • production of leukotrienes and prostaglandins from arachidonic acid
  • degranulation and release of lysosomal enzymes
  • production of ROS
  • synthesis and secretion of cytokines
  • altered expression of cell adhesion molecules
31
Q

what is phagocytosis?

A
  • attachment mediated by opsonins (IgG, C3B, collectins) on targets and specific leukocyte receptors (Fc receptor for IgG, complement receptors)
  • engulfment into a phagocytic vacule
  • lysosomal degranulation by fusion with the phagosome
  • oxidative burst releasing ROS (superoxide, hydrogen peroxide, hypochlorous radical)
  • other mechanisms of intracellular killing; lysozyme, major basic protein, defensins and bactericidal permeability- increasing protein
32
Q

what is the morphologic hallmark for acute inflammation and begin to accumulate within 6-24 hours?

A

neutrophils (PMNs)

33
Q

what is the cell described below:

  • infiltrate tissue in response to tissue necrosis (e.g. myocardial infarction) and bacterial and some fungal infections
  • undergo apoptosis after phagocytosis and digestion
  • release ROS and lysososomal enzymes
A

neutrophils (PMNs)

34
Q

what cell replaces PMNs, usually beginning within 48 hours

A

monocytes (Macrophages/ histiocytes)

35
Q

monocytes are called histiocytes or macrophages after…

A

entering into tissue

36
Q

what is the half life for circulating monocytes

A

half life is months compared to one day

37
Q

activated macrophages have several functions including:

A
  • Phagocytize and digest cellular debris

- take up and metabolize antigens and present membrane bound antigen to immunocompetent T cells

38
Q

what are various factors that monocytes elaborate?

A
  • enzymes (proteases)
  • complement and coagulation factors
  • cytokines (e.g. IL-1, TNF)
  • ROS and NO
  • prostaglandins
  • growth factors
39
Q

what are other cells of inflammation under monocytes:

A
  • lymphocytes, plasma cells
  • eosinophils (allergic reactions, parasitic infections)
  • mast cells - surface IgE (release hsitamine)
40
Q

definition of cellulitis

A

diffuse, permeative infiltration of neutrophils with edema

41
Q

definition of abscess

A

localized area of liquefactive necrosis

42
Q

definition of ulcer

A

erosion of an epithelial surface exposing underlying connective tissue

43
Q

how does acute inflammation differ from chronic inflammation in terms of time?

A

acute inflammation - 10-14 days

chronic - months to years

44
Q

acute inflammation is innate whereas chronic inflammation relies upon …

A

specific, adaptive immune system

45
Q

T/F.
Acute inflammation may be reversible or fatal.
Chronic inflammation may be reversible or fatal.

A

Both are true

46
Q

causes for chronic inflammation include:

A
  1. persistant infections
  2. prolonged exposure to a toxic agent
  3. immune mediated inflammatory disease
47
Q

non specific chronic inflammation is often associated with tissue ____

A

repair (granulation tissue/ fibrosis

48
Q

in regards to non-specific chronic inflammation, the cellular infiltrate may contain….

A

macrophages, lymphocytes, plasma cells, and/or eosinophils

*few neutrophils my also be present

49
Q

which type of inflammation is linked to the delayed type IV hypersensitivity immune reaction

A

granulomatous inflammation

50
Q

morphology of granulomatous inflammation includes:

A

epithelioid (activated) histiocytes - granular pink cytoplasm with indistinct borders

  • Central caseous necrosis often present
  • epithelioid histiocytes coalesce to form multinucleated giant cells Langerhans or foreign body type
  • a collar of mononuclear cells often surrounds the aggregated epithelioid histiocytes, older granulomas develop a rim of fibroblasts and CT
51
Q

how does granulomatous inflammation heal?

A

heals by fibrosis

52
Q

Diseases characterized by granulomatous inflammation include:

A
  • bacterial infection - TB, cat scratch fever
  • parasitic infection - schistosomiasis, toxoplasmsis
  • fungal infection - coccidioidomycosis, histoplasmosis
  • inorganic matter - silicosis, inert foreign material
  • unknown - sarcoidoss, Crohn’s disease
53
Q

What is the source and function of histamine?

A

source: mast cell
function: vasodilation, increase vascular permeability

54
Q

What is the source and function of bradykinin

A

source: plasma protein
function: increase vascular permeability, pain

55
Q

What is the source and function of nitric oxide?

A

source: endothelial cells and other cells
function: vasodilation, tissue damage

56
Q

What is the source and function of prostaglandins?

A

source: membrane phospholipids
function: vasodilation, pain, fever, potentiate, other mediators

57
Q

What is the source and function of leukotrienes C4, D4, E4?

A

source: membrane phospholipids
function: increase vascular permeability, vasoconstriction, bronchoconstriction

58
Q

What is the source and function of leukotriene B4?

A

source: leukocytes
function: leukocyte activation, chemotaxis

59
Q

What is the source and function of PAF?

A

source: leukocytes, endothelial cells
function: increase vascular permeability, chemotactic

60
Q

What is the source and function of cytokines (IL-1 and TNF)

A

source: macrophages, endothelial cells
function: endothelial cell and leukocyte activation, fever

61
Q

What is the source and function of C5a and C3a?

A

source: plasma protein
function: chemotaxis (C5a), phagocytosis (C3b), increase vascular permeability (C3a and C5a)

62
Q

histamines are release by physical injury, antigen binding to…

A

IgE, C3a, C5a, cytokines

63
Q

prostaglandins and leukotrienes are derived from arachidonic acid through the action of…

A

cyclo-oxygenase (prostaglandins) or lipo-oxygenase (leukotrienes)

64
Q

aspirin and non-steroidal anti-inflammatory drugs reduce inflammation by blocking…

A

cyclo-oxygenase activity

65
Q

steroids inhibit release of arachidonic acid from…

A

cell membrane phospholipids

66
Q

while prostaglandins generally cause _____, thromboxane A2 causes _______

A

vasodilation; vasoconstriction

67
Q

thromboxane A2 promotes _____ _____ and prostacyclin inhibits _____ _______

A

platelet aggregation

68
Q

what are examples of the intrinsic capacity for proliferation forL continuously dividing cells

A
  1. continuously dividing: hematopoietic cells, surface epithelium
69
Q

what are examples of the intrinsic capacity for proliferation for: stable cells

A

stable: minimal replication in normal conditions, capable of proliferation in response to injury, parenchymal calls of most solid organs, smooth muscle cells, fibroblasts

70
Q

what are examples of the intrinsic capacity for proliferation for: permanent cells

A

Permanent: no capacity for proliferation, neurons, cardiac muscles

71
Q

what are the 7 steps for healing by first (primary) intention

A
  1. blood clot (minutes)
  2. neutrophils (within 24 hours)
  3. early proliferation/ migration of epithelial cells (24-48 hours)
  4. Macrophages replace neutrophils; early granulation tissue (day 3)
  5. Peak neovascularization (day 5)
  6. Progressive collagen deposition (during 2nd week)
  7. increasing wound strength during next 4 months
72
Q

what are the 2 steps in healing by second intention?

A
  1. more inflammation; more granulation tissue

2. wound contraction due to myofibroblasts

73
Q

growth factors and cytokines have a role in…

A 
wound healing
(he says look up on page 62, table 2-9 - aint nobody have time or money for that)
74
Q

factors that affect wound healing (6 of them)

A
  1. infection
  2. nutrition (protein, vitamins)
  3. steroids
  4. mechanical factors
  5. poor perfusion
  6. diabetes mellitus

Pathology Exam 1 (6 decks)

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