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Pathology > Inflammation 2 > Flashcards

Inflammation 2 Flashcards

1
Q

vascular changes associated with acute inflammation

A

vasodilation - increased blood flow

increased vascular permeability - interstital fluid and proteins

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2
Q

steps of leukocyte recruitment

A
  • margination
  • rolling
  • adhesion
  • transmigration
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3
Q

leukocyte activation

A
  • phagocytosis
  • dectruction of phagocytosed material
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4
Q

end result of leukocyte recruitment & activation

A

resolution/scarring/chronic inflammation

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5
Q

leukocyte rolling

A

Sialyl-Lewis X oligosaccharide

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6
Q

E-selectin (CD62E) on endothelial cells are induced by what

A

TNF and IL-1

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7
Q

P-selecting (CD62P) are on what type of cell

A

endothelial cells and platelets

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8
Q

P-selectin (CD62P) release is mediated by

A

histamine

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9
Q

integrin adhesion transmembrane glycoproteins are induced by

A

LTB4 and C5a

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10
Q

name the cellular adhesion molecules on endothelial cells

A

ICAM

VCAM

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11
Q

increased integrin affinity and increased expression of integrin ligands (CAMS) lead to what type of adhesion

A

stable adhesion

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12
Q

function of diapedeis

A

squeeze between cells at intracellular junctions

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13
Q

what is chemotaxis

A

movement toward chemical gradient (LTB4, C5a, IL-8 and bacterial products)

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14
Q

leukocytes secrete

A

collagenases

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15
Q

CD31 (PECAM-1) are found on what cell types

A
  • endothelial cells
  • leukocytes
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16
Q

function of CD31

A

mediates binding

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17
Q

what are the 3 steps of phagocytosis

A
  1. recognition and attachment of particle to ingesting leukocyte
  2. engulfment, with subsequent formation of phagocytic vacuole
  3. killing and degradation of ingested material
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18
Q

what are the opsonins of phagocytosis

A

IgG

C3b

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19
Q

what are the leukocyte receptors of phagocytosis

A

Fc receptor

complement receptors CR1 and CR3

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20
Q

how does engulfment occur during phagocytosis

A

pseudopods extend around object forming phagocytic vacuole

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21
Q

how does phagocytosis kill, degrade and injest material

A
  1. fusion of phagocytic vacuole with lysosome (phagolysosome)
  2. lysosomal enzymes
  3. production of reactive oxygen species
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22
Q

what is the goal of reactive oxygen species

A

kill microbe with HOCl

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23
Q

what is the resolution of acute inflammation

A
  • injurious stimulus cleared
  • mediators and acute inflammatory cells clear
  • neutrophils undergo apoptosis
  • replacement of injured cells
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24
Q

what are the negative outcomes of acute inflammation

A
  1. scarring
  2. chronic inflammation
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25
Q

scarring (fibrosis) of acute inflammation caused by

A
  • extensive tissue was damaged
  • injured tissue filled in with connective tissue
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26
Q

chronic inflammation results from acute inflammation when

A

injured stimulus NOT cleared

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27
Q

what are the 3 defects in Leukocyte Function

A
  1. leukocyte adhesion deficiency
  2. chronic granulomatous disease (CGD)
  3. Chediak-Higashi syndrome
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28
Q

leukocyte adhesion deficieny is defective in what

A

LAD1 - defective CD18 beta subunit of integrin

LAD2 - absence of sialyl-Lewis X due to defect in fucose metabolism

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29
Q

result of leukocyte adhesion deficiency

A
  • impaired adhesion of neutrophils to endothelium and thus impaired acute inflammatory response
  • recurrent bacterial infections which lack neutrophls in tissue
  • increased circulating neutrophils
  • when baby is born, umbilical cord will take longer to separate
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30
Q

what is chronic granulomatous disease (CGD)

A

a defect in the oxidative burst due to a mutation in NADPH oxidase complex

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31
Q

patients with chronic granulomatous disease are suscpetible to what

A

catalase positive organisms, which eliminate the HOCl

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32
Q

what test is performed to confirm chronic granulomatous disease

A

nitroblue tetrazolium test - no dye in CGD

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33
Q

what is Chediak-Higashi syndrome

A
  • disorder in the trafficking of organelles
  • impaired funsion of phagosome with lysosomes
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34
Q

what is observed with Chediak-Higashi Syndrome

A
  • giant granules in leukocytes (granules from Golfi do not distribute properly in cytoplasm)
  • increased death of neutrophils in bone marrow (neutropenia)
  • secretion of lytic secretory granules in T-cells is affected
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35
Q

serous inflammation is triggered by

A
  • agents causing mild dmage to blood vessel walls
  • cytokines assocaited with increased vascular permeability
36
Q

serous inflammation produces

A

exudate composed of watery fluid containing very little protein

37
Q

in serous inflammation where does the exudate accumulate serum

A
  • tissues (skin blister caused by a mild burn)
  • natural cavities like the pericardial sac
  • pleural or peritoneal cavities (plural effusion ascitis)
38
Q

in serous inflammation what causes the exudate to accumulate serum

A

the secretion of reactive mesothelial cells

39
Q

fibrinous exudate may be degraded by

A

-fibrinolysis

40
Q

fibrinous exudate is removed by

A

macrophages resotring the normal tissue structure (resolution)

41
Q

if macrophages fail to completely remove the fibrin, what happens

A

the fibrin will organize into granulation tissue with newly formed blood vessels resulting in scar formation (organization)

42
Q

what happens if the fibrinous exudate is present in the pleural cavity

A

the process may end with the formation of dense scar tissue that bridges and obliterates the pleural cavity (fibrnous adhesion)

43
Q

purulent or suppurative inflammation is a result of

A

severe inflammatory insult

44
Q

in purulent or suppurative inflammation the exudate is composed mainly of

A

a large # of neutrophils (purulent exudate)

45
Q

why does necrosis occur in purulent or suppurative inflammation

A

many neutrophils die or degenerate in the inflammed area releasing their lysosomal granules causing necrosis

46
Q

what is pus

A

gelatinous mixture of a large number of neutrophils, many of them degenerated, necrotic tissue debris, and fibrinous material

47
Q

ulcer results from

A

necrosis caused by an acute inflammator episode involving the mucosal lining or surface of an organ

48
Q

ulcer formation is followed by sloughing of

A

the nectoric tissue and formation of a crater

49
Q

causes of ulcer

A

bacterial or fungal infection, tissue injury by chemical or physical agents and ischemia

50
Q

appearace of ulcers

A

May be deep or shallow, depending on the nature of the injurious agent and the length of the inflammatory process

51
Q

healing process of ulcers

A

May heal either by resolution with no sequelae or by leaving behind a crater lined by fibrous tissue.

52
Q

when do monocytes peak

A

2-3 days

53
Q

where are monocytes found

A

in the blood

54
Q

mechanisms of monocytes

A
  • migration
  • roll
  • adhese
  • transmigrate
55
Q

monocytes develop into

A

macrogphes in tissue

56
Q

monocytes and macrophages participate in what type of immune systems

A

both innate and adpative or specific immune systems

57
Q

monocytes represent what % of the circulating white cells

A

1 to 6%

58
Q

monocytes can move into tissue and differentiate into

A

macrophages

59
Q

monocytes can also differentiate into

A

dendritic cells (specialized antigen presenting cell)

60
Q

life span of macrophages

A

can survive in tissue for several months

61
Q

where can macrophages reside

A

fixed locations:

  • alveolar macrophages in lung
  • Kupfer cells in liver
  • microglial cells in brain
62
Q

macrophages can act as

A

antigen presenting cells

63
Q

what are the 3 functions of macrophages that act as APC

A
  1. Digest and cleaved the original protein antigen into several small peptides. (13 to 18 amino acids)
  2. Load these short peptides into the groove of MHC class I or II proteins
  3. Display the antigen-MHC complex to an appropriate T cell in order to be activated
64
Q

what are cytokines

A

poplypeptides functioning as mediators of inflammation and immune responses

65
Q

cytokines are AKA

A

interleukins (communication btwn leukocytes)

66
Q

cytokine of acute inflammation

A

TNF, IL-1, IL-6 recruit leukocytes and also cause systemic systems (fever)

67
Q

function of IL-8

A

recruits neutrophils

68
Q

function of IL-10 and TGF-B

A

anti-inflammatory

69
Q

Th1 helper T-cells produce

A

IFN-Y

70
Q

TH2 helper T cells produce

A

IL-4, IL-5 IL-10

71
Q

when does chronic inflammation occur

A
  • persistent infection
  • infection with viruses, mycobacteria, fungi
  • autoimmune disease
  • foreign material
  • malignancies
72
Q

what are T lymphocytes

A

TCR and CD3 complex on cell surface recognize antigen on MHC molecules

73
Q

function of CD4+ helper T cells

A
  • recognize MHC class II on APC
  • B7 molecule on APC binds CD28 on T cell
74
Q

activated Th1 cells produce

A

IFNg (Classical pathway of macrophage activation), anti-virus

75
Q

activated Th2 cells produce

A

IL-5 (eos activator) and IL4 & IL-13 (Alternative pathway, macrophage), anti-parasite

76
Q

function of CD8+ cytotoxic T cells

A

recognize MHC 1 on all nucleated cells

77
Q

CD8+ cytotoxic T cells are activated by

A

IL-2 from Th1 type T helper cell

78
Q

CTLs kill by

A

performin/granzyme or activated CTLs

79
Q

activated CTLs can express

A

Fas ligand and bine a target cell expressing Fas death receptor CD95

80
Q

what are B lymphocytes

A

naive B cells made in bone marrow

81
Q

function of B lymphocytes

A

recognize antigen with surface Ig molecules

82
Q

stimulated B cells can differentiate into

A

plasma cells

83
Q

what are granulomatous inflammation

A
  • distinctive pattern of chronic inflammation
  • lymphocytes and mutlinucleated giant cells
84
Q

granulomatous inflammation characterized by

A

activated epithelioid hustiocytes

85
Q

function of granulomatous inflammation

A

attempt to “wall-off” offending agents

86
Q

granulomatous inflammation can be caused by

A
  • Mycobacteria
  • Fungi (Histoplasmosis, Blastomycosis)
  • Sarcoidosis
  • Reaction to foreign material
  • Crohn’s disease
  • Wegener Granulomatosis
87
Q

E-selectin (CD62E) are found on what type of cell

A

endothelial cells

Pathology (18 decks)

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