Inflammation 2 Flashcards
1
Q
vascular changes associated with acute inflammation
A
vasodilation - increased blood flow
increased vascular permeability - interstital fluid and proteins
2
Q
steps of leukocyte recruitment
A
- margination
- rolling
- adhesion
- transmigration
3
Q
leukocyte activation
A
- phagocytosis
- dectruction of phagocytosed material
4
Q
end result of leukocyte recruitment & activation
A
resolution/scarring/chronic inflammation
5
Q
leukocyte rolling
A
Sialyl-Lewis X oligosaccharide
6
Q
E-selectin (CD62E) on endothelial cells are induced by what
A
TNF and IL-1
7
Q
P-selecting (CD62P) are on what type of cell
A
endothelial cells and platelets
8
Q
P-selectin (CD62P) release is mediated by
A
histamine
9
Q
integrin adhesion transmembrane glycoproteins are induced by
A
LTB4 and C5a
10
Q
name the cellular adhesion molecules on endothelial cells
A
ICAM
VCAM
11
Q
increased integrin affinity and increased expression of integrin ligands (CAMS) lead to what type of adhesion
A
stable adhesion
12
Q
function of diapedeis
A
squeeze between cells at intracellular junctions
13
Q
what is chemotaxis
A
movement toward chemical gradient (LTB4, C5a, IL-8 and bacterial products)
14
Q
leukocytes secrete
A
collagenases
15
Q
CD31 (PECAM-1) are found on what cell types
A
- endothelial cells
- leukocytes
16
Q
function of CD31
A
mediates binding
17
Q
what are the 3 steps of phagocytosis
A
- recognition and attachment of particle to ingesting leukocyte
- engulfment, with subsequent formation of phagocytic vacuole
- killing and degradation of ingested material
18
Q
what are the opsonins of phagocytosis
A
IgG
C3b
19
Q
what are the leukocyte receptors of phagocytosis
A
Fc receptor
complement receptors CR1 and CR3
20
Q
how does engulfment occur during phagocytosis
A
pseudopods extend around object forming phagocytic vacuole
21
Q
how does phagocytosis kill, degrade and injest material
A
- fusion of phagocytic vacuole with lysosome (phagolysosome)
- lysosomal enzymes
- production of reactive oxygen species
22
Q
what is the goal of reactive oxygen species
A
kill microbe with HOCl
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
24
Q
what are the negative outcomes of acute inflammation
A
- scarring
- chronic inflammation
25
scarring (fibrosis) of acute inflammation caused by
- extensive tissue was damaged
- injured tissue filled in with connective tissue
26
chronic inflammation results from acute inflammation when
injured stimulus NOT cleared
27
what are the 3 defects in Leukocyte Function
1. leukocyte adhesion deficiency
2. chronic granulomatous disease (CGD)
3. Chediak-Higashi syndrome
28
leukocyte adhesion deficieny is defective in what
LAD1 - defective CD18 beta subunit of integrin
LAD2 - absence of sialyl-Lewis X due to defect in fucose metabolism
29
result of leukocyte adhesion deficiency
- 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
30
what is chronic granulomatous disease (CGD)
a defect in the oxidative burst due to a mutation in NADPH oxidase complex
31
patients with chronic granulomatous disease are suscpetible to what
catalase positive organisms, which eliminate the HOCl
32
what test is performed to confirm chronic granulomatous disease
nitroblue tetrazolium test - no dye in CGD
33
what is Chediak-Higashi syndrome
- disorder in the trafficking of organelles
- impaired funsion of phagosome with lysosomes
34
what is observed with Chediak-Higashi Syndrome
- 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
35
serous inflammation is triggered by
- agents causing mild dmage to blood vessel walls
- cytokines assocaited with increased vascular permeability
36
serous inflammation produces
exudate composed of watery fluid containing very little protein
37
in serous inflammation where does the exudate accumulate serum
- tissues (skin blister caused by a mild burn)
- natural cavities like the pericardial sac
- pleural or peritoneal cavities (plural effusion ascitis)
38
in serous inflammation what causes the exudate to accumulate serum
the secretion of reactive mesothelial cells
39
fibrinous exudate may be degraded by
-fibrinolysis
40
fibrinous exudate is removed by
macrophages resotring the normal tissue structure (resolution)
41
if macrophages fail to completely remove the fibrin, what happens
the fibrin will organize into granulation tissue with newly formed blood vessels resulting in scar formation (organization)
42
what happens if the fibrinous exudate is present in the pleural cavity
the process may end with the formation of dense scar tissue that bridges and obliterates the pleural cavity (fibrnous adhesion)
43
purulent or suppurative inflammation is a result of
severe inflammatory insult
44
in purulent or suppurative inflammation the exudate is composed mainly of
a large # of neutrophils (purulent exudate)
45
why does necrosis occur in purulent or suppurative inflammation
many neutrophils die or degenerate in the inflammed area releasing their lysosomal granules causing necrosis
46
what is pus
gelatinous mixture of a large number of neutrophils, many of them degenerated, necrotic tissue debris, and fibrinous material
47
ulcer results from
necrosis caused by an acute inflammator episode involving the mucosal lining or surface of an organ
48
ulcer formation is followed by sloughing of
the nectoric tissue and formation of a crater
49
causes of ulcer
bacterial or fungal infection, tissue injury by chemical or physical agents and ischemia
50
appearace of ulcers
May be deep or shallow, depending on the nature of the injurious agent and the length of the inflammatory process
51
healing process of ulcers
May heal either by resolution with no sequelae or by leaving behind a crater lined by fibrous tissue.
52
when do monocytes peak
2-3 days
53
where are monocytes found
in the blood
54
mechanisms of monocytes
- migration
- roll
- adhese
- transmigrate
55
monocytes develop into
macrogphes in tissue
56
monocytes and macrophages participate in what type of immune systems
both innate and adpative or specific immune systems
57
monocytes represent what % of the circulating white cells
1 to 6%
58
monocytes can move into tissue and differentiate into
macrophages
59
monocytes can also differentiate into
dendritic cells (specialized antigen presenting cell)
60
life span of macrophages
can survive in tissue for several months
## Footnote
61
where can macrophages reside
fixed locations:
- alveolar macrophages in lung
- Kupfer cells in liver
- microglial cells in brain
62
macrophages can act as
antigen presenting cells
63
what are the 3 functions of macrophages that act as APC
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
what are cytokines
poplypeptides functioning as mediators of inflammation and immune responses
65
cytokines are AKA
interleukins (communication btwn leukocytes)
66
cytokine of acute inflammation
TNF, IL-1, IL-6 recruit leukocytes and also cause systemic systems (fever)
67
function of IL-8
recruits neutrophils
68
function of IL-10 and TGF-B
anti-inflammatory
69
Th1 helper T-cells produce
IFN-Y
70
TH2 helper T cells produce
IL-4, IL-5 IL-10
71
when does chronic inflammation occur
- persistent infection
- infection with viruses, mycobacteria, fungi
- autoimmune disease
- foreign material
- malignancies
72
what are T lymphocytes
TCR and CD3 complex on cell surface recognize antigen on MHC molecules
73
function of CD4+ helper T cells
- recognize MHC class II on APC
- B7 molecule on APC binds CD28 on T cell
74
activated Th1 cells produce
IFNg (Classical pathway of macrophage activation), anti-virus
75
activated Th2 cells produce
IL-5 (eos activator) and IL4 & IL-13 (Alternative pathway, macrophage), anti-parasite
76
function of CD8+ cytotoxic T cells
recognize MHC 1 on all nucleated cells
77
CD8+ cytotoxic T cells are activated by
IL-2 from Th1 type T helper cell
78
CTLs kill by
performin/granzyme or activated CTLs
79
activated CTLs can express
Fas ligand and bine a target cell expressing Fas death receptor CD95
80
what are B lymphocytes
naive B cells made in bone marrow
81
function of B lymphocytes
recognize antigen with surface Ig molecules
82
stimulated B cells can differentiate into
plasma cells
83
what are granulomatous inflammation
- distinctive pattern of chronic inflammation
- lymphocytes and mutlinucleated giant cells
84
granulomatous inflammation characterized by
activated epithelioid hustiocytes
85
function of granulomatous inflammation
attempt to "wall-off" offending agents
86
granulomatous inflammation can be caused by
* Mycobacteria
* Fungi (Histoplasmosis, Blastomycosis)
* Sarcoidosis
* Reaction to foreign material
* Crohn’s disease
* Wegener Granulomatosis
87
E-selectin (CD62E) are found on what type of cell
endothelial cells
