Lectures 6-11 Flashcards
(114 cards)
1
Q
cellular infiltrate in acute inflammation
A
neutrophils
2
Q
cellular infiltrate in chronic inflammation
A
monocytes/macrophages and lymphocytes
3
Q
what do TLRs do when activated?
A
stimulate release of cytokines (TNF)
4
Q
role of inflammasome
A
cytoplasmic complex recognizing parts of dead cells; triggers activation of caspase-1 which activates IL-1, which, in turn, triggers leukocyte recruitment
5
Q
key difference between TLRs and inflammasome
A
TLR recognizes extracellular microbes while inflammasome recognizes products of dead cells and some microbes
6
Q
what cytokines activation endothelium at initiation of inflammation, leading to leukocyte binding?
A
IL-1 and TNF
7
Q
vasodilation is caused by what mediators?
A
histamine and nitric oxide
8
Q
increased vascular permeability is caused by what mediators?
A
histamine, bradykinin
9
Q
histamine: source, effect
A
mast cells and basophils; vasodilation, increased vascular permeability, smooth muscle contraction
10
Q
nitric oxide: source, effect
A
endothelial cells; vasodilation
11
Q
bradykinin: effect
A
vasodilation, increased permeability, pain
12
Q
transudate: protein and cell content, inflammatory/non-inflammatory, specific gravity
A
hypocellular and low protein content; non-inflammatory; low specific gravity (<1.012)
13
Q
exudate: protein and cell content, inflammatory/non-inflammatory, specific gravity
A
cellular and protein rich; inflammatory; high specific gravity (>1.020)
14
Q
specific gravity in infection
A
high
15
Q
selectins: location, mechanism
A
on endothelial cells, platelets, leukocytes, not present on cell surfaces until cell is activated by mediators; aid in rolling and loose attachment of leukocytes to endothelial cells
16
Q
integrins: location, mechanism
A
on leukocytes, TNF and IL-1 secreted by macrophages at site of injury increase endothelial cell ligand expression; results in stable attachment of leukocytes
17
Q
what chemokine drives diapedesis?
A
CD31 (PECAM1)
18
Q
cytokines that cause fever
A
TNF and IL-1
19
Q
types of acute inflammation
A
serous, fibrous, suppurative, ulcer
20
Q
serous inflammation: describe, examples
A
outpouring of protein-poor fluid from plasma or serosal cavity linings; congestive heart failure, skin blister from burn
21
Q
congestive heart failure, skin blister from burn are examples of what type of acute inflammation?
A
serous
22
Q
fibrinous inflammation: describe, examples
A
secondary to more severe injury than serous, affects linings (meninges, percardium, pleura, peritoneum), may lead to scarring; pericarditis, pleuritis, peritonitis
23
Q
suppurative inflammation: describe, examples
A
occurs with infections, pus formation, abscess; acute appendicitis, acute meningitis
24
Q
type of acute inflammation seen with acute appendicitis, acute meningitis, acute bronchopneumonia
A
suppurative
25
local defect on surface of organ or tissue in patients with circulatory insufficiency or diabetes
ulcer
26
role of eosinophils in chronic inflammation
produce major basic protein which is toxic to parasites and epithelial cells
27
two major characteristics of chronic inflammation
angiogenesis and fibrosis
28
what type of inflammation is characterized by aggregates of epithelioid macrophages, multinucleated giant cells, fibrosis, and angiogenesis?
granulomatous inflammation (a type of chronic inflammation)
29
granulomatous inflammation: morphology
aggregates of epithelioid macrophages, multinucleated giant cells, fibrosis, and angiogenesis
30
three characteristics of systemic inflammation
fever, elevated acute-phase proteins, leukocytosis
31
acute phase proteins: source, 3 proteins, function
synthesized in liver, stimulated by IL-6; C-reactive protein, fibrinogen, serum amyloid A protein; aid in elimination of microbes, fibrinogen binds to RBCs causing stacks that sediment more rapidly than normal, causing increased ESR (erythrocyte sedimentation rate)
32
increased erythrocyte sedimentation rate: mechanism, what it is indicative of
fibrinogen binds to RBCs causing stacks that sediment more rapidly than normal; infection or autoimmune disease
33
what cytokines stimulate leukocytosis in systemic inflammation?
TNF and IL-1
34
neutrophilia is indicative of what? what is left shift?
bacterial infection; accelerated release of immature neutrophils
35
lymphocytosis is indicative of what?
viral infection
36
which stage of an immune response is clinically silent?
sensitization stage (primary response)
37
spring allergen, summer allergen, fall allergen
tree, grass, weed
38
early phase (15-30 min.) of type 1 hypersensitivity is marked by what?
tryptase
39
degranulation mechanism
mast cells and basophils express FcRI (high affinity receptor for IgE), and when IgE binds and the receptor is crosslinked, the mast cell/basophil degranulates, releasing preformed mediators
40
single best marker of mast cell degranulation
tryptase
41
role of IL-4 and IL-13
class switching to IgE
42
role of IL-3, IL-5, and GM-CSF
survival and activation of eosinophils
43
cytokines responsible for class switching to IgE
IL-4 and IL-13
44
cytokines responsible for survival and activation of eosinophils
IL-3, IL-5, and GM-CSF
45
leukotrienes: source, role in type 1 hypersensitivity reactions
mast cells; eosinophil migration, smooth muscle contraction, vascular permeability, mucus hypersecretion
46
elevated eosinophils is an indication of what?
NAACP mnemonic: neoplasia, asthma, allergy, connective tissue disease, parasitic disease
47
how do eosinophils get to the site of inflammation?
they have CCR3, a receptor for eotaxin, which is a chemokine found at sites of allergic inflammation
48
effects of corticosteroids on eosinophils
steroids induce rapid apoptosis of eosinophils; steroids inhibit the production of IL-5, causing decreased release of eosinophils form the marrow; this effect is mediated by steroid binding to GR-alpha and inhibiting AP-1 and NFkappaB
49
major basic protein: source, function
eosinophil; mast cell activation, helminthotoxic
50
eosinophil cationic protein (ECP): function
mast cell activation, helminthotoxic, neurotoxic
51
platelet activating factor (PAF): source, function
eosinophil; bronchoconstriction, activates platelets
52
LTC4 (leukotriene C4): source, function
eosinophil; bronchoconstriction, mucus hypersecretion, edema
53
allergic rhinitis: mechanism
symptoms due to crosslinking of IgE in nasal mucosa and ocular conjunctiva with specific antigen exposure
54
asthma: differential diagnoses
vocal cord dysfunction (localized obstruction), COPD (generalized obstruction)
55
asthma: components in inflammatory cell infiltrate
eosinophils and lymphocytes
56
asthma: mechanism
symptoms are due in part by IgE-mediated disease in lower airways: wheezing, shortness of breath due to increased airway constriction (prevents exhalation), increased mucus secretion and production
57
mediators of anaphylaxis
histamine, leukotrienes, nitric oxide
58
histamine function via H1
smooth muscle contraction, vascular permeability
59
histamine function via H2
vascular permeability
60
histamine function via H1+H2
vasodilation, pruritus
61
what antibodies are involved in type 2 hypersensitivity?
IgG and IgM
62
how do some drugs induce an antibody response?
they become antigenic when bound to RBCs or platelets
63
basis of type 3 hypersensitivity
production of IgG against a soluble antigen --\> immune complex forms and activates complement
64
where do immune complexes preferentially deposit?
sites with increased vascular permeability, sites of increased antigen
65
serum sickness: what is it, what type of hypersensitivity, when does it happen and why
systemic reaction from injection of large quantities of foreign (non-human) protein; type 3; occurs 7-10 days after first exposure to antigen (this time is needed to switch from IgM to IgG --\> form complexes)
66
serum sickness: sequence of events
1. IgM is made and clears some of the foreign serum proteins 2. IgM is class-switched to IgG and antigen-antibody complexes start to form and cause symptoms 3. when antigen becomes limited, complexes do not form and symptoms go away
67
farmer's lung: what type of hypersensitivity, what happens
type 3; alveolitis (destruction of alveolar wall) due to type 3 reaction against hay dust or mold spores --\> impairment in gas exchange
68
usual target organ of type 4 hypersensitivity
skin
69
IFNgamma: source, role in type 4 hypersensitivity
T cells; induces expression of adhesion molecules and activates macrophages
70
TNF and lymphotoxin: source, role in type 4 hypersensitivity
T cells; local tissue destruction, induces expression of adhesion molecules
71
IL-3 and GM-CSF: source, role in type 4 hypersensitivity
T cells; stimulates monocyte production from bone marrow
72
what cell mediates a tuberculin response?
TH1
73
Rhus dermatitis: mechanism
chemical from poison ivy leaf bind with self proteins and generates extensive macrophage-mediated inflammation
74
is antigen soluble or cell-associated for each hypersensitivity reaction?
1: soluble 2: cell (or matrix) associated 3: soluble 4: soluble for TH1 cells and cell associated for CD8 CTLs
75
components of repair (3)
remnants of injured tissue, endothelial cells, fibroblasts
76
what kind of cells repair by connective tissue (scar)?
non-dividing cells
77
asymmetric replication
with cell division, a daughter cell differentiates, but the other daughter cell remains a stem cell
78
what growth factors induce angiogenesis?
VEGF and FGF
79
what growth factors produce ECM proteins?
PDGF and TGF-beta
80
PDGF and TGF-beta: source, functions
platelets, macrophages, epithelium, and smooth muscle cells; produce ECM proteins
81
two basic forms of ECM and where each is synthesized
interstitial matrix: fibroblasts basement membrane: mesenchyme and epithelium
82
provides scaffold essential for healing without scar
ECM
83
Ehlers-Danlos syndrome: mechanism, clinical presentation
genetic defects in collagen synthesis; hyperextensible skin, hypermobile joints and ligaments, rupture of internal organs and large arteries
84
hyperextensible skin, hypermobile joints and ligaments, rupture of internal organs and large arteries
Ehlers-Danlos syndrome
85
Marfan syndrome: mechanism, clinical presentation
mutation affecting fibrillin (major component of ECM abundant in aorta, lens, ligaments); aneurysm and dilatation of aorta, dislocated lens, long legs, arms, fingers
86
aneurysm and dilatation of aorta, dislocated lens, long legs, arms, fingers
Marfan syndrome
87
4 sequential steps of repair by connective tissue
angiogenesis, fibroblast migration and proliferation, scar formation, remodeling
88
granulation tissue: when does it appear
present by 3-5 days
89
growth factors responsible for fibroblast migration and proliferation
TGF-beta, PDGF, FGF
90
what growth factor is necessary for both angiogenesis and fibroblast migration/proliferation?
FGF
91
remodeling of scar is accomplished by what?
matrix metalloproteinases (MMP) containing zinc degrades collagen and other ECM proteins
92
matrix metalloproteinases (MMP): role
degrades collagen and other ECM proteins = remodeling of scar
93
healing by first intention: when are neutrophils replaced with macrophages
by day 3
94
how do hormones affect healing?
steroids inhibit TGF-beta and decreases fibrosis
95
raised scar due to excess collagen
keloid
96
keloid
raised scar due to excess collagen
97
protrudes above surrounding skin without skin covering
exuberant granulation
98
wound healing: when does a thin layer of epithelial cells cover wound?
48 hours
99
wound healing: when is epidermis at full thickness?
day 5
100
wound healing: when is granulation tissue present?
day 3 to second week
101
wound healing: when is there connective tissue remodeling?
after one month
102
wound healing: when is wound strength 70-80%?
by three months
103
rank HIV transmission risk: mom-baby (without prophylaxis), IVDU, percutaneous (blood), receptive vaginal intercourse, receptive anal intercourse
IVDU \> mom-baby \> receptive anal intercourse \> percutaneous (blood) \> receptive vaginal intercourse
104
window period: what is it, and how long
HIV can be detected in blood but antibodies to HIV are not present; 6-8 weeks
105
HIV: when do signs and symptoms begin?
1-4 weeks after exposure
106
HIV: how long do symptoms last?
\<14 days
107
HIV: when is viral load the highest?
first 2-3 months
108
immune reconstitution inflammatory syndrome: when does it develop?
within 8 weeks of starting antiretroviral treatment
109
microbial translocation in HIV: mechanism
massive mucosal CD4 T cell depletion results in increased gut permeability --\> increased plasma LPS levels; gut permeability increases over time
110
main difference between direct and indirect alloantigen recognition
direct: graft APCs indirect: host APCs
111
major players in chronic rejection (3)
CD4 T cells, macrophages, cytokines
112
what are minor histocompatibility antigens?
cleaved and processed endogenous proteins that occupy the binding groove of MHC class I and II
113
GVHD: mechanism
incoming donor T cells recognize host APCs, become activated, attack tissues of recipient and cause immediate tissue damage
114
what can exacerbate the symptoms off GVHD?
preconditioning can cause tissue damage that allows LPS to cross the gut barrier or cytokines to be released by damaged tissues --\> activated macrophages amplify the function of donor T cells
