Term Test 2 - Inflammation Flashcards
1
Q
what leukocyte is present in most lesions of acute inflammation
A
neutrophils (at least some)
2
Q
pus implies what
A
bacterial infection
3
Q
what are some examples of causes of neutrophilic inflammation
A
trauma, burns, immune complexes, foreign material, thrombosis, necrosis
4
Q
neutrophils enter tissues within _______
A
hours
5
Q
pus takes __________ days to form
A
several
6
Q
abscess has what specific connotations
A
implies fibrosis, which takes at least a week (4-5 days to start)
7
Q
What is the fate of a neutrophil
A
typically death once they enter a tissue
8
Q
What are the four outcomes of suppurative inflammation
A
1) resolution - if the stimulus is removed
2) chronic suppurative inflammation - if stimulus persists
3) stimulation of fibrosis
4) containment - abscess formation
9
Q
Do neutrophilic infections always produce pus
A
NO. If the neutrophils are contained in many compartments (ex. alveoli) or non-liquid, pus will not be produced
10
Q
What are the steps in neutrophil recruitment (8 total)
A
1) bacteria enter tissue
2) bacteria are recognized by antibodies, phagocytes, complement…
3) release of inflammatory mediators
4) inflammatory mediators act on the endothelium and leukocytes
5) rolling adhesion (mediated by selectins)
6) firm adhesion (mediated by integrins)
7) diapedesis
8) chemotaxis
11
Q
What are 3 mediators of chemotaxis
A
IL-8, C5a, LTB4
12
Q
Rolling is mediated by ______ on leukocytes and ___________ on endothelium
A
carbohydrates ; L-selectin/P-selectin
13
Q
Firm adhesion is mediated by ______ on leukocytes and ___________ on endothelium
A
integrins (ex. LFA1 aka CD11a/CD18); ICAM-1
14
Q
How do neutrophils undergo chemotaxis
A
Extension of lamellipodia that adhere to the tissue matrix
15
Q
What is an example of a chemotactic molecule for neutrophils
A
IL-8
16
Q
What is an example of a chemotactic molecule for eosinophils
A
RANTES
17
Q
What is an example of a chemotactic molecule for both neutrophils and eosinophils
A
C5a
18
Q
IgG binds to _________ and is an opsonin of ____________ immunity
A
FcγR; acquired
19
Q
C3b binds to ________ and is an opsonin of ____________ immunity
A
CR3; innate and acquired
20
Q
SP-A and MBL are opsonins of _____________ immunity
A
innate
21
Q
What TLR recognizes bacterial lipoproteins
A
TLR1, 2, 6
22
Q
What TLR recognizes bacterial LPS
A
TLR4
23
Q
What TLR recognizes CpG DNA
A
TLR9
24
Q
What TLR recognizes dsRNA
A
TLR3
25
What TLR recognizes flagellin
TLR5
26
What TLR recognizes ssRNA
TLR7,8
27
what are 4 mechanisms by which neutrophils kills bacteria
bactericidal proteins, oxidative killing, proteolytic enzymes, NETs
28
what are 4 types of antimicrobial proteins in neutrophil granules
lactoferrin, lysozyme, defensins, cathelicidins
29
what are 4 types of ROS
superoxide anion (O2-), hypochlorite (HOCl-) , peroxide (H2O2), myeloperoxidase
30
what are 3 types of proteolytic enzymes
elastase, collagenase, cathepsin G
31
How do leukocytes recognize bacteria (3)
1) opsonins, 2) PAMPs, 3) cytokines from other cells
32
How do leukocytes kill bacteria (4)
1) bactericidal enzymes, 2) oxidative killing, 3) proteolytic enzymes, 4) NETs
33
What is the stimulus for eosinophils (2)
Parasites and allergy
34
What are eosinophil effector functions
1) not phagocytic
2) oxidative injury
3) damage to cell membranes from granule proteins
35
What are eosinophil granule proteins (3)
Eosinophil myeloperoxidase, eosinophil major basic protein; eosinophil cationic protein
36
T/F low amounts of immune complexes are characteristic of many immune reactions
True
37
In what cases do immune complexes cause disease
Persistent infection/immune response or defective removal via phagocytosis and complement
38
Where do circulating immune complexes tend to deposit
synovium, glomeruli, skin
39
what is the Arthus reaction
when antigen localized to vessel walls reacts with circulating antibody
40
What is a granuloma
nodular mass of activated (epitheloid) macrophages, with or without giant cells, surrounded by lymphocytes and/or fibrous tissue
41
what is granulomatous inflammation
inflammation dominated by activated macrophages
42
T/F granulomatous inflammation often includes giant cells, epitheloid macrophages and fibrosis
T
43
What is pyogranulomatous inflammation
Dominated by activated macrophages and neutrophils
44
T/F granulomatous inflammation can be acute or chronic
FALSE, it is ALWAYS CHRONIC
45
What are four causes of granulomatous inflammation
1) foreign material
2) fungi
3) mycobacterium
4) DTH reaction
46
What is the pathogenesis of granulomatous inflammation
Response to inert foreign material OR immune response stimulated by Th1 cells
47
What are some sequelae of granulomatous inflammation
cachexia, space occupying lesion, impingement on a vital structure
48
How do macrophages become activated during granulomatous inflammation
Macrophages present antigen to Th1 cells -> Th1 cells produce IFNγ -> IFNγ activates the macrophages
49
What are the effector functions of macrophages
Phagocytosis and killing of bacteria
50
How does granulomatous inflammation differ from neutrophilic inflammation
In granulomatous, there are resident populations of macrophages that are ready for rapid responses AND there is better coordination between the immuno-inflammatory responses
51
What are some common causes of delayed type hypersensitivity
plants, textile fibres, dyes, cleansers, topical medications, shampoos, disinfectants, rubber, latex, plastics, metals
52
What is the time from exposure to the stimulus to onset of immune complex mediated disease
8 hours
53
What is the time from exposure to the stimulus to onset of delayed type hypersensitivity
24-72 hours
54
How would you describe the exudate formed by neutrophilic inflammation on mucosal surfaces
catarrhal or mucopurulent
55
What is hypopyon
neutrophilic inflammation in the anterior chamber of the eye; interferes with vision
56
endothelial activation is associated with an _______ in tissue factor _______ in protein C and ________ in thrombomodulin
increase, decrease, decrease
57
what colour does eosinophilic inflammation impart on tissues
green
58
What are three ways that neutrophils may damage host tissue
space occupying lesion, proteolytic/oxidative injury, induction of fibrosis and scarring
59
what are giant cells
macrophages with multiple nuclei (5-20)
60
T/F there are tons of lymphocytes in a granulomatous reaction to foreign bodies
FALSE
61
What are histiocytes
macrophages, monocytes, dendritic cells
62
Inflammatory lesions formed by lymphocytes +/- plasma cells without other leukocytes suggests
protozoal, viral, or immune-mediated disease
63
What is SIRS
Systemic consequences of localized or disseminated inflammation
64
What is sepsis
SIRS caused by infection
65
What is bacteremia
Bacteria in systemic circulation (with or without clinical disease)
66
What is septicemia
Bacteremia + clinically apparent disease
67
Name examples of systemic distribution of the causes of SIRS
- bacteremia
- anaphylaxis
68
Name examples of localized distribution of the causes of SIRS
- sterile pancreatitis
- bacterial pneumonia
69
What are examples of cytoplasmic receptors
NOD like receptors and RIG-I like receptors
70
What are three examples of soluble receptors
complement, antibody, collectins
71
What are examples of cell surface receptors
TLRs, Fc receptors, complement receptors
72
Changes in tissue factor, thrombomodulin and protein c promote _____________ when local
endothelial activation and hypercoagulability -> thrombosis
73
Changes in tissue factor, thrombomodulin and protein c promote __________ when disseminated
cogaulation -> DIC -> consumptive coagulοpathy
74
Name 5 consequences of SIRS
1. acute phase response
2. vasodilation (systemic hypotension)
3. increased vascular permeability (edema)
4. leukocyte activation (release of proteases and free radicals)
5. endothelial activation
75
What tissues are the first to suffer from SIRS
liver, heart, brain, kidney, intestine, lung
76
T/F acute phase response is static
False, it is adaptive
77
Define the acute phase response
systemic changes in physiologic processes during disease; adaptive
78
Name 3 acute phase proteins
CRP, fibrinogen, haptoglobin
79
Name 3 beneficial functions of acute phase proteins
control pathogens, quell inflammation, minimize tissue damage
80
Name 2 acute phase proteins in ruminants
haptoglobin, fibrinogen
81
Name 2 acute phase proteins in dogs
SAA, CRP
82
Name 2 acute phase proteins in cats
SAA, α1 acid glycoprotein
83
Which is most likely to trigger an acute phase response
A) bacterial pneumonia
B) dehiscence of GI tract
C) liver abscess
D) granuloma in cat liver
B (tons of bacteria, huge surface area affected)
84
Where is edema commonly localized to during SIRS
lung
85
Define autoimmune disease; what breaks down
Disease caused by an immune response against self-antigens (Ab mediated and cell mediated); breakdown of self tolerance
86
Name three mechanisms of tissue damage in autoimmune diseases and give an example of each
1) immune complex disease (vasculitis, polyarthritis, glomerulonephritis, uveitis)
2) antibody-mediated cytotoxicity (IMHA, thrombocytopenia, myasthenia gravis, pemphigus)
3) T cell-mediated cytotoxicity (myositis, discoid lupus)
87
What is inflammation
The active response of tissues to injury which stimulates a return to homeostasis
88
Neutrophils eliminate
extracellular bacteria
89
Eosinophils eliminate
metazoan parasites (worms)
90
Macrophages eliminate
Mycobacteria, fungi, foreign material
91
Cytotoxic T cells eliminate
viruses, protozoa
92
Name 4 goals of inflammation
1) eliminate the injurious stimulus or pathogen
2) contain the injury
3) remove necrotic tissue
4) initiate tissue repair
93
Humoral responses of inflammation include (5)
Fibrinogen, edema, antibody, innate defense proteins, complement
94
What occurs physiologically during cachexia and why
Catabolism of muscle to provide amino acids for tissue repair
95
The plasma concentration of acute phase protein increases within _____________ hours after the onset of tissue injury
5-10
96
The plasma concentration of acute phase proteins returns to normal within by _________ hours after the inflammatory response subsides
48 (2 days)
97
Measuring the concentration of _____________ is helpful to detect inflammatory responses in ruminants
plasma haptoglobin
98
What are the most frequent sites for bacteremic spread
pericardium, pleura, peritoneum, meninges, synovial surfaces
99
What well vascularized tissues are prone to population from bacteria
Cancellous bone, growth plate of bones, spleen, liver, kidney, lung, uvea, heart valves
100
What is a consequence of hypercoagulability in horses
laminitis
101
What are four ways in which autoimmune diseases damage tissues
1) antibody mediated opsonization/complement activation
2) formation of immune complexes
3) pro inflammatory/cytotoxic effects of autoreactive T cells
4) actions of T helper cells
102
What three changes indicate that an inflammatory reaction is occuring in a patient
1) fever
2) leukocytosis
3) changes in acute phase proteins
103
What are the three MAIN organs that get affected during SIRS/sepsis
kidney, liver, lung
104
T/F neutrophils secrete cytokines that can trigger thrombosis, leading to ischemia
T
105
what is activated upon immune complex deposition
1. activation of complement
2. activation of macrophages and neutrophils
106
what causes vasculitis
neutrophil-mediated damage to vessel walls (by being recruited to the vessel wall)
107
T/F well vascularized tissues are the most susceptible to immune complex disease
T
108
What are two consequences of immune complex deposition
1. vasculitis (due to the neutrophils)
2. activation of platelets and thrombosis -> infarction and ischemia
109
T/F Mycobacterium = mycoplasma
F
110
T/F macrophages activated by IFNγ are better equipped at killing intracellular pathogens
T
111
upon re-exposure to an antigen that elicited a TH1 response, what happens
TH1 cells secrete cytokines that induce an inflammatory response and IFNγ that activates macrophages
112
Type 1 sensitivity takes how many mins to develop
30
113
Type III sensitivity takes how long to develop
8 hours
114
Type IV sensitivity takes how long to develop
24-72h
115
what are three consequences of vasculitis from immune complex deposition
edema, petechiae, infarcts
116
How does the histologic appearance of a chronic allergic disease differ from that of the immediate reaction following injection of an allergen?
chronic: mast cells, eosinophils, lymphocytes
acute: degranulated mast cells, edema
117
In pemphigus foliaceus, how does the immune response cause pustules/ vesicles/ blisters in the epidermis?
Autoantibodies target desmosomal proteins
