PATHOMA Acute inflammation 10/30 Flashcards

1
Q

In acute what 2 presence in tissue?

A

edema and neutrophils

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2
Q

Acute infl arises in response to?

A

Infection (to eliminate pathogen) or tissue necrosis (to clear necrotic debris)

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3
Q

whats the point of acute infl in infection?

A

to eliminate pathogen

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4
Q

whats the point of acute infl in tissue necrosis?

A

to clear necrotic debris

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5
Q

response and specificity in acute?

A

IMMEDIATE response with LIMITED specificy

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6
Q

type of immunity in acute?

A

innate immunity

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7
Q

Mediators of acute infl? 5 groups

A
Toll like receptors (TLRs);
Arachidonic acid (AA) metabolites;
Mast cells;
Complement;
Hageman factors.
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8
Q
  1. where are present TLRs?
A

present on cells on the innate immune system (eg. macrophages and dendritic cells)
and ALSO ON ADAPTIVE IMMUNITY (eg lymphocytes).

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9
Q
  1. What does activate TLRs?
A

Activated by pathogen-associated molecular patterns (PAMPs) that are commonly shared by microbes

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10
Q
  1. example of PAMPs?
A

lipopolysacharide

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11
Q
  1. what is co-receptor for TLR4 on macrophages?
A

CD14

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12
Q
  1. PAMPs and TLRs interaction example?
A

CD14 on macrophages recognizes LPS (a PAMP) on the outer membrane of gram negative bacteria.

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13
Q
  1. TLR activation results in what?
A

upregulation of NF-kappaB.

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14
Q
  1. what does NF-kappaB?
A

its a nuclear transcription factor that activates immune response genes leading to production of multiple immune mediators.

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15
Q
  1. why TLR plays important role also in chronic inflammation?
A

TLR are present on ADAPTIVE IMMUNITY (eg lymphocytes) cells and, hence, play important role in mediating chronic inflammation.

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16
Q
  1. Arachidonic acid (AA) is released from the ….?
A

phospholipid cell membrane by phospholipase A2.

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17
Q
  1. AA is released by?
A

Arachidonic acid (AA) is released from the phospholipid cell membrane by phospholipase A2.

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18
Q
  1. once AA is released from the phospholipid cell membrane by phospholipase A2, whats next?
A

acted upon by cyclooxygenase or 5-lipoxygenase

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19
Q
  1. If AA is acted upon by cyclooxygenase, what is produced?
A

prostaglandins (PG).

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20
Q
  1. What PG mediate vasodilation and incr. permeability?
A

PGI2, PGD2, PGE2

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21
Q
  1. what PG mediates pain and fever?
A

PGE2

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22
Q
  1. PGE2 does what?
A

mediate vasodilation and incr. permeability

mediates pain and fever

23
Q
  1. What does PGI2, PGD2?
A

mediate vasodilation and incr. permeability

24
Q
  1. If AA is acted upon by 5-lipoxygenase, what is produced?
A

leukotrienes (LT)

25
2. What LT attracts and activates neutrophils?
LTB4
26
2. What LT mediate vasoconstriction, bronchospasm and increased vascular permeability?
LTC4, LTD4, LTE4
27
2. what are slow reacting substances for anaphylaxis?
LTC4, LTD4, LTE4
28
2. what does LTB4?
attracts and activates neutrophils
29
2. What does LTC4, LTD4, LTE4?
mediate vasoconstriction, bronchospasm and increased vascular permeability + they are slow reacting substances for anaphylaxis
30
3. mast cells are distributed in what tissue?
connective tissue
31
3. what activates mast cells?
1. Tissue trauma; 2. Complement proteins C3a and C5a or 3. cross-linking of cell-surface IgE by antigen
32
3. IMMEDIATE response of mast cell once they are activated?
release of preformed histamine granules, which mediate VASODILATION of arterioles and increased vascular permeability
33
3. release of preformed histamine granules from mast cells results in?
release of preformed histamine granules, which mediate vasodilation of arterioles and increased vascular permeability
34
3. DELAYED response of mast cell involves what?
production of arachidonic acid metabolites, particularly leukotrienes.
35
4. What is complement?
proinflammatory serum proteins that ,,complement" inflammation
36
4. Complement proteins circulate in what form?
inactive precursors
37
4. What activates complement? classical pathway
C1 binds IgG or IgM that bound to antigen
38
4. What activates complement? alternative pathway
microbial products directly activate complement
39
4. What activates complement? mannose-binding lectin (MBL) pathway
MBL binds to mannose on m/os and activates complement
40
4. All complement cascade pathways result in production of what?
C3 convertase
41
4. What mediates C3 convertase?
C3 to C3a and C3b
42
4. Due to activity of convertase eventually is produced what?
C5 convertase (C5 --> C5a and C5b)
43
4. What does C5b?
C5b complexes with C6-C9 to form MAC
44
4. What are anaphylatoxins?
C3a and C5a
45
4. What does anaphylatoxins?
trigger mast cell degranulation, resulting in histamine-mediated vasodilation and increased vascular permeability.
46
4. What other function has C5a?
chemotactic for neutrophils
47
4. what does C3b?
opsonin for phagocytosis
48
4. What does MAC?
lyses microbes by creating a hole in the cell membrane
49
5. What is Hageman factor?
Factor XII
50
5. How is caller factor XII?
Hageman factor
51
5. where is produced Hageman factor (factor XII)?
is inactive proinflammatory protein produced in liver
52
5. when is activated factor XII?
activated upon exposure to subendothelial or tissue collagen.
53
5. activated factor XII leads to activation of what?
1. Coagulation and fibrinolytic systems; 2. Complement; 3. Kinin system
54
5. what does Kinin system?
Kinin cleaves high-molecular-weight kininogen (HMWK) to bradykinin, which mediates vasodilation and increased vascular permeability (similar to histamine), as well as pain.