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1 STEP UWorld pathology > PATHOMA Acute inflammation 10/30 > Flashcards

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
Q
  1. What LT attracts and activates neutrophils?
A

LTB4

26
Q
  1. What LT mediate vasoconstriction, bronchospasm and increased vascular permeability?
A

LTC4, LTD4, LTE4

27
Q
  1. what are slow reacting substances for anaphylaxis?
A

LTC4, LTD4, LTE4

28
Q
  1. what does LTB4?
A

attracts and activates neutrophils

29
Q
  1. What does LTC4, LTD4, LTE4?
A

mediate vasoconstriction, bronchospasm and increased vascular permeability + they are slow reacting substances for anaphylaxis

30
Q
  1. mast cells are distributed in what tissue?
A

connective tissue

31
Q
  1. what activates mast cells?
A
  1. Tissue trauma;
  2. Complement proteins C3a and C5a or
  3. cross-linking of cell-surface IgE by antigen
32
Q
  1. IMMEDIATE response of mast cell once they are activated?
A

release of preformed histamine granules, which mediate VASODILATION of arterioles and increased vascular permeability

33
Q
  1. release of preformed histamine granules from mast cells results in?
A

release of preformed histamine granules, which mediate vasodilation of arterioles and increased vascular permeability

34
Q
  1. DELAYED response of mast cell involves what?
A

production of arachidonic acid metabolites, particularly leukotrienes.

35
Q
  1. What is complement?
A

proinflammatory serum proteins that ,,complement” inflammation

36
Q
  1. Complement proteins circulate in what form?
A

inactive precursors

37
Q
  1. What activates complement? classical pathway
A

C1 binds IgG or IgM that bound to antigen

38
Q
  1. What activates complement? alternative pathway
A

microbial products directly activate complement

39
Q
  1. What activates complement? mannose-binding lectin (MBL) pathway
A

MBL binds to mannose on m/os and activates complement

40
Q
  1. All complement cascade pathways result in production of what?
A

C3 convertase

41
Q
  1. What mediates C3 convertase?
A

C3 to C3a and C3b

42
Q
  1. Due to activity of convertase eventually is produced what?
A

C5 convertase (C5 –> C5a and C5b)

43
Q
  1. What does C5b?
A

C5b complexes with C6-C9 to form MAC

44
Q
  1. What are anaphylatoxins?
A

C3a and C5a

45
Q
  1. What does anaphylatoxins?
A

trigger mast cell degranulation, resulting in histamine-mediated vasodilation and increased vascular permeability.

46
Q
  1. What other function has C5a?
A

chemotactic for neutrophils

47
Q
  1. what does C3b?
A

opsonin for phagocytosis

48
Q
  1. What does MAC?
A

lyses microbes by creating a hole in the cell membrane

49
Q
  1. What is Hageman factor?
A

Factor XII

50
Q
  1. How is caller factor XII?
A

Hageman factor

51
Q
  1. where is produced Hageman factor (factor XII)?
A

is inactive proinflammatory protein produced in liver

52
Q
  1. when is activated factor XII?
A

activated upon exposure to subendothelial or tissue collagen.

53
Q
  1. activated factor XII leads to activation of what?
A
  1. Coagulation and fibrinolytic systems;
  2. Complement;
  3. Kinin system
54
Q
  1. what does Kinin system?
A

Kinin cleaves high-molecular-weight kininogen (HMWK) to bradykinin, which mediates vasodilation and increased vascular permeability (similar to histamine), as well as pain.

1 STEP UWorld pathology (10 decks)

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