2.1 - Acute inflammation Flashcards

1
Q

which CD located on macrophages is a coreceptor for TLR4?

A

CD14

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2
Q

CD14 on macrophages recognizes what bacterial component?

A

LPS

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3
Q

which CD on macrophages is responsible for recognition of LPS?

A

CD14

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4
Q

TLR activation results in upregulation of ______, a nuclear transcription factor

A

NFkB

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5
Q

PGE2 is responsible for mediating ______ and _______

A

pain and fever

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6
Q

5-lipoxygenase produces ______________

A

leukotrienes

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7
Q

what are the neutrophil chemoattractants? (4)

A
  • LTB4
  • C5a
  • IL-8
  • bacterial products
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8
Q

mast cells are activated by what 3 factors?

A
  • tissue trauma
  • C3a and C5a
  • cross linking of cell surface IgE by antigen
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9
Q

the second phase of the mast cell response is mediated by ____________

A

leukotrienes

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10
Q

what are the 3 main complement pathways, and activators?

A
  • classical: C1 binds IgG or IgM
  • alternative: microbial products
  • mannose-binding lectin: MBL binds mannose on microorganisms
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11
Q

all complement pathways converge in production of:

A

C3 convertase

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12
Q

what are the complement anaphylatoxins?

A

C3a and C5a

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13
Q

hageman factor is responsible for activation of what 3 systems?

A
  • coagulation / fibrinolytic
  • complement
  • kinin
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14
Q

in inflammation, vascular permeability occurs in what vessel type, specifically?

A

post-capillary venules

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15
Q

in inflammation, what two molecules are responsible for sensitization of nerve endings?

A
  • bradykinin

- PGE2

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16
Q

what is the pathophysiology behind fever?

A
  • pyrogens cause macrophages to release IL-1 and TNF, which increase cyclooxygenase activity in perivascular cells of the hypothalamus
  • increased PGE2 raises temperature set point
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17
Q

in fever production, macrophages release what compounds? what do they act on? where?

A
  • IL-1 and TNF

- increase cyclooxygenase activity in perivascular cells of hypothalamus

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18
Q

what PG is responsible for raising the temperature set point in fever?

A

PGE2

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19
Q

weibel palade bodies contain what mediators?

A
  • von willebrand factor (“W”)

- P-selectin (“P”)

20
Q

in the rolling phase of neutrophil chemotaxis, P-selectin is mediated by ______________

21
Q

in the rolling phase of neutrophil chemotaxis, E-selectin is induced by what two compounds?

A
  • TNF

- IL-1

22
Q

in the rolling phase of neutrophil chemotaxis, where are selectins located?

A

endothelial cells

23
Q

in the adhesion phase of neutrophil chemotaxis, where are CAMs located?

A

endothelium

24
Q

what 2 molecules are responsible for upregulation of ICAM and VCAM in the adhesion phase of neutrophil chemotaxis?

A

TNF and IL-1

25
in the adhesion phase of neutrophil chemotaxis, where are integrins located?
leukocytes
26
in the adhesion phase of neutrophil chemotaxis, leukocytes are upregulated by what two molecules?
C5a and LTB4
27
what is the inheritance of leukocyte adhesion deficiency?
AR
28
leukocytes adhesion deficiency is a defect of what molecule type, and on what cell type? what is the result?
- integrins (CD18 subunit) on leukocytes | - delayed separation of umbilical cord, lack of pus
29
leukocytes transmigrate across endothelium of what vessel type, specifically?
postcapillary venules
30
chediak higashi syndrome is a defect in what process? what is the underlying cause?
impaired phagolysosome formation due to protein trafficking defect
31
what is the inheritance of chediak higashi syndrome?
AR
32
the following sequelae correspond to what syndrome? - increased risk of pyogenic infections - neutropenia - giant granules in leukocytes - defective primary hemostasis - albinism - peripheral neuropathy
chediak higashi syndrome
33
the neutropenia seen in chediak higashi syndrome is due to________________
intramedullary death of neutrophils
34
the giant granules in leukocytes seen in chediak higashi syndrome is due to________________
fusion of granules arising from golgi apparatus
35
the defective primary hemostasis seen in chediak higashi syndrome is due to________________
abnormal dense granules in platelets
36
chronic granulomatous disease is characterized by a defect in what process?
poor oxygen dependent killing
37
chronic granulomatous disease is due to a defect in what ENZYME?
NADPH oxidase
38
what are the main catalase positive organisms responsible for infections in chronic granulomatous disease?
- pseudomonas cepacia********** - s. aureus - serratia marcescens - nocardia - aspergillus
39
what is the test used to diagnose chronic granulomatous disease? how does it work?
- nitroblue tetrazolium - leukocytes are incubated with NBT dye, which turns blue if NADPH oxidase can convert oxygen to superoxide radical but remains colorless if NADPH oxidase is defective
40
NBT test returns with a colorless result - what is the interpretation? why?
- defect in NADPH oxidase | - NADPH oxidase cannot convert oxygen to superoxide radical
41
myeloperoxidase is responsible for what step in oxygen dependent killing?
conversion of H2O2 to HOCl
42
MPO deficiency predisposes to infection by what organism?
candida
43
in MPO deficiency is the NBT test normal or abnormal? why or why not?
- normal | - conversion from oxygen to superoxide radical is intact (NADPH oxidase function is normal, which is what NBT tests)
44
during the resolution phase of neutrophil arrival and function, neutrophils regress via what mechanism?
apoptosis
45
do macrophages typically use oxygen dependent or independent killing?
independent (with lysozyme, eg)
46
in inflammation, macrophages are responsible for what main processes / pathways?
- resolution and healing - continued acute inflammation - abscess - chronic inflammation macrophages are the "managers" of inflammation - they dictate if a good job has been done and resolution can occur, or if more work needs to be done and more mediators need to be recruited
47
during the resolution and healing phase of acute inflammation, macrophages secrete what 2 cytokines? what is their general purpose?
- IL-10 and TGFB | - anti-inflammatory