inflammation Flashcards

1
Q

what activates mast cells

A

C5a

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2
Q

what do mast cell release

A

histamine

PGD2

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3
Q

what are possible results of acute inflammation

A

resolution
abscess
scarring
chronic inflammation

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4
Q

where is PGD2 found

A

in mast cells granules

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5
Q

what does PGD2 cause

A

vasodilation, pain, fever

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6
Q

what does histamine cause

A

increased vascular permeability and vasodilation, leading to increased blood flow, swelling, heat and redness

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7
Q

injury of basement membrane causes

A

injury to collagen, which activates Hageman factor (factor XII)

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8
Q

Hageman factor is also part of what

A

coagulation cascade

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9
Q

mechanisms by which mediators are signaled to go to infection site

A

chemotaxis

leukocyte recruitment

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10
Q

key inflammatory cytokines

A

TNF
IL-1
IL-6

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11
Q

what mediators upregulate adhesion molecules for leukocytes on endothelial surface

A

histamine
TNF
IL-1

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12
Q

what chemokines stimulate chemotaxis toward infection sites

A

C3a

C5a

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13
Q

what do inflammasomes produce

A

IL-1

IL-18

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14
Q

autoinflammatory syndromes are caused by

A

dysregulation activation of inflammasomes
leads to excess IL-1
gain-of-function mutation

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15
Q

first line of defense against extracellular bacteria

A

neutrophils

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16
Q

steps of neutrophil extravasation

A
margination/stasis
rolling
binding
extravasation
(then chemotaxis to infection site)
17
Q

P-selectin

A

stored in Weibel-Palade bodies
binds PGSL-1 (selectin ligand)
this interaction slows neutrophil
low affinity interaction that leads to rolling of neutrophil

18
Q

LFA-1

A

integrin
binds to ICAM-1 (integrin ligand)
high affinity interaction that causes binding of neutrophil

19
Q

PECAM-1

A

concentrated at endothelial cell junctions
aka CD31
allows neutrophil extravasation

20
Q

what type of macrophage has anti-microbial activity

21
Q

what type of macrophage has anti-inflammatory/pro-resolving activity

22
Q

M1

A

classically activated
anti-microbial activity
produce ROS, NO, and lysosomal enzymes to kill microbes
produce pro-inflammatory cytokines (IL-1, 12, and 23)

23
Q

M2

A

once microbe is gone, M1 becomes M2
alternatively activated
anti-inflammatory/pro-resolving activity (IL-10 and TGF beta)

24
Q

TGF beta is secreted by

A

macrophages

initiates wound healing

25
TGF beta function
initiates wound healing by inducing migration of fibroblasts to site and proliferation of them
26
conditions that cause chronic inflammation
TB syphilis (treponema pallidum) chronic exposure to toxic agents autoimmune diseases (lupus, RA)
27
hallmarks of chronic inflammation
infiltration of macrophages and lymphocytes tissue destruction angiogenesis and fibrosis (attempts at healing)
28
systemic effects of inflammation
fever neutrophilia acute phase response shock
29
production of fever
pro-inflammatory cytokines IL-1 and TNF lead to production of arachidonic acid AA --> PGE2 PGE2 acts on hypothalamus --> cAMP (resets body temp)
30
how do NSAIDs reduce fever
inhibit cyclooxygenase and block PGE2 synthesis
31
production of neutrophilia
pro-inflammatory cytokines IL-1 and TNF stimulate accelerated release of PMNs from bone marrow sustained release by macrophage- and T lymphocyte-derived release of granulocyte colony stimulating factor
32
advantages of fever
immune system functions more effectively at higher temp host cells are protected from deleterious effects of TNF alpha at elevated temps pathogens grow more poorly at elevated temps
33
what is observed in neutrophilia
an increase in band forms (immature leukocytes)
34
acute phase response
macrophage-derived IL-6 acts on hepatocytes to synthesize and release acute phase proteins (e.g., CRP), which act as opsonins increase in plasma levels of acute phase proteins, leading to accelerated ESR
35
shock
TNF causes vasodilation and vascular permeability subsequent intravascular volume loss leads to hypotension and shock TNF acts on heart, causing low output systemic activation of coagulation system --> DIC --> cut off of blood supply to organs --> organ system and bleeding
36
precursor of lipid mediators (PGD2, leukotrienes)
arachidonic acid