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Pathology Exam 1 > Inflammation Part 1 > Flashcards

Inflammation Part 1 Flashcards

1
Q

what are the four causes of inflammation

A
  1. infections: (bacterial, viral, fungal, parasitic) and microbial toxins cause distinct patterns of inflammation
  2. tissue necro - causes inflam regardless of cause
  3. foreign bodies: exogenous or endogenous
  4. immune rxns (hypersensitivity - autoimmune diseases or environmental substances (allergies or microbes)
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2
Q

in general, three ways cells recognize need for inflammatory response?

A
  1. TLRs
  2. inflammasome
  3. complement
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3
Q

where are TLRs present

A
  • on cell membrane of the innate immune sys (macrophages and dendritic cells)
  • endosomes
  • on cells of adaptive immunity (lymphocytes)
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4
Q

how are TLRs activated

A

by PAMPs that are commonly shared by microbes

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5
Q

examples of a specific TLR

A

CD14 (a TLR) on macrophages recognizes lipopolysaccharide (a PAMP) on the outer membrane of gram-neg bacteria

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6
Q

TLR activation results in upregulation of what

A

NF-KB, a nuclear transcription factor that activates immune response genes leading to production of multiple immune mediators

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7
Q

what is the inflammasome

A

a multiprotein cytoplasmic complex

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8
Q

what does the inflammasome do

A

senses dead cell products (uric acid, ATP from damaged mito etc.) and induces activation of IL-1 –> leukocyte recruitment

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9
Q

what does inflammasome induce activation of

A

IL-1

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10
Q

what does IL-1 do

A

leukocyte recruitment

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11
Q

where is arachidonic acid (AA) released from and what is it released by

A

the phospholipid cell membrane by phospholipase A2

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12
Q

after released from phospholipid cell membrane, what is AA acted upon by

A
  • cyclooxygenase
  • 5-lipoxygenase
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13
Q

what does cyclooxygenase produce

A
  • prostaglandins (PG)
  • thromboxane A2 (TXA2)
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14
Q

what do PGI2, PGD2, and PGE2 all mediate

A

vasodilation (at the arteriole) and increased vasc. permeability (at the post-capillary venule)

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15
Q

what does PGE2 individually mediate

A

pain and fever

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16
Q

what does PGI2 individually mediate

A

inhibits platelet aggregation

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17
Q

what does TXA2 do

A

causes vasoconstriction and platelet aggregation

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18
Q

what does PGI2 cause

A

vasodilation (at the arteriole) and increased vasc. permeability (at the post-capillary venule)

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19
Q

what does PGE2 cause

A

vasodilation (at the arteriole) and increased vasc. permeability (at the post-capillary venule)

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20
Q

what does PGD2 do (along with two others)

A

vasodilation (at the arteriole) and increased vasc. permeability (at the post-capillary venule)

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21
Q

what does 5-lipoxygenase produce

A

leukotrienes (LT)

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22
Q

what does LTB4 do

A

attracts (chemotaxis) and activates neutrophiles

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23
Q

what do LTC4, LTD4, and LTE4 all do

A

(slow reacting substances of anaphylaxis) mediate vasoconstriction, bronchospasm, and increased vasc. permeability

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24
Q

what do lipoxins do

A

inhibit neutrophil chemotaxis and adhesion
- (counteracts LTB4)

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25
Q

what do corticosteroids do and examples

A

inhibit phospholipase
- cortisone and prednisone

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26
Q

what do NSAIDS do

A

inhibit cyclooxygenase (COX)

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27
Q

where is COX-1 expressed

A

in most tissues (homeostasis of electrolytes in kidney and protection of GI tract)

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28
Q

when is COX-1 increased

A

during inflammation

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29
Q

where is COX-2 expressed

A

absent from most normal tissues

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30
Q

when is COX-2 induced

A

during inflammation

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31
Q

examples of COX-1 inhibitors

A

aspirin, ibuprofen (advil, motrin) and naproxen (aleve)

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32
Q

example of COX-2 inhibitor

A

celebrex

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33
Q

what is used to treat asthma

A

lipoxygenase inhibitors and leukotriene receptor antagonists (singulair)

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34
Q

where are mast cells widely distributed

A

throughout connective tissue

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35
Q

what are mast cells activated by

A
  1. tissue trauma
  2. complement proteins C3a and C5a
  3. cross-linking of cell-surface IgE by antigen
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36
Q

describe immediate response of mast cells

A

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

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37
Q

what does histamine do

A
  1. vasodilation
  2. increased vasc. permeability
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38
Q

describe delayed response of mast cells

A

production of arachidonic acid metabolites, particularly leukotrienes
—> this prolongs the inflammatory response over hours

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39
Q

what are cytokines secreted from

A

activated lymphocytes, macrophages, and dendritic cells but also endothelial, epithelial and CT cells

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40
Q

what are the major cytokines in acute inflammation

A

TNF, IL-1 and IL-6

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41
Q

what are the major cytokines in chronic inflammation

A

IFN-y, IL-12, and IL-17

42
Q

what are the cytokines involved with negative feedback to downregulate inflammation

A

IL-10 and TGF-B

43
Q

what do TNF and IL-1 both do

A
  • activate endothelium
  • induce secretion of other cytokines and chemokines
44
Q

what do TNF, IL-1 and IL-6 all do

A

promote systemic inflammatory state

45
Q

what is the systemic inflammatory state

A
  • fever
  • lethargy
  • stimulate the liver to make acute phase proteins (ex. C-reactive protein)
46
Q

what does TNF individually do

A

metabolic wasting (cachexia)

47
Q

what are chemokines

A

cytokines that act as chemotactic agents for major imflammatory cells

48
Q

example of a chemokine

A

CXCL8 (formerly IL-8)

49
Q

what does nitric oxide (NO) do

A

vasodilation

50
Q

what are the three complement pathways

A
  • classical
  • alternative
  • mannose binding lectin (MBL)
51
Q

specific steps of classical pathway

A

C1 binds IgG or IgM that is bound to antigen

52
Q

specific steps of alternative pathway

A

microbial products directly activate complement without antigen/Ab complexes

53
Q

specific steps of MBL pathway

A

MBL binds to mannose on microorganisms and activates complement

54
Q

what are the steps in complement pathway that are common between all three pathways

A
  • production of C3 converatse
    —-> which mediates C3 into C3a and C3b
  • which produces C5 convertase
    —-> which mediates C5 into C5a and C5b
  • C5b complexes with C6-C9 to form the membrane attack complex (MAC)
55
Q

C3a and C5a are also called

A

anaphylatoxins

56
Q

what do C3a and C5a both do

A
  • trigger mast cell degranulation
    —> histamine release causes vasodilation and increased vasc. permeability
  • activate leukocytes
57
Q

what does C5a individually do

A

chemotactic for neutrophils

58
Q

is C3a or C5a more potent

A

C5a more potent that C3a

59
Q

what does C3b do

A

opsonin for phagocytosis
—> acts as the ‘eat me’ signal

60
Q

what does the MAC do

A

lyses microbes by creating a hole in the cell membrane

61
Q

what is Hagemen Factor (Factor XII)

A

inactive proinflammatory protein produced in liver

62
Q

when is Hageman Factor activated

A

upon exposure to subendothelial or tissue collage

63
Q

what does Hageman Factor in turn, activate

A
  • coagulation and fibrinolytic systems
  • complement
  • kinin system
64
Q

what is the kinin system

A
  • kinin cleaves high-molecular-weight kininogen (HMWK) to bradykinin
  • bradykinin causes vasodilation, increased vasc. permeability and pain
65
Q

what are the cardinal signs of acute inflammation

A
  • redness (rubor)
  • warmth (calor)
  • swelling (tumor)
  • pain (dolor)
  • fever
66
Q

what is redness and warmth due to

A
  • vasodilation –> increased blood flow
  • via relaxation of arteriolar s muscle
  • key mediators = histamine, prostaglandins, and bradykinin
67
Q

what is swelling due to

A

increased vasc. permeability causing leakage of fluid from postcapillary venules into the interstitial space

68
Q

what is pain due to

A

bradykinin and PGE2 sensitize sensory nerve endings

69
Q

what is fever due to

A
  • pyrogens cause macrophages to release IL-1 and TNF, which increase COX activity in perivascular cells of the hypothalamus
  • this leads to increased PGE2 which raises T set point
70
Q

is acute inflammation delayed or immediate and short-term or long-term

A

immediate and short term

71
Q

what is the hallmark cell of acute inflammation

A

neutrophils

72
Q

what are the vascular changes during acute inflammation

A
  • brief vasoconstr.
  • vasodil.
  • increased permea.
  • exudate leaving the circulation
  • increase in blood viscosity
  • decrease in blood flow through the microcirculation
73
Q

what are the cellular events of acute inflammation in order

A
  1. margination
  2. rolling
  3. adhesion
  4. transmigration and chemotaxis
  5. phagocytosis
  6. destruction of phagocytosed material
  7. resolution
74
Q

what happens during margination

A
  • vasodilation of arterioles slows blood flow
  • cells marginate from center of flow to periphery
75
Q

what happens during rolling

A

-“aka loose attachment”
- selectin speed bumps are upregulated on endothelial cells
- selectins bind SIalyl-Lewis X on leukocytes
- interaction results in rolling of leukocytes along vessel wall

76
Q

what does P-selectin do during rolling

A

P-selectin release from Weibel-Palade bodies (storage granules in endothelial cells) is mediated by histamine

77
Q

what is E-selectin induced by

A

TNF and IL-1

78
Q

what happens during adhesion (3)

A
  • cellular adhesion molecules are upregulated on endothelium by TNF and IL-1
  • integrins become high affinity and are upregulated on leukocytes by C5a and LTB4
  • interaction between CAMs and integrins results in firm adhesion of leukocytes to the vessel wall
79
Q

what is a leukocyte adhesion deficiency a defect in?

A

defect in integrins

80
Q

what are the cellular adhesion molecules and what are they upregulated by

A

ICAM and VCAM and upregulated by TNF and IL-1

81
Q

what happens during transmigration and chemotaxis

A
  • leukocytes transmigrate across the endothelium of postcap. venules and move towards chemical attractants
82
Q

what are neutrophils attracted by

A

bacterial products, IL-8, C5a, and LTB4

83
Q

what happens during phagocytosis

A
  • consumption of pathogens or necrotic tissue
  • pseudopods extend from leukocytes to form phagosomes, which are internalized and merge with lysosomes to produce phagolysosomes
84
Q

what is phagocytosis enhanced by

A

opsonins (IgG and C3b)

85
Q

what is Chediak-Higashi syndrome

A

impaired phagolysosome formation with increased risk of pyogenic infections

86
Q

what is the most effective mechanism of destroying phagocytosed material

A

OXYGEN dependent killing

87
Q

what is HOCL’ (hypochlorous radical) generated by

A

oxidative burst in phagolysosomes and destroys phagocytosed microbes

88
Q

how does oxygen go to superoxide

A

NADPH oxidase

89
Q

what can superoxide go to and how

A

go to H2O2 by superoxide dismutase

90
Q

what can H2O2 go to and how

A

go to HOCl’ (bleach) by myeloperoxidase (MPO) which is contained in the azurophilic granules (lysosomes) of PMNs

91
Q

what is chronic granulomatous disease characterized by

A

poor OXYGEN-dependent killing
–> due to inherited NADPH oxidase defect
–> leads to recurrent infection and granuloma formation

92
Q

is oxygen-independent or oxygen-dependent killing more effective

A

oxygen dependent more effective

93
Q

how does oxygen independent killing occur

A

via enzymes present in leukocytes secondary granules

94
Q

what happens during resolution

A

neutrophils undergo apopto and disappear within 24 hrs after resolution of the inflammatory stimulus

95
Q

what are the three main patterns of acute inflammation

A
  • serous
  • purulent or suppurative
  • fibrinous
96
Q

describe serous inflammation

A
  • due to burn or viral infection, tend to be watery
97
Q

what is effusion

A

fluid in a serous cavity

98
Q

describe purulent or suppurative inflammation

A
  • common in bacterial infections
  • thick and yellow (rich in neutrophils)
99
Q

describe fibrinous inflammation

A
  • rich in fibrin which makes it sticky. covering called a pseudomembrane
  • noted when inflammation occurs in a body cavity. can resolve but if scarring occurs could restrict function
100
Q
A

Pathology Exam 1 (5 decks)

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