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Pathology > Inflammation > Flashcards

Inflammation Flashcards

1
Q

Acute inflammation (definition)

A

Local reaction of vascularized tissue to injury

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2
Q

Principal processes of acute inflammation

A

Increased blood flow to injured site
Exudation of fluid from vessels
Attraction of leukocytes to injury
Activation of chemical mediators
Proteolytic degradation of extracellular debris
Restoration of injured tissue to normal structure/function

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3
Q

Inflammation is protective because

A

It rids organism of initial cause of cell injury (microbes, toxins) & consequences of injury (necrotic tissue)

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4
Q

Inflammation may be harmful because

A

underlie common chronic disease, can cause life-threatening hypersensitivity reaction, & can produce scarring that is constricting

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5
Q

6 cardinal signs of acute inflammation

A

Heat & redness, Swelling, Pain, Loss of function, systemic changes

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6
Q

Causes of acute inflammation

A

Infection, trauma, physical injury from thermal extremes or ionizing radiation, chemical injury, immunologic injury, & tissue death (inflammation close to necrotic areas)

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7
Q

Outcomes of acute inflammation

A

Resolution, healing by scarring, abscess, & progression to chronic inflammation

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8
Q

Resolution of acute inflammation

A

complete tissue restoration - from mild injury with little tissue damage

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9
Q

Healing by scarring occurs after

A

substantial tissue destruction, abundant fibrin exudation, & in tissues that do not regenerate

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10
Q

Serous inflammation

A

protein-poor, thin fluid from blood plasma or effusion;

Skin blisters

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11
Q

Fibrinous inflammation

A

Accumulation of fibrinous exudates ( meshwork of threads - fibrinogen)
Occurs from more severe injuries & greater vascular permeability; inflammation of body cavities

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12
Q

In fibrinous inflammation, scarring occurs if

A

fibrin is not removed; ingrowth of fibroblasts & blood vessels stimulated

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13
Q

Suppurative or Purulent Inflammation

A

production of large amounts of pus (neutrophils, necrotic cells, & edema fluid)
Abscesses, pyogenic bacteria, acute appendicitis

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14
Q

Abscesses

A

focal localized collections of pus
Produced by deep seeded bacteria
Have central region - mass of dead cells & tissue with zone of preserved neutrophils around
Can be walled off to keep from spreading

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15
Q

Ulcers

A

local defect, excavation produced by shedding of inflammatory necrotic tissue
Must be on or near surface
Mucosa of mouth, stomach, intestines, GU tract or subcutaneous tissue of legs in older people
Neutrophils at margins

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16
Q

Acute inflammation duration

A

0 - 48 hours

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17
Q

Subacute inflammation duration

A

2 - 10 days

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18
Q

Chronic inflammation duration

A

More than 2 weeks

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19
Q

Cellular elements of acute inflammation

A

neutrophils

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20
Q

Cellular elements of chronic inflammation

A

monocytes, lymphocytes, plasma cells, macrophages, granuloma cells

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21
Q

Eosinophils

A

predominant inflammatory cells in allergic reactions & parasitic infections

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22
Q

Key events of acute inflammation

A

Alteration in vascular = increase in blood flow & allow luekocytes and plasma proteins to leave circulation
Leukocyte accumulation at site of injury

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23
Q

Vasodilation is initially preceded by

A

Vasoconstriction (immediate, variable, cutaneous arterioles)

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24
Q

Transudation

A

increase in hydrostatic pressure (congestive heart failure) or decreased osmotic pressure (renal disease)
Fluid will leak out of vasculature but spaces between endothelial cells tight (no protein leakage)

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25
Q

Exudation

A

Inflammation, junctions between endothelial cells widened
Proteins & cell components leak out
Can occur from injury

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26
Q

Margination

A

Leukocytes (neutrophils) line up along endothelial cell surface

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27
Q

Adhesion

A

Leukocytes bind to endothelial cell surface

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28
Q

Emigration

A

Leukocytes migrate between endothelial cells and across basement membrane to interstitial space

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29
Q

Chemotaxis

A

directed movement along chemical gradient towards injury

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30
Q

Cell Adhesion Molecules (CAM)

A

Membrane proteins that promote leukocyte attachment for inflammatory response
Selectins, Immunoglobulin family, Integrins

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31
Q

Selectins

A

Homing receptors & mediate rolling (slowing down) of leukocytes along endothelium at sites of inflammation
Surface of endothelium, platelets, & leukocytes

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32
Q

P-Selectin (CD62P)

A

Comes from platelets
When activated by TNF or IL-1, migrates to cell surface
Binds to PSGL-1 & Lewis X oligosacharides

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33
Q

E-Selectin (CD62E)

A

Comes from endothelial cells
Synthesized by activation by TNF or IL-1
Enhances later recruitment of leukocytes

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34
Q

L-Selectin (CD62L)

A

Comes from lymphocytes & neutrophils - bind to endothelium & lymph nodes
Binds to GlyCAM-1 & MadCAM-1

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35
Q

Intercellular adhesion molecule-1 (ICAM-1)

A

Ig family
Assists in localization of leukocytes to tissue injury
On surface endothelium
Binds to integrins LFA-1 & Mac-1 on neutrophils & macrophages

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36
Q

VCAM-1 (Vascular cell adhesion molecule)

A

Ig Family
On endothelium
Binds to integrin VLA-4 on lymphocytes, monocytes, eosinophils, basophils

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37
Q

PECAM-1 (Platelet endothelial cell adhesion molecule)

A

Ig Family
On endothelium
CD-31, binds in homophilic manner (to other CD31 on apposing cell)
Diapedesis step of leukocyte emigration

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38
Q

Integrins

A

Adhesion molecules act in regulation of cell-matrix and cell-cell adhesion
Transmembrane proteins

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39
Q

Beta 1 integrins (CD49/CD29 -VLA molecules)

A

VLA-4
Expressed on leukocytes (WBC)
Binds to VCAM-1 on endothelium (Ig Family)

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40
Q

Beta 2 integrins (CD11/CD18 - LFA)

A

Activation of phagocytic cells by chemotactic stimuli increases surface expression of these integrins
LFA-1 & complement receptor type 3 & 4 bind to ICAM-1 (on endothelium) - assist in localization of phagocytes to injury sites & extravasation

41
Q

Phagocytosis recognition/attachment

A

Enhnaced by Opsonins

Leukocyte receptors

42
Q

Engulfment

A

pseudopods surround object forming phagosome that fuses with lysosome creating phagolysosome

43
Q

Phagocyte killing through

A

Oxygen-dependent - oxidative burst (HOCl)

Oxygen-independent: leukocyte granule proteins & enzymes

44
Q

Histamine & Serotonin

A

Causes arteriolar dilation & increase permeability of postcapillary venules
(quick effect & short lasting)

45
Q

Histamine & Serotonin are stored in

A

preformed granules of mast cells & basophils and platelets

46
Q

Critical step of complement activation

A

Cleavage of C3

47
Q

Classic complement pathway activation

A

initiated by binding of antigen antibody complex to C1

48
Q

Alternate complement pathway

A

C3 directly activated by bacterial endotoxins, complex polysaccharides, aggregated globulins

49
Q

Lectin pathway

A

C1 activation by binding of mannose-binding lectin to carbohydrates on microbes

50
Q

C3a, C4a, C5a

A

Stimulate histamine release from mast cells

Increased vascular permeability & vasodilation

51
Q

C5a

A

chemotaxis, increased expression of leukocyte CAM, activates lipoxygenase pathway

52
Q

C3b

A

opsonization

53
Q

C5-9

A

membrane attack complex

Forms macropores - lysis

54
Q

Hageman Factor

A

Factor 12
Triggers kinin system & clotting cascade
Converts Prekallikrein into Kallikrein

55
Q

Kallikrein

A 
(Kinin system)
Amplifies activation of Hageman Factor
Activates Bradykinin (through cleavage)
Converts plasminogen to plasmin
Chemoattractant for neutrophils & converts C5 to C5a
Increases CAM expression
56
Q

Bradykinin

A

Causes pain

Increases vascular permeability, vasodilation, contracts non-vascular smooth muscle

57
Q

Bradykinin is inactivated by

A

plasma kininase

58
Q

Coagulation-Fibrinolytic system

A

Cascade of reactions resulting in fibrin clot which is then dissolved by fibrinolytic system

59
Q

Thrombin

A

Cleaves fibrinogen to create fibrin - create clot

& inflammation: mobilize P-selectin, produce chemokines, stimulate endothelial adhesion molecule, induce COX-2

60
Q

Plasmin

A

Lyses fibrin clots
Activates Hageman factor, cleaves C3 to C3a, degrades fibrin to form fibrin split products
Formed by cleaving of plasminogen by kallikrein (PA)

61
Q

Arachidonic acid

A

Released from membrane by stimuli including C5a

2 pathways: Cyclooxygenase (COX) pathway & Lipoxygenase (LOX) pathway

62
Q

COX pathway

A

COX converts arachidonic acid into prostaglandin intermediates that form: TXA2, PGI2, PGE2, PGD2, PGF2a

63
Q

TXA2 (Thromboxane A2)

A

Platelet aggregator & vasoconstrictor

64
Q

PGI2

A

Vasodilator & inhibitor of platelet aggregation

65
Q

PGE2

A

Sensitizes skin to painful stimuli & fever, also causes vasodilation & edema

66
Q

PGD2 & PGF2a

A

vasodilation & potentiate edema

67
Q

LOX pathway

A

converts AA into leukotriens & lipoxins

68
Q

LT B4

A

Chemoattractant causes neutrophil aggregation & adhesion, ROS generator, lysosome release

69
Q

LT C4, D4, E4

A

Intense vasoconstriction & bronchospasm, & increase vascular permeability

70
Q

Lipoxins (Lipoxin A4 & B4)

A

Negative regulators of leukotriene action

Inhibit leukocyte recruitment, cellular activities of inflammation, & neutrophil adhesion/chemotaxis

71
Q

Aspirin inhibits

A

Cyclooxygenase - prevent platelet aggregation through COX pathway

72
Q

Platelet Activating Factor

A

Causes platelet aggregation & release of products (histamine, serotonin)
Vasoconstriction, bronchoconstriction, but vasodilation & venular permeability at low concentration

73
Q

Cytokines & Chemokines

A

Polypeptides - cellular hormones

74
Q

IL-1 & TNF (cytokines)

A

Produced by macrophages
Acute Phase Reactions - fever, neutrophilia
Endothelial effects: increase leukocyte adherence, PGI synthesis, coagulation, & production of IL-1, IL-6, IL-8, PDGF
Collagen synthesis
Increases cytokine secretion (IL-1, IL-6)

75
Q

Chemokines

A

Stimulate leukocyte recruitment (chemotactic property)

Contain cysteine residues

76
Q

C-X-C (Alpha chemokines)

A

Act on neutrophils

IL-8

77
Q

C-C (Beta-chemokines)

A

Attract cells other than neutrophils

78
Q

C (Gamma-chemokines)

A

Specific for lymphocytes

79
Q

CX3C chemokines

A

Fractalkine - strong attractant for monocytes & T-cells

80
Q

Nitric Oxide (NO)

A

Free radical gas
Produced by macrophages, endothelium, neurons
Acts through cGMP
Vasodilation - smooth muscle relaxation
Reduces platelet aggregation & adhesion, & WBC recruitment
Microbicidal

81
Q

Reactive oxygen metabolites cause

A

Endothelial cell damage, inactivation of antiproteases, injury to other cells

82
Q

Substance P & Neurokinin A

A

Made in CNS & PNS

Transmit Pain & increase permeability

83
Q

Vasodilation

A

PG, NO

84
Q

Vascular Permeability

A

Vasoactive amines, C3a & C5a, Bradykinin, Leukotrienes (C4, D4, E4), PAF, Substance P

85
Q

Chemotaxis & leukocyte activation

A

C5a, Leukotriene B4, Chemokines

86
Q

Fever

A

IL-1, IL-6, TNF, PG

87
Q

Pain

A

PG, Bradykinin

88
Q

Tissue damage

A

Lysosomal, enzymes, oxygen metabolites, NO

89
Q

Chommon inflammation frequently begin

A

insidiously, as low grade, smoldering response without signs of acute inflammation (most common & disabling)

90
Q

Chronic inflammation looks like:

A

Infiltration with mononuclear cells (no neutrophils), tissue destruction (induced by persistent stimuli or inflammatory cells), attempts at healing (fibrosis)

91
Q

Key cell in chronic & granulomatous inflammation

A

Macrophages (derived from monocytes)

92
Q

Kupffer cells

A

Macrophages in liver

93
Q

Osteoclasts

A

Macrophages in bone

94
Q

Macroglia

A

Macrophages in brain

95
Q

Activated Macrophages

A

Increase in size, lysosome, lysosomal enzymes & ability to kill bacteria
Appear large, flat, & pink

96
Q

Macrophages produce

A

Cytokines (IL1 & TNF) growth factors, ROS, NO, Complement components, coagulation factors

97
Q

Macrophages are activated by

A

INF-gamma

98
Q

Recruitment of eosinophils is dependent on

A

eotaxin

Pathology (6 decks)

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