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Inflammation Flashcards

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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
Exudation
Inflammation, junctions between endothelial cells widened Proteins & cell components leak out Can occur from injury
26
Margination
Leukocytes (neutrophils) line up along endothelial cell surface
27
Adhesion
Leukocytes bind to endothelial cell surface
28
Emigration
Leukocytes migrate between endothelial cells and across basement membrane to interstitial space
29
Chemotaxis
directed movement along chemical gradient towards injury
30
Cell Adhesion Molecules (CAM)
Membrane proteins that promote leukocyte attachment for inflammatory response Selectins, Immunoglobulin family, Integrins
31
Selectins
Homing receptors & mediate rolling (slowing down) of leukocytes along endothelium at sites of inflammation Surface of endothelium, platelets, & leukocytes
32
P-Selectin (CD62P)
Comes from platelets When activated by TNF or IL-1, migrates to cell surface Binds to PSGL-1 & Lewis X oligosacharides
33
E-Selectin (CD62E)
Comes from endothelial cells Synthesized by activation by TNF or IL-1 Enhances later recruitment of leukocytes
34
L-Selectin (CD62L)
Comes from lymphocytes & neutrophils - bind to endothelium & lymph nodes Binds to GlyCAM-1 & MadCAM-1
35
Intercellular adhesion molecule-1 (ICAM-1)
Ig family Assists in localization of leukocytes to tissue injury On surface endothelium Binds to integrins LFA-1 & Mac-1 on neutrophils & macrophages
36
VCAM-1 (Vascular cell adhesion molecule)
Ig Family On endothelium Binds to integrin VLA-4 on lymphocytes, monocytes, eosinophils, basophils
37
PECAM-1 (Platelet endothelial cell adhesion molecule)
Ig Family On endothelium CD-31, binds in homophilic manner (to other CD31 on apposing cell) Diapedesis step of leukocyte emigration
38
Integrins
Adhesion molecules act in regulation of cell-matrix and cell-cell adhesion Transmembrane proteins
39
Beta 1 integrins (CD49/CD29 -VLA molecules)
VLA-4 Expressed on leukocytes (WBC) Binds to VCAM-1 on endothelium (Ig Family)
40
Beta 2 integrins (CD11/CD18 - LFA)
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
Phagocytosis recognition/attachment
Enhnaced by Opsonins | Leukocyte receptors
42
Engulfment
pseudopods surround object forming phagosome that fuses with lysosome creating phagolysosome
43
Phagocyte killing through
Oxygen-dependent - oxidative burst (HOCl) | Oxygen-independent: leukocyte granule proteins & enzymes
44
Histamine & Serotonin
Causes arteriolar dilation & increase permeability of postcapillary venules (quick effect & short lasting)
45
Histamine & Serotonin are stored in
preformed granules of mast cells & basophils and platelets
46
Critical step of complement activation
Cleavage of C3
47
Classic complement pathway activation
initiated by binding of antigen antibody complex to C1
48
Alternate complement pathway
C3 directly activated by bacterial endotoxins, complex polysaccharides, aggregated globulins
49
Lectin pathway
C1 activation by binding of mannose-binding lectin to carbohydrates on microbes
50
C3a, C4a, C5a
Stimulate histamine release from mast cells | Increased vascular permeability & vasodilation
51
C5a
chemotaxis, increased expression of leukocyte CAM, activates lipoxygenase pathway
52
C3b
opsonization
53
C5-9
membrane attack complex | Forms macropores - lysis
54
Hageman Factor
Factor 12 Triggers kinin system & clotting cascade Converts Prekallikrein into Kallikrein
55
Kallikrein
``` (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
Bradykinin
Causes pain | Increases vascular permeability, vasodilation, contracts non-vascular smooth muscle
57
Bradykinin is inactivated by
plasma kininase
58
Coagulation-Fibrinolytic system
Cascade of reactions resulting in fibrin clot which is then dissolved by fibrinolytic system
59
Thrombin
Cleaves fibrinogen to create fibrin - create clot | & inflammation: mobilize P-selectin, produce chemokines, stimulate endothelial adhesion molecule, induce COX-2
60
Plasmin
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
Arachidonic acid
Released from membrane by stimuli including C5a | 2 pathways: Cyclooxygenase (COX) pathway & Lipoxygenase (LOX) pathway
62
COX pathway
COX converts arachidonic acid into prostaglandin intermediates that form: TXA2, PGI2, PGE2, PGD2, PGF2a
63
TXA2 (Thromboxane A2)
Platelet aggregator & vasoconstrictor
64
PGI2
Vasodilator & inhibitor of platelet aggregation
65
PGE2
Sensitizes skin to painful stimuli & fever, also causes vasodilation & edema
66
PGD2 & PGF2a
vasodilation & potentiate edema
67
LOX pathway
converts AA into leukotriens & lipoxins
68
LT B4
Chemoattractant causes neutrophil aggregation & adhesion, ROS generator, lysosome release
69
LT C4, D4, E4
Intense vasoconstriction & bronchospasm, & increase vascular permeability
70
Lipoxins (Lipoxin A4 & B4)
Negative regulators of leukotriene action | Inhibit leukocyte recruitment, cellular activities of inflammation, & neutrophil adhesion/chemotaxis
71
Aspirin inhibits
Cyclooxygenase - prevent platelet aggregation through COX pathway
72
Platelet Activating Factor
Causes platelet aggregation & release of products (histamine, serotonin) Vasoconstriction, bronchoconstriction, but vasodilation & venular permeability at low concentration
73
Cytokines & Chemokines
Polypeptides - cellular hormones
74
IL-1 & TNF (cytokines)
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
Chemokines
Stimulate leukocyte recruitment (chemotactic property) | Contain cysteine residues
76
C-X-C (Alpha chemokines)
Act on neutrophils | IL-8
77
C-C (Beta-chemokines)
Attract cells other than neutrophils
78
C (Gamma-chemokines)
Specific for lymphocytes
79
CX3C chemokines
Fractalkine - strong attractant for monocytes & T-cells
80
Nitric Oxide (NO)
Free radical gas Produced by macrophages, endothelium, neurons Acts through cGMP Vasodilation - smooth muscle relaxation Reduces platelet aggregation & adhesion, & WBC recruitment Microbicidal
81
Reactive oxygen metabolites cause
Endothelial cell damage, inactivation of antiproteases, injury to other cells
82
Substance P & Neurokinin A
Made in CNS & PNS | Transmit Pain & increase permeability
83
Vasodilation
PG, NO
84
Vascular Permeability
Vasoactive amines, C3a & C5a, Bradykinin, Leukotrienes (C4, D4, E4), PAF, Substance P
85
Chemotaxis & leukocyte activation
C5a, Leukotriene B4, Chemokines
86
Fever
IL-1, IL-6, TNF, PG
87
Pain
PG, Bradykinin
88
Tissue damage
Lysosomal, enzymes, oxygen metabolites, NO
89
Chommon inflammation frequently begin
insidiously, as low grade, smoldering response without signs of acute inflammation (most common & disabling)
90
Chronic inflammation looks like:
Infiltration with mononuclear cells (no neutrophils), tissue destruction (induced by persistent stimuli or inflammatory cells), attempts at healing (fibrosis)
91
Key cell in chronic & granulomatous inflammation
Macrophages (derived from monocytes)
92
Kupffer cells
Macrophages in liver
93
Osteoclasts
Macrophages in bone
94
Macroglia
Macrophages in brain
95
Activated Macrophages
Increase in size, lysosome, lysosomal enzymes & ability to kill bacteria Appear large, flat, & pink
96
Macrophages produce
Cytokines (IL1 & TNF) growth factors, ROS, NO, Complement components, coagulation factors
97
Macrophages are activated by
INF-gamma
98
Recruitment of eosinophils is dependent on
eotaxin

Pathology (6 decks)

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