Inflammation Flashcards

(88 cards)

1
Q

Definition of inflammation

A

Protective response to dilute, isolate and eliminate the cause of injury, and to repair tissue damage resulting from the injury

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2
Q

Repair begins during what phase of inflammation

A

Early on

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3
Q

How is injured tissue replaced in inflammation

A

By regeneration of native parenchymal cells, filling with fibroblasts, or a combination of the two

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4
Q

The inflammatory process is primarily a reaction of what?

A

Blood vessels resulting in the accumulation of fluid, electrolytes, plasma proteins and leukocytes in extravascular tissues

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5
Q

Vasodilation is responsible for…

A

Heat and redness

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6
Q

Increased vascular permeability is responsible for…

A

Swelling

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7
Q

Mediator release is responsible for…

A

Pain and loss of function

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8
Q

Connective tissue cells involved in inflammatory response

A

Mast cells, fibroblast, macrophages

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9
Q

Cells in the blood vessels involved in inflammation

A

Polymorphonuclear leukocyte, lymphocyte, platelets, monocytes, clotting factors, eosinophils, basophils

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10
Q

Cells in the connective tissue involved in inflammation

A

Elastic fibers, collagen fibers, proteoglycans

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11
Q

Acute inflammation

A

Rapid, short lived, exudation of fluid and plasma proteins, neurtophils

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12
Q

Chronic inflammation

A

Long, lymphocytes and macrophages, fibrosis, tissue necrosis

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13
Q

3 major components of acute inflammation

A

Vasodilation (increase blood flow), endothelial permeability (leukocytes leave circulation), activation of leukocytes

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14
Q

Vasodilation is induced by…

A

The action of mediators on vascular smooth muscle

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15
Q

Vasodilation mediators

A

MO, bradykinin, PGD2, LTB4

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16
Q

Why does blood stasis occur with vasodilation

A

There is increased viscosity of the blood

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17
Q

Increased vascular permeability leaves in a ______ in intravascular osmotic pressure and ____ interstitial fluid osmotic pressure

A

Decrease; increase

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18
Q

Transudate vs exudate: which happens in the arterioles, capillaries and venules during acute inflammation

A

Transudate in arterioles, exudate in capillaries and venules

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19
Q

8 cells of inflammation

A

Neutrophils, eosinophils, basophils & mast cells, monocytes & macrophages, lymphocytes, platelets, endothelial cells, fibroblasts

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20
Q

What are the first WBCs to attain the inflammatory site

A

Neutrophils

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21
Q

What is the main function of neutrophils in the inflammatory response

A

Kill, eliminate foreign material, and limit growth

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22
Q

What are neutrophil extracellular traps?

A

Activated neutrophils release granule proteins and chromatin that form extracellular fibers to bind gram positive and negative bacteria

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23
Q

Eosinophils can induce histamine release from what cells?

A

Mast cells and basophils

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24
Q

Mast cells are located…

A

Perivascular

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25
Basophils are located...
In circulation
26
Where are basophils and mast cells most numerous
At sites of contact with the external environment
27
What Ig do mast cells and basophils bind to?
IgE (Fc portion)
28
What is the hallmark of chronic inflammation?
Macrophages
29
What are two cellular events in inflammation
Leukocyte extravasation and phagocytosis
30
What is margination
When WBCs collect along the endothelium
31
What is rolling
When WBCs adhere transiently to the endothelium wall
32
Leukocyte adhesion to the endothelium is controlled by what?
Selectins and integrins and their ligands
33
TNF and IL-1 induce endothelial expression of...
ICAM-1 and VCAM-1, which binds integrins in the surface of WBCs
34
What is another name for transmigration
Diapedesis
35
Where does transmigration predominantly occur
In the venules
36
What acts on the rolling WBCs in the venules to stimulate their activation and migration through the endothelium
Chemokines
37
What WBCs usually transmigrate first
Neutrophils
38
Steps of the leukocyte adhesion cascade
Rolling, activation by chemokines and cytokines, stable adhesion and migration through the endothelium
39
Chemotaxis
Movement toward the site of injury along a chemical gradient
40
Chemotactic factors
C5a, arachidonic acid metabolites, LPS, histamines, PAF, chemokines
41
The production of chemokines is induced by...
Exogenous irritants
42
3 steps of leukocyte phagocytosis and degranulation
Recognition and attachment, engulfment, killing or degradation
43
Mannose receptors on leukocytes bind
Glycoproteins and glycolipids on microbial cell walls
44
Scavenger receptors on leukocytes bind
Microbes and modified LDL particles
45
Macrophage integrins bind
Microbes
46
Opsonization
Coating of the extraneous matter with opsonin's which bind to leukocytes
47
3 main opsonins
Fc fragment of IgG, C3b and plasma proteins such as mannose-binding lectin
48
Microbial killing is accomplished largely by...
Reactive oxygen species and nitric oxide and lysosomal enzymes
49
3 situations that lead to leukocyte-induced tissue injury
Lysosome rupture, regurgitation during feeding, frustrated phagocytosis
50
Mediators of vasodilation
PGD2, NO, leukotrienes, histamine and bradykinin
51
Mediators of increased vascular permeability
Histamine, serotonin, C3a/C5a, leukotrienes, cytokines
52
Mediators of chemotaxis and leukocyte activation
C5a, leukotriene, chemokines, LPS, cytokines
53
Mediators of fever
Cytokines and prostaglandins
54
Mediators of pain
Prostaglandins and bradykinin
55
Mediators of tissue damage
Neutrophil and macrophage lysosomal enzymes
56
Vasoactive amines
Histamine and serotonin
57
Plasma proteins
Kinins, clotting system, complement system
58
Activation of the kinin system results in the release of
Bradykinin
59
The kinin system is activated by...
The intrinsic coagulation pathway (Hageman, factor XII)
60
What inactivates bradykinin
Kininase
61
What represents the main link between the coagulation system and inflammation?
Protease thrombin
62
What is the complement system important in?
Inflammation, opsonization, cell lysis
63
3 pathways of complement system
Classical, alternative, lectin
64
What is the membrane attack complex
Polymerization of C9 forming a channel in lipid membranes, it allows for fluid and ions to enter the cell and cause lysis
65
Membrane attack complex complement proteins
C5b-C9
66
Vascular effects complement proteins
C3a and C5a
67
AA metabolism complement proteins
C5a
68
Leukocyte activation, adhesion and chemotaxis complement protein
C5a
69
Phagocytosis complement protein
C3b
70
The breakdown of arachidonic acid results in what metabolites?
Prostaglandins, thromboxanes, lipoxins and leukotrienes
71
Two pathways of AA metabolism
Cyclooxygenase and lipoxygenases
72
AA metabolites participate in...
Every aspect of acute inflammation
73
Platelet-activating factor (PAF) is produced by
Leukocytes, platelets and endothelial cells
74
What are cytokines
Proteins produced by many cell types that modulate functions of other cell types
75
2 major cytokines that mediate inflammation
TNF and IL-1
76
Outcomes of acute inflammation
Complete resolution, healing, chronic inflammation, abscess formation
77
How is tissue damage repaired?
By parenchymal regeneration or by connective tissue replacement (fibrosis)
78
When will scar formation occur
When there is damage to the tissue framework, damaged connective tissue
79
Labile cells
Constant turnover, easily replaceable
80
Quiescent cells
In resting phase, G0 cells have to cycle
81
Permanent cells
Replaced by scar or cavity
82
Steps of fibrosis and scarring
Formation of new blood vessels, migration/proliferation of fibroblasts, deposits of ECM components, maturation/organization of fibrous tissue
83
Granulation tissue is due to...
The formation of new small blood vessels, edema, proliferation of fibroblasts and presence of macrophages
84
Angiogenesis can occur by...
Mobilization of endothelial precursor cells from the bone marrow and by pre-existing vessels
85
Growth factors in angiogenesis
VEGF, angiopoietins 1 and 2, FGFs, PDGF, TGF-B
86
3 processes of fibrosis
Emigration and proliferation of fibroblasts, deposition of ECM components, tissue remodeling
87
Migration and proliferation of fibroblasts is controlled by...
Growth factors and cytokines
88
Growth factors are mainly derived from...
Platelets, inflammatory cells, and endothelium