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Immunity > Inflammation I > Flashcards

Inflammation I Flashcards

1
Q

A set of host responses to injury in which there is an attempt to destroy or limit the spread of the injurious agent

A

Inflammation

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2
Q

These responses are mediated by the microvasculature and involve both

A

Innate and adaptive immunity

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3
Q

Attributed bacterial killing solely to the effects of soluble substances that we now recognize as antibodies and that are present in the blood plasma

A

Paul Ehrlich’s “humoral theory” of inflammation

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4
Q

Established that chemical substances such as histamine, locally generated in inflammation, can mediate vascular changes of inflammation

A

Thomas Lewis, a British cardiologist

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5
Q

Illustrated in the “triple” response, which can be induced by firmly stroking the skin with a hard object

A

Action of histamine

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6
Q

Almost anything that can adversely influence cell viability can induce some aspect of

-ex: sunburn

A

Inflammation

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7
Q

The bacteria bind to mast cell surfaces, inducing degranulation of vasoactive amines and secretion of cytokines in

A

Acute inflammation from bacterial invasion

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8
Q

These agents cause arteriolar dilation and then venular leakage of fluid and proteins. The result is the development of

A

Interstitial edema

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9
Q

About 12 hours following injury, the walls of the post-capillary venules begin to be lined with

A

Neutrophils

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10
Q

They then penetrate the wall and emigrate (diapedesis) to the site of injury through the interstitium. This is followed by the

A

Phagocytosis of bacteria

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11
Q

If the inflammation lasts more than a day, we will see emigration of

-peak at 2 days

A

Macrophages

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12
Q

The macrophages will engulf the remaining

A

Neutrophil debris

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13
Q

Provides an example of a severe acute inflammatory reaction

A

Bacterial bronchopneumonia

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14
Q

What is the difference between bronchopneumonia from lobar pneumonia?

A

Lobar involves entire lobe

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15
Q

As a bacterial pneumonia develops, the initial phase is an edematous phase with few inflammatory cells in which the alveoli fill with

A

Exudate

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16
Q

This is followed by the so-called “red-hepatization” stage in which we see a prominent

A

Neutrophil response

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17
Q

The next phase is the so-called “grey-hepatization” stage in which neutrophils are replaced by a less dense array of

A

Macrophages

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18
Q

During the grey-hepatization, we see the alveolar accumulation of

A

Fibrin

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19
Q

Filled with membrane-bound vesicles that contain a variety of potent vasoactive agents

A

Mast cells

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20
Q

Released following different stimuli that occur through injury, non-immune and immune reactions

A

Mast cell vasoactive agents

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21
Q

One of the principal activations of mast cells that result in degranulation is mediated through the

A

IgE Fc antibody receptor

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22
Q

Signaling is initiated by aggregation followed by signaling sequence of phosphorylations. It results in histamine, cytokine and arachidonic acid metabolite production, and release of

A

Histamine (via degranulation)

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23
Q

A variety of local and systemic (e.g. fever) effects are mediated by

A

Arachidonic acid metabolites

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24
Q

What are the two synthetic pathways for these eicosanoids?

A
  1. ) Prostaglandins and prostacyclins

2. ) Leukotrines

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25
Q

The products of the pathway mediate such processes as vasodilation, vasoconstriction, edema, fever and

A

Leukocyte chemotaxis

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26
Q

Aspirin and other non-steroidal anti-inflammatory agents (NSAIDs) act by blocking

A

Cyclooxygenase

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27
Q

Potent anti-inflammatoryagents that prevent the synthesis of arachidonicacid

A

Glucocorticoids

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28
Q

Phagocytose foreign bodies and are antigen-presenting cells, using cytokines to stimulate specific antigen dependent responses by B and T cells and non-specific responses by other cell types

A

Macrophages

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29
Q

Secrete a variety of factors to coordinate and stimulate immune responses to specific antigen

A

T cells

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30
Q

Several cytokines act on conjunction with colony-stimulating factors to increase the bone marrow production of different classes of

A

Leukocytes

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31
Q

We see shifts in the population of leukocytes in

A

Acute infections

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32
Q

Inflammation from a severe infection will result in immature forms of

-important diagnostic indicator

A

Neutrophils

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33
Q

Refers to the presence of increased proportions of younger, less well differentiated neutrophils and neutrophil-precursor cells in the blood

A

“Left Shift”

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34
Q

Increase in blood lymphocytes to greater than 4000

-can be caused by acute viral infections

A

Lymphocytosis

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35
Q

The capillary and venules present two barriers to the migration of fluid, solutes and cells into the tissue spaces. What are they?

A
  1. ) Endothelium

2. ) Basal Lamina

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36
Q

There are three main types of microvascular leakage that follow an injury. The most specific and “physiological” of these is the

A

Histamine type response

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37
Q

More severe injury, in which permanent damage occurs to the microvascular walls, results in the more prolonged leakages seen with

A

Mild direct and severe direct injury

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38
Q

In the more severe form of direct injury, the leakage is seen across a destroyed wall and is limited by local

A

Thrombosis

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39
Q

Mediates an increased in transcytosis across the endothelial cell in the microvasculature

-recently reckognized

A

VEGF

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40
Q

One way of studying the events of inflammation with the light microscope is to use

A

Fluorescent dextran

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41
Q

The leakage for the dextrin does not occur from all vessels. Rather, it occurs selectively from the post-capillary venules that are intermediate in size between

A

Capillaries and arterioles

42
Q

Quantitation reveals that the leakage follows a stereotypic time course within a given

A

Vascular bed

43
Q

The time course of leakage is independent of the duration of histamine treatment, suggesting a

A

Gating phenomenon

44
Q

Furthermore, there is a refractory period within which a second histamine injection does not produce a

A

Second leakage peak

45
Q

Post-capillary venules do not possess smooth muscle in their walls, unlike arterioles. Nonetheless, venular constriction is observed following

A

Histamine exposure

46
Q

Whereas endothelial cell transport normally is mediated primarily by small vesicles, there is no increase of vesicular transport during

A

Inlammation

47
Q

Studies on horseradish peroxidase transport indicate that macromolecules instead rapidly pass down

A

Inter-endothelial junctions

48
Q

At an ultrastructural level, endothelial gaps are seen to form at the inter-endothelial junctions of previously

-induced by histamine

A

Continuous venule

49
Q

Seen as an exudate that is localized and has high protein concentration

A

Inflammatory Edema

50
Q

The transudate of general edema is of low protein concentration and occurs from an imbalance

A

Hydrostatic and osmotic pressures

51
Q

In inflammation, pre-capillary sphincters open up, increasing hydrostatic pressure AND the venules become leaky such that the osmotic gradient across the wall is

A

Removed

52
Q

As fluid leaves the vasculature, the blood in the microcirculation, now becomes more viscous with increasing

A

Hematocrit

53
Q

The sequence of events in leukocyte infiltration can be divided into which 4 steps?

A
  1. ) Margination
  2. ) Sticking
  3. ) Emigration
  4. ) Phagocytosis
54
Q

In a typical course of inflammatory events, vasodilation, transudation, and then slowing of circulation occurs as the

A

Blood viscosity increases

55
Q

As stasis develops, one begins to see the peripheral orientation of leukocytes along the vascular epithelium, principally

A

Neutrophils

56
Q

Leukocytes first stick transiently and then more

A

Avidly

57
Q

How does induction of the neutrophil interaction with the endothelium occur?

A
  1. ) Redistribution of intracellular receptor stores to the cell surface
  2. ) Induction of expression
  3. ) Activation of receptors
58
Q

Normally is intracellular in endothelium and unavailable for cell surface glycoconjugate binding

A

P-selectin

59
Q

Will induce new expression of receptors on the endothelial surface

A

Cytokines

60
Q

Cell surface integrins can be activated by soluble agents that bind to other receptors. This phenomenon has been called

A

Inside-out signaling

61
Q

Transmembrane heterodimeric adhesion molecules that form noncovalent associations with extracellular matrix and cell surface ligands such as the ICAMs

A

Integrins

62
Q

Integrins associate with the cell surface ligands

A

ICAMs

63
Q

Bind to injured vascular walls and fibrin

A

Platelet integrins

64
Q

Enable leukocyte binding to the venular wall and subsequent migration through that wall

A

Leukocyte integrins

65
Q

In acute inflammation, first, there is an initial and rapid loose adhesion that accounts for

A

Rolling

66
Q

First, there is an initial and rapid loose adhesion that accounts for rolling. It involves mainly the

A

P-selectin, L-selectin, and E-selectin

67
Q

Factors such as histamine and thrombin induce the cell surface movement of

A

Selectins

68
Q

These same agents [i] indirectly initiate arteriolar vasodilation by inducing the endothelial cell to secrete vasoactive prostacyclin and

A

Nitric oxide

69
Q

Cytokines such as IL-1, TNF, IFN-y appear to induce synthesis of the endothelial cell

A

ICAMs

70
Q

The leukocytes are activated by agents made by endothelium or other cells, to increase the avidity of their

A

Integrins

71
Q

These integrins bind stably to endothelium, largely through the interaction of

A

B2-integrin w/ ICAM-1

72
Q

In the following hours, we see release of themajor soluble ligands

A

IL-1 and TNF

73
Q

These agents produce a more sustained vasodilation and vascular leakage, increased leukocyte delivery, further neutrophil adhesion and chemokinesis, secretion of IL-8 and expression of endothelial ELAM-1

A

IL-1 and TNF

74
Q

Closely associated with sticking is the function of directed cell migration out of the vasculature. This is called

A

Diapedesis

75
Q

Neutrophils and mononuclear phagocytes enter inflammatory foci for the purpose of ingesting and disposing of unwanted particulate material such as bacteria or broken-down cells. This is the process of

A

Phagocytosis

76
Q

Neutrophils possess large numbers of cytoplasmic granules: The primary granules are?

-peroxidase positive

A

Azurophilic granules

77
Q

The neutrophils and macrophages also possess

-peroxidase negative

A

Secondary granules

78
Q

Larger dense granules that contain various lysosomal hydrolases such as acid phosphatase, cationic proteins, myeloperoxidase and the antibacterial protein lysozyme

A

Azurophilic granules

79
Q

The smaller specific granules also contain lysozyme, but also have

A

Alk-phos and lactoferrin

80
Q

Have gelatinase and cathepsins. These are released at the leading edge of migrating neutrophils and are thought to act primarily in disrupting extracellular matrix

A

Tertiary particles (from tertiary granules)

81
Q

Phagocytosis can be subdivided into which three phases?

A

Recognition/attachment, engulfment, digestion

82
Q

Coating or “opsinization” of the microbe precedes recognition and attachment by

A

Phagocytes

83
Q

There are two main groups of opsonizationfactors: What are they?

A
  1. ) Heat stabile IgG

2. ) Heat labile C3b (complement)

84
Q

The Fc portion of IgG is recognized by the

A

FcgR receptor

85
Q

C3b is recognized by complement receptors

A

CR-1, 2, and 3

86
Q

In addition, the b2 integrin Mac-1 binds to certain bacterial wall lipopolysaccharide (LPS), mediating so-called

A

Non-opsonic phagocytosis

87
Q

After binding of opsonin molecules to the particle surface, the particle then sticks to the phagocyte surface because the phagocyte has receptors for the

A

Fc portion of antibody and C3b

88
Q

As the phagosome is being formed during ingestion, it is converged on by

A

Lysozymes

89
Q

Phagocytosis is an energy-requiring process that is accompanied by a tremendous burst of metabolic activity in the cell. Oxygen consumption increases

A

2-3 fold

90
Q

The amount of glucose metabolized via the hexose monophosphate shunt (HMS) increases from a resting level of 1% to an active level

A

10%

91
Q

The most important agents for bacterial killing is

A

Superoxide anion and hydrogen peroxide

92
Q

A highly reactive radical derived from oxygen and NADPH

-sequestered in vacuoles

A

Superoxide anion

93
Q

The cell removes any cytoplasmic superoxide with the enzyme

A

Superoxide dismutase

94
Q

An inherited disease usually affecting males (X-linked)

-due to deficiency of NADPH oxidase

A

Chronic Granulomatous Disease (CGD)

95
Q

The major defect of CGD is that the leukocytes fail to show the burst of metabolic activity that normally accompanies

A

Phagocytes

96
Q

This in turn leads to a failure of the halide/myeloperoxidalsystem, which is seen in

A

CGD

97
Q

CGD patients develop serious infections with catalase producing bacteria such as

A

Staphylococcus aureus

98
Q

This is because the catalse negative bacteria essentially commit

A

Suicide

99
Q

Considerably more benign than chronic granulomatous disease, indicating that NADPH oxidase and superoxide production is more important than the peroxidase reaction in bacterial killing

A

Myeloperoxidase

100
Q

Mutations affecting lysosomal membrane trafficking leads to increased CNS infections in

A

Chediak-Higashi syndrome

Immunity (33 decks)

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