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Immunity > Inflammation II > Flashcards

Inflammation II Flashcards

1
Q

What are three mediators in vasodilation?

A

Prostaglandins, nitric oxide, and histamine

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2
Q

C3a and C5a function to increase

A

Vascular permiability

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3
Q

What three mediators function to induce fevers?

A

IL-1, TNF, and prostaglandins

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4
Q

Chronic inflammation can be described by the predominant type of inflammatory cell, i.e

A

Mononuclear inflammatory cells

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5
Q

Parenchymal cell death and tissue destruction that result in growth of new blood vessels and production of connective tissues are examples of

A

Irreversible tissue damage

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6
Q

A dying cell release soluble mediators of inflammation that initiate a response similar to that seen in

A

Acute inflammation

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7
Q

Then, mononuclear emigration replaces neutrophilic emigration. Two new things occur. These are:

A

Angiogenesis and fibroblast migration

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8
Q

As chronic inflammation progresses, we see the development of a transient

A

Granular tissue

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9
Q

A precursor to scar formation

A

Granulation

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10
Q

The process by which new blood vessels are created from preexisting ones

A

Angiogenesis

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11
Q

Occurs at the level of capillaries that consist of a vascular endothelium resting on a basement membrane with an overlay of pericytes

A

Angiogenesis

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12
Q

Angiogenesis is stimulated by

A

Inflammation and hypoxia

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13
Q

Regulate angiogenesis through their receptors leading to the formation of new blood vessels

A

Chemokines

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14
Q

Chemokines indirectly influence endothelial cell behaviors by attracting chemokine receptor-expressing

A

Leukocytes

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15
Q

These subsequently secrete pro-angiogenic factors, such as

-Act on endothelial cells and initate angiogenesis

A

Vascular Endothelial Growth Factor (VEGF)

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16
Q

The coordinated arrangement of endothelial cells in three dimensions to form and maintain a vascular tube requires endothelial cell proliferation, migration, survival, and permeability. These biological responses are mediated mainly by

A

BEGFA-activated VEGFR2

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17
Q

On VEGFA-binding to extracellular Ig-like domains 2 and 3 of VEGFR2, signaling molecules bind to respective

A

Phosphorylation sites

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18
Q

Ultimately, the granulation field becomes relatively accellular, with dense fibrous connective tissue (scar tissue) replacing the

A

Original architecture

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19
Q

The persistent stimulus of chronic inflammation activates macrophages and lymphocytes, leading to the production of growth factors and cytokines, which increase the synthesis of

A

Collagen

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20
Q

Deposition of collagen is enhanced by decreased activity of

A

Metalloproteinases

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21
Q

The principal cells producing the ECM of fibrosis are the myofibroblasts, defined as fibroblasticlike cells that express

A

Alpha-smooth muscle actin

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22
Q

These cells derive from tissue resident mesenchymal cells (fibroblasts and pericytes) following stimulation by various

A

Cytokines

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23
Q

In an MI, the initial infiltrate is replaced by a monocytic response that peaks

A

One day later

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24
Q

Reaches its peak at two weeks of age whereas a full dense scar appears only by several months

A

Granulation

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25
Q

Inflammation of the gallbladder, a condition that can result from gallstones that block the common bile duct

A

Cholecystisis

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26
Q

Gross examination reveals variable thickening of the gallbladder wall. Microscopic exam can reveal chronic inflammation with

A

Rokitansky-Aschoff sinuses

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27
Q

Periportaland receives blood with the highest oxygen concentration

-closer to bile duct and hepatic artery

A

Zone 1 of hepatocyte

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28
Q

In micronodular cirrhosis, the regenerative nodules average 3 mm or less in size. The yellow-brown appearance of these nodules is caused by concomitant

A

Hepatic Steatosis

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29
Q

The most common cause of micronodular cirrhosis and steatosis is

A

Chronic Alcohol abuse

30
Q

A fine reticulin network of type IV collagen is normally present in the liver, but with cirrhosis there is extensive deposition of type

A

I and III collagen

31
Q

The increased hepatocyte proliferation from nodular regeneration increases the risk for

A

Hepatocellular cholangiolar carcinoma

32
Q

Liver injury leads to Kupffer cell activation with release of cytokines, such as

-stimulate stellate cells in the space of Disse to proliferate into myofibroblasticcells that contribute to the fibrogenesis

A

Platelet-derived growth factor and TNF

33
Q

In cirrhosis, the flow of blood over hepatocytes from portal triad to central vein is impeded due to the architectural changes resulting from

A

Fibrosis

34
Q

Achronic inflammatory infiltrate is typically seen in viral pneumonias such as those resulting from

A

Influenza

35
Q

The final common pathway for various severe lung injuries

A

Diffuse Alveolar Damage (DAD)

36
Q

In early DAD, hyaline membranes, as seen here, line the alveoli. Later in the first week after lung injury, the hyaline membranes resolve, and we see proliferation of

A

Macrophages

37
Q

Fibroblasts migrate into the alveolar exudates through defects in the epithelial basement membrane to lay down collagen within the hyaline membranes in the

A

Organization phase of DAD

38
Q

As epithelial cells grow over the newly formed connective tissue, a new basement membrane is formed, thereby incorporating the collagen into the interstitium, a process known as

A

Fibrosis by accretion

39
Q

Involvement of the alveolar ducts results in these structures being lined by a ring of

A

Granulation tissue

40
Q

Less frequently, the organized exudates retain a predominantly intra-alveolar position, resulting in loose buds of granulation tissue similar to those seen in

A

Pneumonia

41
Q

It is claimed that this intra-alveolar pattern of repair is particularly found when the initial damage is caused by

A

Generalized sepsis

42
Q

However, interstitial fibrosis is more characteristic of injury caused by

A

Cytotoxic drugs

43
Q

Fibrotic disease that is often reversible with steroid treatment. Thus there remains a potential of reversibility with fibrosis

A

BOOP

44
Q

Its appearance within air spaces rather than the interstitium, and likely the better preservation of the alveolar cells themselves, that predisposes to recovery

A

Boop

45
Q

An example of extensive and irreversible fibrosis

A

UIP

46
Q

Require stabilizing linkages that extend from the stroma through basement membrane to receptors to cytoskeleton

A

Skeletal muscle fibers

47
Q

The thin extracellular matrix, consisting largely of basement membrane, is important for maintaining theadjacent

A

Myofiber

48
Q

A loss of anyone of the linkage proteins can result in a

A

Muscular dystrophy

49
Q

The most common of these result from X-linked mutations of the gene coding for

A

Dystrophin

50
Q

Caused by a defective dystrophin gene on the X chromosome that leads to an inability to produce the striated muscle sarcolemmal membrane structural protein dystrophin

A

Duchenne Muscular Dystrophy (DMD)

51
Q

What is the inheritance pattern of DMD?

A

X-linked recessive

52
Q

About one third of cases of DMD arise from

A

Spontaneous new mutations

53
Q

While they can be considered as forms of chronic inflammation, retain the leukocyte characteristics seen in acute inflammation

A

Abscesses

54
Q

Encapsulated accumulation of pus (usually neutrophils)

A

Abscess

55
Q

It can be a complication of pneumonia, is seen in aspiration, bronchiectasis, and airway obstruction

A

Pulmonary Abscess

56
Q

Accumulation of pus in an existing body cavity

A

Empyema

57
Q

A circumscribed form of chronic inflammation that occurs in response to a localized inciting agent such as a foreign body or certain bacteria that can be sequestered by inflammatory tissue but that cannot be easily removed from the tissue

A

Granuloma

58
Q

A special type of chronic inflammation characterized by a circumsized collection of macrophages

A

Granuloma

59
Q

The initiating event of granuloma growth is the growth of

A

Myobacterium

60
Q

The initial response is that seen in acute inflammation, in which there is

A

Vasodilation and neutrophilic and mononuclear diapedesis

61
Q

Mononuclear cells surround site of injury and both fuse to form giant cells and adhere to produce

A

Epithelioid macrophages

62
Q

Then, fibroblasts surround the inflammatory cells and we see the walled-off formation of a

A

Granuloma

63
Q

One of the most well-studied cases of granulomas is

A

Tuberculosis

64
Q

The causative organism for tuberculosis stains red with the

A

Acid fast stain

65
Q

Non-caseating and of uncertain cause and need to be distinguished from those of TB and other infectious diseases

A

Sarcoid granulomas

66
Q

The most important factors in determining the extent of the inflammatory reaction are (a) whether there is significant amount of cell death and (b) whether there is destruction of the underlying

A

Basement membrane

67
Q

If the parenchymal cell can rapidly migrate on its basement membrane substrate and re-epithelialize the injured surface, we will see

A

No irreversible changes

68
Q

On the other hand, if this migration and regeneration is impeded, either because the cells can’t divide, or because the underlying basement membrane and stromal architecture is destroyed, then we will see

A

Irreversible angiogenesis and fibrosis

69
Q

Serves as a good example of a severe and yet self-limiting inflammation reaction

A

Gout

70
Q

Unlike gout, results in the development of permanent sequelae

A

Silicosis

71
Q

The result of silicosis is extensive scarring of the

A

Lung

72
Q

One mechanism by which this may operate is that injured macrophages release the cytokines IL-1 and TNF which initiate angiogenesis, recruit fibroblasts and induce

A

Collagen and fibronectin synthesis

Immunity (33 decks)

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