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Morbid > Imflammation I > Flashcards

Imflammation I Flashcards

1
Q

Components of innate immunity (school)

A

Natural Killer cells
Dendritic cells
Epithelial cells
Proteins of the complement system

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2
Q

What cells provide first response to infection (apart from leukocytes)

A

Components of innate immunity

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3
Q

Sequence of events in inflammatory reaction

A
  1. Macrophage recognition
  2. Clotting begins
  3. Chemokines attract phagocytic cells to injury site
  4. Neutrophils and macrophages phagocytose pathogens
  5. Tissue heals
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4
Q

Acute disorders caused by inflammatory reactions

A
  1. Acute respiratory distress syndrome
  2. Asthma
  3. Glomerulonephritis
  4. Septic shock
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5
Q

Cells involved in acute respiratory distress syndrome

A

Neutrophils

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6
Q

Cells involved in asthma

A

Eosinophils; IgE antibodies

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7
Q

Cells involved in glomerulonephritis

A

Antibodies and complement; neutrophils and monocytes

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8
Q

Cells involved in septic shock

A

Cytokines

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9
Q

Chronic diseases caused by inflammatory reactions

A

Arthritis
Asthma
Atherosclerosis
Pulmonary fibrosis

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10
Q

Cells involved in arthritis

A

Lymphocytes, macrophages; antibodies

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11
Q

Cells involved in atherosclerosis

A

Macrophages; Lymphocytes

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12
Q

Cells involved in Pulmonary fibrosis

A

Macrophages; fibroblasts

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13
Q

What are the main characteristics of acute inflammation

A
  1. Exudation of fluid and plasma proteins (edema)
  2. Emigration of leukocytes, predominantly neutrophils
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14
Q

Which phase of inflammation is associated with ‘more tissue destruction’

A

Chronic

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15
Q

Cardinal signs of inflammation

A

Rubor
Tumor
Calor
Dolor
Functio laesa

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16
Q

Causes of inflammation

A
  1. Infections
  2. Tissue Necrosis
  3. Foreign bodies
  4. Deposition of endogenous substances
  5. Immune reactions
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17
Q

Three major components of AI

A
  1. Dilation of small vessels
  2. Increased permeability of the microvasculature
  3. Emigration of the leukocytes from microcirculation, accumulation at site and activation.
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18
Q

What is an exudate

A

An extra vascular fluid that has a high protein concentration and contains cellular debris

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19
Q

What is a transudate

A

A fluid with low protein content(most of which is albumin), low or no cellular debris and low specific gravity

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20
Q

An ultra filtrate of blood plasma that is as a result of osmotic or hydrostatic imbalance across the vessel wall without an increase in vascular permeability

A

Transudate

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21
Q

Edema can be either an exudate or a transudate T/F

A

T

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22
Q

Pus is rich in

A

Leukocytes (neutrophils)
Debris of dead cells
Microbes

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23
Q

What are the states of the pressures involved in transudate production

A
  1. Increased hydrostatic pressure (venous outflow obstruction eg congestive heart failure)
  2. Decreased colloid osmotic pressure (decreased protein synthesis eg liver disease); (increased protein loss eg kidney disease)
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24
Q

There’s vasodilation and stasis in exudate production T/F

A

T

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25
Q

There’s increased interendothelial spaces in transudate formation T/F

A

F. Increased interendothelial spaces in exudate formation

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26
Q

Vasodilation is mediated by

A

Histamine

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27
Q

What vessels are affected in AI vasodilation

A

Arterioles
Capillaries

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28
Q

In acute inflammation, blood flow is increased/decreased/normal

A

Increased

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29
Q

Following vasodilation in acute inflammation, there’s outpouring of fluid into the extra vascular tissues. This fluid is called

A

Exudate. Protein rich fluid

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30
Q

Loss of fluid and increased vessel diameter lead to (3)

A

Slower blood flow
Concentration of red cells in small vessels
Increased viscosity of blood

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31
Q

As stasis develops, what occurs with neutrophils

A

They accumulate along the vascular endothelium

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32
Q

Mechanisms responsible for increased permeability of post capillary venules

A
  1. Contraction of endothelial cells (leakage)
  2. Endothelial injury
  3. Transcytosis
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33
Q

Contraction of endothelial cells is elicited by

A

Histamine
Bradykinin
Leukotrienes
Other mediators

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34
Q

What is called the immediate transient response

A

Contraction of endothelial cells (vascular leakage)

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35
Q

Contraction of endothelial cells (vascular leakage) usually lasts for how long

A

15-30 minutes

36
Q

In some forms of mild injury, vascular leakage begins after a delay of 2-12hrs and lasts hours or days T/F

A

T

37
Q

Late appearing sunburn is a good example of what type of leakage

A

Delayed prolonged leakage

38
Q

Endothelial injury can lead to

A

Endothelial cell necrosis and detachment

39
Q

Direct damage to the endothelium can be caused by

A
  1. Sever injury e.g burns
  2. Induced by the actions of microbes and microbial toxins that target endothelial cells
40
Q

Transcytosis (increased transport of fluids and proteins through the endothelial cell) may involve

A

Intracellular channels stimulated by VGEF(vascular endothelial growth factor)

41
Q

In late stages of inflammation, neutrophils that adhere to the endothelium may also injure the endothelial cells T/F

A

T

42
Q

The constellation of pathologic changes that occur in lymphatic vessels and nodes is termed

A

Reactive or Inflammatory Lymphadenitis

43
Q

The most important leukocytes capable of phagocytosis

A

Neutrophils
Macrophages

44
Q

The journey of leukocytes from the vessel lumen to the tissue is mediated and controlled by

A

Chemokines

45
Q

Phases of the leukocyte journey to the tissue that occur in the lumen

A

Margination
Rolling
Adhesion to endothelium

46
Q

Cytokines are secreted by ……………………. in tissues in response to microbes and other injurious agents

A

Sentinel cells

47
Q

L selectin is expressed on

A

Leukocytes

48
Q

E selectin is expressed on

A

Endothelium

49
Q

P selectin is expressed on only endothelium T/F

A

F. Expressed on both platelets and endothelium

50
Q

Ligands for selections are

A

Sialylated Oligosaccharides bound to mucin-like glycoprotein backbones

51
Q

The expression of selectins and their ligands is regulated by

A

Cytokines

52
Q

What cytokines induce the coordinate expression of numerous adhesion molecules

A

TNF
IL-1

53
Q

What stimulates the redistribution of P selectin from the Weibel Palade bodies

A
  1. Histamine and Thrombin
54
Q

Firm adhesion is mediated by a family of heterodimeric leukocyte surface proteins called

A

Integrins

55
Q

B1 integrin, VLA-4 is to

A

VCAM 1 (Vascular cell adhesion molecule 1)

56
Q

B2 integrins, LFA 1 and Mac 1 are to

A

ICAM 1 (intercellular adhesion molecule 1)

57
Q

Leukocytes normally express integrins in what state

A

Low affinity state

58
Q

Chemokines produced at the site of the injury bind to

A

Endothelial cell proteoglycans

59
Q

Chemokines bind to leukocytes and activate

A

rolling leukocytes

60
Q

Chemokines activate the conversion of VLA-4 and LFA1 integrins on the leukocytes to what state

A

High affinity state

61
Q

The migration of the leukocytes through the endothelium is called

A

Transmigration or Diapedesis

62
Q

Transmigration of leukocytes occurs mainly in

A

Post capillary venules

63
Q

Molecules between endothelial cells involved in the migration of leukocytes are

A

CD31 or PECAM 1(Platelet endothelial cell adhesion molecule)

64
Q

Only exogenous substances can act as chemoattractants T/F

A

F. Exogenous and endogenous substances can act as chemoattractants

65
Q

The most common exogenous chemoattractants are

A

Bacterial products
Some lipids

66
Q

Endogenous chemoattractants include:

A
  1. IL-8 (cytokines)
  2. C5a (components of the complement system)
  3. LTB4 (arachidonic acid metabolites)
67
Q

Chemotactic agents bind to specific ……… on the surface of leukocytes

A

7 trans membrane GPCRs

68
Q

Signals from the leukocyte GPCRs activate second messengers that (2)

A
  1. Increase cytosolic calcium
  2. Activate small GTPs of the Rac/Rho/cdc42 family
69
Q

Leukocyte surface signals induce

A
  1. Polymerization of actin at the leading edge of the cell
  2. Localization of MYOSIN filaments at the back
70
Q

In most forms of AI, neutrophils predominate the inflammatory infiltrate during

A

The first 6 to 24hours

(Replaced by monocytes in the next 24 to 48 hours)

71
Q

What cells become the dominant population in prolonged inflammatory reactions

A

Monocytes

72
Q

In what situation is the cellular infiltrate dominated by continuously recruited neutrophils for several days?

A

Pseudomonas bacteria

73
Q

In viral infections, what cells are the first to arrive

A

Lymphocytes

74
Q

Hypersensitivity reactions are dominated by

A

Lymphocytes
Macrophages
Plasma cells

75
Q

What’s the dominant population of the cellular infiltrate in allergic reactions

A

Eosinophils

76
Q

Agents that block ………… are among the most successful developed therapeutics for Chronic Inflammatory Do

A

TNF

77
Q

Recognition of what cells induces leukocyte activation for clearance

A

Microbes or Dead cells

78
Q

In phagocytosis and clearance, Leukocyte activation results in

A
  1. Increases in cytosolic Ca2+
  2. Activation of enzymes (pkC, PLA2)
79
Q

What are the Three steps in Phagocytosis

A

Recognition and Attachment
Engulfment
Killing or Degradation

80
Q

Examples of phagocytic receptors

A

Mannose receptors
Scavenger receptors
Receptors for various opsonins

81
Q

The ……………. receptor recognizes microbes and not host cells

A

Mannose

82
Q

Mac 1 may also bind microbes for phagocytosis T/F

A

T

83
Q

The major opsonins are

A
  1. IgG antibodies
  2. the C3b breakdown product of complement
  3. Certain plasma lectins (mannose-binding lectin)
84
Q

Extensions of the cytoplasm used for engulfment

A

Pseudopods

85
Q

Vesicle that encloses foreign particle

A

Phagosome

86
Q

Phagocytosis is dependent on

A

Polymerization of actin filaments

87
Q

Killing of microbes is accomplished by

A

Reactive Oxygen species
Reactive Nitrogen species
Lysosomal enzymes

Morbid (8 decks)

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