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Year 2 > Inflammation and Repair > Flashcards

Inflammation and Repair Flashcards

1
Q

What is LAD-1?

A

Inherited disorder resulting in

defective leukocyte integrins.

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2
Q

What is LAD-2?

A

Absence of sialylated glycoprotein on leukocytes for E-selectin.

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3
Q

What is Chediak-Higashi syndrome?

A

A.R. impaired fusion of lysosomes and phagosomes, impaired secretion of lytic granules by cytotoxic T cells.

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4
Q

What are some general causes of

leukocyte defects?

A

Rare mutations in TLR signaling pathways; mutations in T or B cell differentiation.

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5
Q

Unrelenting fever caused by increased function of cryopin is treated with what?

A

Antagonists to IL-1.

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6
Q

A defect in which molecule causes a defect in neutrophil rolling?

A

Selectin

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7
Q

The “burst” of oxygen consumption by neutrophils during an acute inflammatory response is for what?

A

The generation of microbicidal activity.

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8
Q

What are the 3 general features of acute inflammation?

A

1) Vascular Changes
2) Neutrophil Recruitment
3) Limited tissue injury

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9
Q

What are the 4 general characteristics of injury resolution?

A

1) Clearance of injurious stimuli
2) Clearance of mediators and acute inflammatory cells.
3) Replacement of injured cells.
4) Return to normal function.

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10
Q

What is an abscess?

A

A collection of neutrophils. It is a localized foci of suppurative (purulent) inflammation.

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11
Q

What are the 4 general features of chronic inflammation?

A

1) Angiogenesis
2) Mononuclear cell infiltrate
3) Scarring (fibrosis)
4) Progressive tissue injury

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12
Q

What is serous inflammation?

A

When exudate is protein poor, resulting in watery fluid that accumulates in area of injury or in body cavities.

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13
Q

What is an example of serous inflammation?

A

Skin blister

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14
Q

What is fibrous inflammation?

A

Occurs from a severe injury and results in greater vascular permeability that allows fibrin to pass the endothelial barrier. There is a greater outflow of protein into the extravascular spaces.

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15
Q

If fibrinogen gets into the body cavities, what can it cause?

A

A clotting/sticking fibrin mass that coats the surface of the cavity and causes the organ to adhere to the body wall.

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16
Q

What causes permanent organ adhesion to the body wall?

A

If fibrinolysis doesn’t occur fast enough. Fibroblasts and new blood vessels migrate into the fibrin mesh, forming granulation tissue. This leads ultimately to fibrosis/scarring.

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17
Q

What is an ulcer?

A

Any break in epithelium.

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18
Q

True or false: There is a lot of fibrin formation in an ulcer.

A

True.

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19
Q

What are the characteristics of suppurative (purulent) inflammation?

A

Large numbers of neutrophils; edema; necrotic debris (pus).

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20
Q

What kind of bacterial infections cause purulent inflammation?

A

Pyogenic bacterial infections.

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21
Q

What is an example of a chemical mediator of inflammation that is stored in intracellular granules and rapidly released?

A

Histamine.

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22
Q

What are examples of chemical mediators of inflammation that are synthesized de novo in response to a stimulus?

A

Prostaglandins; cytokines produced by leukocytes and other cells.

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23
Q

What are examples of chemical mediators of inflammation that circulate inactively but are activated at the site of inflammation?

A

Complement/ coagulation system; Kinins.

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24
Q

What are examples of chemical mediators of inflammation that do not require receptors?

A

Reactive oxygen species; lysosomal proteases.

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25
Q

Which cells produce cell derived chemical mediators of inflammation?

A

Tissue macrophages. mast cells, endothelial cells, and recruited leukocytes.

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26
Q

What kind of cells store histamines?

A

Perivascular mast cells, circulating basophils, and platelets.

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27
Q

What are the stimuli that cause histamine release?

A

Cold/heat; binding of IgE antibodies to Fc receptor; C3a or C5a; cytokines (IL-1, IL-8); neuropeptides.

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28
Q

What is the effect of histamine?

A

Arteriolar vasodilation.

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29
Q

Histamine is the main mediator for which phase of increased vascular permeability?

A

The immediate reversible phase (endothelial cell contraction).

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30
Q

What inactivates histamine?

A

Histaminase.

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31
Q

What type of cells store serotonin?

A

Platelet granules.

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32
Q

What causes platelet aggregation?

A

Contact of platelets with extravascular collagen; PAF, PAD; antigen-antibody complexes.

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33
Q

What is the effect of serotonin?

A

Vasoconstriction

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34
Q

Where is serotonin mainly produced?

A

Neurons and enterochromaffin cells.

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35
Q

What is a function of serotonin aside from mediating inflammation?

A

It is a neurotransmitter and regulates intestinal motility.

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36
Q

What are the major sources of arachidonic acid?

A

Leukocytes, mast cells, endothelial cells, and platelets.

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37
Q

How is arachidonic acid released from the cell membrane?

A

It is released from phospholipids by phospholipase A2 or by inflammatory mediators such as C5a.

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38
Q

The cyclooxygenase pathway cleaves arachidonic acid and stimulates the synthesis of what?

A

Prostaglandins and thromboxanes.

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39
Q

The lipoxygenase pathway cleaves arachidonic acid and stimulates the synthesis of what?

A

Leukotrienes and lipoxins.

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40
Q

Prostacyclin (PGI2) is a prostaglandin that that causes what?

A

Vasodilation and inhibition of platelet aggregation.

41
Q

Thromboxane A2 has what effects?

A

Vasoconstriction and promotion of platelet aggregation.

42
Q

PGD2 and PGE2 has what effects?

A

Vasodilation and increased vascular permeability.

43
Q

What are the effects of LTC4, LTD4, and LTE4?

A

Bronchospasm; increased vascular permeability.

44
Q

What are the effects of LXA4 and LXB4?

A

Inhibition of neutrophil adhesion and chemotaxis.

45
Q

What is an important source of lipoxin?

A

Platelets activated and adherent to leukocytes.

46
Q

Can platelets synthesize LXA4 and LXB4 alone?

A

No, it can form them via an intermediate derived from adjacent neutrophils by a transcellular pathway.

47
Q

How do NSAIDs treat pain and fever?

A

They inhibit cyclooxygenase activity. This results in less prostaglandin synthesis (aka less inflammation).

48
Q

Why are glucocorticoids potent inhibitors of inflammation?

A

They up regulate the gene for lipocortin 1, which inhibits phospholipase A2, thus preventing release of arachidonic acid.

49
Q

How are omega 3 fatty acids involved in reducing inflammation?

A

They compete with omega 6 fatty acids for metabolism in the plasma membrane. EPA is the phospholipid that becomes present in the membrane. Lipoxygenase and cyclooxygenase converts this to LT5 and PG3, which are less potent inflammatory mediators.

50
Q

What is the main function of Platelet Activating Factor?

A

It is a very potent positive regulator of inflammation. 1000x more so than histamine.

51
Q

True or false: Platelet Activating Factor has no effect on the synthesis of arachidonic acid metabolites.

A

False. Platelet activating factor enhances the synthesis of arachidonic acid metabolites.

52
Q

True or false: The process of bronchoconstriction can be considered anti-inflammatory.

A

False. Bronchoconstriction is pro-inflammatory.

53
Q

What are the major cytokines in acute inflammation?

A

IL-1, TNF, IL-6 and chemokines.

54
Q

What are the 2 main functions of chemokines?

A

Recruit leukocytes to site of inflammation; control normal anatomic segregation of cells in lymphoid and other tissues.

55
Q

What subset of chemokines attracts mainly neutrophils?

A

CXC subset.

56
Q

What subset of chemokines attracts monocytes, eosinophils, and memory T cells?

A

CC subset

57
Q

Which receptors are co-receptors for HIV binding/ entry into lymphocytes?

A

CXCR4 and CCR5

58
Q

Which cells release ROS?

A

Activated neutrophils and macrophages.

59
Q

True or false: High levels of ROS will increase endothelial permeability.

A

True. High levels of ROS can lead to endothelial damage.

60
Q

Catalase, superoxide dismutase and glutathione are all examples of what?

A

Antioxidants.

61
Q

What are the functions of Nitric Oxide (NO)?

A

Vasodilation; inhibits all stages of platelet activation; reduces leukocyte recruitment at inflammatory sites; microbicidal agent in activated macrophages.

62
Q

What is the function of neutral proteases in mediating inflammation?

A

Neutral proteases break down the ECM and cleave precursors to form vasoactive mediators C3a and C5a; and bradykinin from kininogen.

63
Q

True or false: Serum and tissue fluids normally do not contain anti-proteases.

A

False. Anti-proteases need to be present. Deficiency can lead to tissue destruction.

64
Q

How do C3a and C5a cause vasodilation and increased vascular permeability?

A

By inducing mast cells to release histamine.

65
Q

What are the 3 main functions of C5a?

A

Leukocyte activation; adhesion to endothelium; chemotaxis.

66
Q

What is the function of C3b?

A

It acts like opsonin to enhance phagocytosis.

67
Q

What is the membrane attack complex?

A

Made by multiple copies of C9. Kills bacteria by creating pores.

68
Q

Inherited deficiency in C1 inhibitor gives rise to what disease?

A

Hereditary angioedema.

69
Q

Acquired deficiency of decay-accelerating factor leads to what disease?

A

Paroxysmal nocturnal hemoglobinuria.

70
Q

What is Hageman Factor (XII)?

A

It is a plasma protein synthesized by the liver.

71
Q

What does Hageman Factor do?

A

Activates the kinin system.

72
Q

What are the effects of bradykinin?

A

Early vasodilation; increased vascular permeability of venules and pain; extravascular smooth muscle (bronchial) contraction.

73
Q

Are the effects of bradykinin long or short lived?

A

Short lived b/c they are degraded by kininases present in plasma and tissues.

74
Q

What is the function of kallikrein?

A

It is a potent activator of Hageman Factor. It links kinins to the clotting system.

75
Q

What is the function of fibrinopeptides?

A

They increase vascular permeability and are chemotactic for leukocytes.

76
Q

What are the functions of thrombin?

A

It cleaves fibrinogen to fibrin and small fibrinopeptides. Thrombin also enhances leukocyte adhesion and converts C5 to C5a.

77
Q

What does factor Xa do?

A

Increases vascular permeability and promotes transmigration of leukocytes from venules.

78
Q

How is plasminogen activated to plasmin?

A

Plasminogen activator and kallikrein cleave plasminogen in the clot to active plasmin.

79
Q

What are the functions of plasmin?

A

It solubilizes the fibrin clot and increases vascular permeability via “fibrin split products”.

80
Q

What are more functions of plasmin?

A

It can activate Hageman Factor; cleave C3 to C3a and C3b.

81
Q

What is classical macrophage activation?

A

Induced by bacterial LPS, foreign material and interferon G secreted by T cells. Results in actively microbicidal macrophages.

82
Q

Which interleukins does classical macrophage activation release?

A

IL-1 and IL-12

83
Q

What is alternative macrophage activation?

A

Induced by cytokines such as IL-4 and IL-13. Macrophages are NOT actively microbicidal.

84
Q

What can induce macrophages to fuse and become multinucleated giant cells?

A

IFN-g.

85
Q

What are the 3 types of CD4+ helper T cells?

A

TH1 cells, TH2 cells, and TH17 cells.

86
Q

What is the function of TH1 cells?

A

They produce cytokine IFN-g, activating macrophages by the classical pathway.

87
Q

What is the function of TH2 cells?

A

They secrete IL-4, IL-5, IL-13, which recruit/activate eosinophils and stimulate alternative pathway of macrophage activation.

88
Q

What is the function of TH17 cells?

A

They secrete IL-17, which induces secretion of chemokines that recruit neutrophils and monocytes.

89
Q

Which type of CD4+ helper T cell is common in allergic reactions?

A

TH2.

90
Q

What is the function of

eotaxin?

A

Recruits eosinophils.

91
Q

What is a major stimulator of monocytes and macrophages?

A

Interferon gamma.

92
Q

Granulomatous inflammation forms under what 3 settings?

A

1) Persistent T cell response in which T cell cytokines maintain macrophage activation. 2) Immune-mediated inflammatory disease. 3) Sarcoidosis and in response to foreign, inert bodies.

93
Q

True of false: Classical granulomatous inflammation has necrosis.

A

True.

94
Q

True or false: The granuloma in tuberculosis exhibits central caseous necrosis.

A

True.

95
Q

True or false: The granuloma in sarcoidosis exhibits central caseous necrosis.

A

False.

96
Q

IL-6 stimulates hepatocytes to secrete what?

A

C-reactive protein (CRP).

97
Q

True or false: Serum levels of CRP have no correlation with inflammation.

A

False. You can use serum levels of CRP to measure the level of inflammation.

98
Q

What is the function of Colony Stimulating Factor (CSF) in the bone marrow?

A

It increases the production of white cells.

Year 2 (9 decks)

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