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Pathology > 2- Acute and Chronic Inflammation > Flashcards

2- Acute and Chronic Inflammation Flashcards

1
Q

What are the 5 signs of inflammation?

A 
Rubor (redness)
Tumor (Swelling)
Calor (heat)
Dolor (pain)
Loss of function (function laesa)- added later on
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2
Q

What are the 3 signs of acute inflammation?

A
  1. Increased blood flow
  2. Leakage of plasma proteins –> edema
  3. Neutrophil emigration into the tissue
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3
Q

What is exudate?

A

When plasma proteins, blood and fluids into the tissues.

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4
Q

What is the specific gravity of exudate?

A

sg > 1.020

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5
Q

What generally causes exudate to leak into the tissues from the blood?

A

increased vascular PERMEABILITY

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6
Q

What is transudate?

A

Fluid in tissues with low protein content

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7
Q

What is the specific gravity of transudate?

A

< 1.012

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8
Q

What generally causes transudate to enter the tissues from the blood?

A

An increase in vascular PRESSURE

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9
Q

What is the first sign of inflammation?

A

Vasodilation

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10
Q

What type of vessels dilate in the circulatory system?

A

Arterioles

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11
Q

What factors induce vasodilation?

A

Histamine and NO

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12
Q

Vasodilation leads to protein-rich fluid to squeeze through into the tissues. What type of fluid is this (transudate or exudate)?

A

Exudate

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13
Q

Why does vasodilation eventually lead to stasis?

A

Loss of fluid –> increased viscosity –> stasis of blood

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14
Q

Stasis of the blood leads to the accumulation of what important cells along the vascular endothelium?

A

Neutrophils

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15
Q

How do neutrophils enter the tissues from the blood? (generally)

A

The vascular endothelium expresses adhesion molecules which bind to the neutrophils, which then squeeze through and into the tissues.

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16
Q

What is the “hallmark” of acute inflammation?

A

Increased vascular permeability

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17
Q

What is the most common mechanism of increased vascular permeability?

A

Contraction of endothelial cells

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18
Q

Which mediators cause endothelial contraction to lead to increased vascular permeability?

A

Elicited by histamine, bradykinin, leukotrienes, the neuropeptide substance P, and many other mediators

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19
Q

Is the contraction of endothelial cells long or short lived?

A

Short lived (15-30mins)

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20
Q

How can endothelial injury cause increased vascular permeability?

A

Injury (by necrosis or direct injury)leads to the escape of exudate from the blood and into the tissues.

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21
Q

What is transcytosis?

A

The passage of fluid and proteins through the endothelial cell, causing exudate to build in the tissues.

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22
Q

Which mediator causes transcytosis?

A

VEGF

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23
Q

What happens to lymph vessels during inflammation of a tissue?

A

They grow and proliferate to drain the excess interstitial fluid.

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24
Q

What is the term when the lymph VESSEL is inflamed?

A

Lymphangitis

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25
Q

What is called when the lymph NODE is inflammed?

A

Lymphadenitis

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26
Q

Let’s go back to neutrophils going into the tissues. What causes the margination of the neutrophils to the endothelial lining?

A

Stasis

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27
Q

Which molecules cause the “rolling” of the neutrophils along the endothelium?

A

Selectins

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28
Q

Which molecules allow the adhesion of the neutrophil to the endothelium?

A

Integrins

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29
Q

Which signals cause the neutrophil to undergo diapedesis through the endothelium?

A

Chemokines

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30
Q

What causes the neutrophil attraction, once inside the tissue, to the point of injury?

A

Chemokines

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31
Q

What is the role of macrophages in repair?

A

They stimulate repair (fibroblast stimulation, collagen synthesis, stimulate enzymes that remodel connective tissues)

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32
Q

What enzymes are contained within the granules of the neutrophils?

A

Elastase, Defensins, Cathlicidins, and Lysozymes.

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33
Q

What is the protein in eosinophils that kills parasites?

A

Major Basic Protein (MBP)

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34
Q

Chediak-Higashi is a syndrome where there is a defect in what?

A

Phagolysosome formation

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35
Q

What are the symptoms of Chediak-Higashi syndrome?

A

Susceptibility to infections
Abnormalities in melanocytes (leading to albinism)
Cells of the nervous system (associated with nerve defects)
Platelets (causing bleeding disorders)
Leukocyte abnormalities
Neutropenia (decreased numbers of neutrophils)
Defective degranulation
Delayed microbial killing

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36
Q

What is defective in chronic granulomatous disease?

A

Phagocyte oxidase

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37
Q

What are the symptoms of chronic granulomatous disease?

A

Many granuloma formations from macrophages walling off bacteria that they cant kill

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38
Q

What happens in leukocyte adhesion deficiency?

A

Selectins and Integrins defective –> leukocyte can’t adhere to endothelium –> no leukocyte diapedesis to infected sites in tissues –> recurrent infections

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39
Q

Radiation and chemotherapy can cause what type of acquired leukocyte deficiency?

A

Bone marrow suppression

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40
Q

Generally, where are cell-derived mediators sequestered?

A

Granules

41
Q

What types of cells release mediators?

A

all granulocytes, mesenchymal cells, most epithelia

42
Q

Where are most plasma-derived mediators made?

A

The liver

43
Q

What is special about plasma-derived mediators as they float around in the blood?

A

They are in the inactive form (like complement proteins and kinins) and must be activated to elicit a response.

44
Q

What are the 2 major vasoactive amines?

A

Histamine and serotonin

45
Q

Which cell has the highest supply of histamine? (think allergies)

A

Mast cells

46
Q

Which types of stimuli cause mast cell degranulation (thus releasing histamine)?

A 
Physical injury
Antibody binding 
Complement (C5a and C3a are anaphylatoxins)
Cytokines
Other nonimportant stuff
47
Q

What does histamine do to arterioles?

A

Dilate them

48
Q

What does histamine do to venules?

A

Increase their permeability

49
Q

Which cells in the blood store serotonin?

A

Platelets

50
Q

What are the main actions of serotonin?

A

Similar to histamine (Vasodilation,blah blah)

51
Q

Cycloogenases synthesize which important eicosanoids?

A

Prostaglandins

52
Q

Lipoxygenases synthesize which important eicosanoids?

A

Leukotrienes and lipoxins

53
Q

Where are prostaglandins made?

A

Produced by mast cells, macrophages, endothelial cells, and many others

54
Q

Which mediator is a potent vasodilator, inhibitor of platelet aggregation, and stimulates other mediators?

A

Prostacyclin (PGI2)

55
Q

Which prostaglandin is made by mast cells, and works with PGE2 to cause vasodilation and increased permeability of venules?

A

PGD2

56
Q

Which prostaglandin stimulates the contraction of uterine and bronchial smooth muscle and small arterioles?

A

PGF2α

57
Q

Which prostaglandin is a chemoattractant for neutrophils?

A

PGD2

58
Q

Which prostaglandin is a hyperalgesic, makes skin hypersensitive to pain, and is involved with cytokine-induced fevers in infections?

A

PGE2

59
Q

Which prostaglandin is produced by activated platelets and causes platelet aggregation and synthesis?

A

TXA2

60
Q

What are the main roles of leukotrienes?

A

Produced by lipoxygenase enzymes
Secreted mainly by leukocytes
Chemoattractants for leukocytes
Vascular effects

61
Q

Which lipoxygenase is the predominant one in neutrophils and converts AA to 5-hydroxyeicosatetraenoic acid?

A

5 lipoxygenase

62
Q

Which leukotriene is a potent chemotactic agent and activator of neutrophils, causes aggregation and adhesion of the cells to venular endothelium, and generates ROS?

A

LTB4

63
Q

Which leukotrienes cause intense vasoconstriction, bronchospasm and increased vascular permeability, as well as releases lysosomal enzymes?

A

Cysteinyl-containing leukotrienes C4, D4, and E4 (LTC4, LTD4, LTE4)

64
Q

What is the role of lipoxins?

A

They are negative regulators of leukotrienes by inhibiting inflammation and neutrophil attraction.

65
Q

What are the 3 main actions of PAF?

A

Platelet aggregation,bronchoconstriction and vasoconstriction

66
Q

At really low concentrations of PAF, what happens?

A

Vasodilation and increased vascular permability

67
Q

What cells release NO?

A

Consuela-like cells. Just kidding. Endothelial cells.

68
Q

What are the 2 main actions of NO?

A
  1. Vasodilation by relaxing muscles.

2. Inhibiting inflammation

69
Q

What are the 2 main cytokines that are produced from macrophages and mediate inflammaiton?

A

TNF and IL-1

70
Q

What are the systemic effects of IL-1 and TNF?

A

Fever, decrease appetite (which is why you arent hungry when sick), increase sleep,increases acute phase proteins.

71
Q

What does IL1 and TNF do to the vascular endothelium?

A

Stimulates exprression of adhesion molecules for neutrophils, also acts as a procoagulant

72
Q

What do IL1 and TNF do to neutrophils?

A

Activate them

73
Q

What do TNF and IL1 do to fibroblasts?

A

Activate them –> proliferation –> increase collagen synthesis –> tissue repair

74
Q

Which chemokine causes activation and chemotaxis of neutrophils, with limited activity on monocytes and eosinophils?

A

C-X-C chemokines (alpha)

75
Q

Which chemokine generally attracts monocytes, eosinophils, basophils, and lymphocytes but not neutrophils?

A

C-C chemokines (beta)

76
Q

Which chemokine is a specific lymphotactin?

A

C chemokine (gamma)

77
Q

Which chemokine has a soluble and surface bound protein form, and is also known as Fractalkine?

A

CX3C chemokine

78
Q

C5a activates which prostaglandin enzymes? (COX or Lipoxygenase)

A

Lipoxygenase

79
Q

Which complement factor is an opsonin?

A

C3b

80
Q

Which complement product lyses cells?

A

the MAC

81
Q

Where are kinins derived from?

A

Plasma proteins (kininogens)

82
Q

Which factor converts prekallikrein to kallikrein?

A

XIIa

83
Q

Activated kallikrein (a protease) converts HMWK to which important molecule?

A

Bradykinin

84
Q

What are the actions of bradykinin?

A

Increases vascular permeability
Causes contraction of smooth muscle
Dilation of blood vessels
Pain when injected into the skin

85
Q

Kallikrein (in addition to cleaving HMWK) cleaves palsminogen into what factor?

A

Plasmin

86
Q

What are the 2 main actions of plasmin?

A

Converts C3 –> C3a and cleaves fibrin clots.

87
Q

Which enzyme from the neutrophil can not only degrade extracellular components but can activate the complement?

A

Proteases

88
Q

Which neuropeptide from nerves can transmit pain signals, regulate blood pressure, stimulate secretion from endocrine cells, and increase vascular permeability?

A

Substance P

89
Q

What type of outcome results when inflammation is short lived and injury is limited?

A

Complete resolution

90
Q

When do scars form?

A

after substantial tissue destruction when the tissues are incapable of regeneration

91
Q

What will happen if the acute inflammatory response cannot be resolved?

A

Chronic inflammation

92
Q

An ulcer is a defect where there is shedding of what type of cell damage?

A

Necrosis

93
Q

Which cells are the dominant player in chronic inflammation?

A

Macrophages

94
Q

Granulomatous inflammation, a type of chronic inflammation, occurs because of what problem?

A

When the body can’t kill an organism,like in TB, it will wall it off and quarantine the pathogen and form a granuloma.

95
Q

Why do foreign body granulomas occur?

A

incited by inert foreign bodies that are too big to be engulfed by phagocytosis

96
Q

What is special about foreign body granulomas?

A

They do not illicit an inflammatory immune response

97
Q

What happens in defective inflammation?

A

results in increased susceptibility to infections, but also delayed wound healing because inflammation is essential for clearing damaged tissues and debris, and starting the repair process

98
Q

What are some examples of excessive inflammation?

A

allergies and possibly atherosclerosis, ischemic heart disease and some neurodegenerative diseases like Alzheimers

99
Q

Peter and the Giant Chicken get into multiple fights stemming from what initial problem?

A

An expired coupon

Pathology (4 decks)

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