Inflammation Flashcards

1
Q

____-____ receptors recognize microbes.
___-___ receptors can sense cell damage.

A

Toll-like
NOD-like

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2
Q

Inflammation leads to the recruitment of _____.

A

Leukocytes

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3
Q

Causes of inflammation:

A

Infection
Tissue necrosis
Foreign body
Immune reactions, such as hypersensitivity

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4
Q

Cardinal signs of inflammation:

A

Redness, warmth, swelling, pain, loss of function

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5
Q

_____ is due to leakage of the fluid from a post capillary venules into the interstitial space. key mediators are ____ which causes endothelial cell contraction, and ___ ____ resulting in endothelial cells disruption.

A

Swelling
Histamine
Tissue damage

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6
Q

____ and ____ are due to vasodilation which results in increased blood flow via relaxation of arteriolar smooth muscle. Key mediators are ___, ____, and ____.

A

Redness
Warmth
Histamine
Prostaglandins
Bradykinin

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7
Q

Loss of function is from cellular and tissue damage related to ___ ___ ___ created by lysosomal enzymes.

A

Reactive oxygen species

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8
Q

The most important mediators of acute inflammation are:

A

Vasoactive amines, arachidonic acid derivative lipid products such as prostaglandins and leukotrienes, cytokines including chemokine, and products of complement activation

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9
Q

_____ come from mast cells and leukocytes. It causes vasodilation, pain and fever.

A

Prostaglandins

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10
Q

____ is produced by mast cells, basophils and platelets. It causes vasodilation, increase vascular permeability, and endothelial activation.

A

Histamine

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11
Q

_____ is produced by mast cells and leukocytes. It increases vascular permeability, chemotaxis, and leukocyte adhesion and activation

A

Leukotrienes

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12
Q

Cytokines such as ____, ___, and ____ are produced by macrophages, endothelial cells, and mast cells. Locally, they cause endothelial activation. Systemically, they produce a fever, metabolic abnormalities, and hypotension (shock)

A

TNF, IL-1, and IL-6

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13
Q

_____ are produced by leukocytes and activated macrophages. They cause chemotaxis and leukocyte activation.

A

Chemokines

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14
Q

____ comes from Plasma and is produced in the liver. It causes leukocyte chemotaxis and activation, direct target killing, and vasodilation

A

Complement

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15
Q

Diagram of mediators of inflammation:

A
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16
Q

Principal actions of arachidonic acid metabolites in inflammation:

A
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17
Q

Prostaglandins, bradykinin, and substance P are the main mediators of ____.

A

Pain

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18
Q

Lysosomal enzymes and reactive oxygen species are the main mediators of tissue damage, and ___ ___ ___.

A

Loss of function

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19
Q

Histamines and prostaglandins are the main mediators of ___ and ___.

A

Redness
Warmth

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20
Q

Histamines, serotonin, C3a and C5a, leukotrienes C4, D4, and E4 are the main mediators of increased ____ ____.

A

Vascular permeability

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21
Q

TNF, IL-1, chemokines, C3a and C5a, leukotriene B4 are the main mediators of ____ recruitment and activation.

A

Leukocyte

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22
Q

Inflammation allows inflammatory cells such as neutrophils and macrophages, lymphocytes, etc., plasma proteins, and fluid to exit the ___ ___ and enter the ___ ___.

A

Blood vessels
Interstitial space

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23
Q

____ inflammation is fast, onset in minutes or hours. Mainly neutrophils with prominent local and systemic signs.

A

Acute

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24
Q

____ inflammation can take days. It is mainly monocytes/macrophages and lymphocytes. The tissue injury is often severe and progressive. There are less local and systemic signs.

A

Chronic

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25
Q

Acute inflammation arises in response to ____ or ___ ____. It is characterized by the presence of edema and neutrophils. It is immediate response with limited ____.

A

Infection
Tissue necrosis
Specificity

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26
Q

Three Major components of the acute inflammatory response:

A

Vascular changes
Leukocyte recruitment
Leukocyte activation

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27
Q

Acute inflammation:
____ is mediated by histamines serotonin prostaglandins, leukotrienes, and complement. It increases blood flow and produces ____ (redness).

A

Vasodilation
Erythema

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28
Q

Acute inflammation:
____ ___ ____ is mediated by histamines serotonin, and kinins. The result is gaps between endothelial cells that allows for leakage of fluid, which causes ___.

A

Increased vascular permeability
Edema

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29
Q

Vascular changes allow movement of ___ ___ and ___ ___ from vascular space to site of infection/injury.

A

Inflammatory cells
Plasma proteins

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30
Q

When there is no inflammation there is a ___ hydrostatic pressure and ___ colloid osmotic pressure.

A

Higher
Lower

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31
Q

When exudates and transudates form, hydrostatic pressure ____ and colloid osmotic pressure ____.

There is ____ interendothelial spaces allowing for fluid and protein leakage. When

A

Increases
Decreases
Increased

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32
Q

Decreased colloid osmotic pressure is caused from ____ protein synthesis (liver disease) or ____ protein loss (kidney disease).

A

Decreased
Increased

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33
Q

Increased hydrostatic pressure is caused from venous ____ obstruction (congestive heart failure).

A

Outflow

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34
Q

____ refers to when vasodilation slows blood flow and cells move to periphery of vessels

A

Margination

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35
Q

____ refers to the up regulation of selectins on endothelial cells. Leukocytes have ____ __ __ on the surface, which binds to selectins.

A

Rolling
Sialyl Lewis X

36
Q

Endothelial adhesion molecules, ____ and ___, are up regulated by TNF and IL-1. Leukocyte ____ are upregulated by C5a and LTB4 and converted to their high affinity form. ICAM and VCAM are ligands for Integrins. This process is referred to as ____, which stops the cell rolling.

A

ICAM
VCAM
Integrins
Adhesion

37
Q

Leukocyte adhesion deficiency is most commonly due to an autosomal recessive defect of ____.

A

Integrins

38
Q

Migration:
_____ is expressed on both leukocytes and endothelial cells. It facilitates transmigration. This process is driven by ____ produced at the site of injury (chemotaxis). Neutrophils are attracted by bacterial products, ___, ___, and ___.

A

PECAM-1 (CD31)
Chemokines
IL-8
C5a
LTB

39
Q

Diagram of acute inflammation- leukocyte recruitment:
Rolling, adhesion, and migration

A
40
Q

_____ is a cytokine that is produced by macrophages, mast cells, and T lymphocytes. It stimulates expression of endothelial adhesion molecules and secretion of other cytokines. It has its systemic effects.

A

TNF

41
Q

____ is a cytokine that is produced by macrophages, endothelial cells, and some epithelial cells. It is similar to TNF, but plays a greater role in fever.

A

IL-1

42
Q

____ is a cytokine produced by T lymphocytes. It recruits neutrophils and monocytes.

A

IL-17

43
Q

____ is a cytokine that is produced by macrophages and other cells. It produces systemic effects (acute phase response).

A

IL-6

44
Q

_____ are cytokines that are produced by macrophages endothelial cells, T lymphocytes, and mast cells. It recruits leukocytes to sites of inflammation and plays a role in migration of cells in normal tissues.

A

Chemokines

45
Q

There are 10 different kinds of ___-___ receptors, each for a different set of microbial molecules

A

Toll-like

46
Q

_____ receptors bind to mannose, C3b, and Fc (antibodies).

A

Phagocytic

47
Q

Picture of myocardial infarct, showing acute inflammation:

A
48
Q

Graph of acute inflammation:

A
49
Q

Removal of the offending agent:
_____ is mediated by phagocytic receptors ( ____, ___, ____ ___). It is facilitated by coating (opsonization) by the ____ IgG, C3b, and others.

A

Phagocytosis
Mannose, opsonin, scavenger receptors
Opsonins

50
Q

Destruction of phagocytosed material is performed by ___ ___ ___. ___ ___ (NADPH oxidase) produces superoxide anion. ___ ___ ___ (NOS) with superoxide produces peroxynitrite.

___ ___ (proteases) also assist with destruction, but are less effective than ROS.

A

Reactive oxygen species
Phagocyte oxidase
Nitric oxide synthetase

Granule enzymes

51
Q

Diagram of removal of offending agents:

A
52
Q

Altered phagocytosis:
_______ syndrome is a protein trafficking defect characterized by impaired phagolysosome formation. Immunodeficiency, diminished hemostasis.

A

Chediak-Higashi

53
Q

Altered phagocytosis:
____ ____ disease (CGD) is characterized by poor oxygen, dependent, killing due to NADPH oxidase defect. It is X-linked or autosomal recessive. Characterized by recurrent infections.

A

Chronic granulomatous

54
Q

Altered phagocytosis:
____ ___ results in defective hypochlorite formation. Increased risk for candida infections, however, most patients are asymptomatic

A

MPO deficiency

55
Q

During resolution of acute inflammation, neutrophils undergo ____ and disappear within 24 hours after resolution.

A

Apoptosis

56
Q

____/____ can result after acute inflammation in the healing connective tissue

A

Scarring/fibrosis

57
Q

_____ of acute and chronic inflammation results in an ____ with persistent acute inflammation and surrounding chronic inflammation.

A

Combination
Abscess

58
Q

Diagram of inflammation:

A
59
Q

If unchecked or inappropriately directed against host tissues, the ____ itself becomes the offender. This underlies, many acute and chronic human diseases. Adjacent tissues to inflammation may suffer ___ ___.

A

Leukocyte
Collateral damage

60
Q

The inflammatory response may be inappropriately directed against host tissues, causing ___ ___.

A

Autoimmune disease

61
Q

The host may react excessively against usually harmless, environmental substances, causing ___ ___ and ___.

A

Allergic reactions
Asthma

62
Q

Table of disorders caused by inappropriate immune system actions:

A
63
Q

____ inflammation is characterized by the presence of macrophages lymphocytes and plasma cells in tissue. It is a delayed response but more ____.

A

Chronic
Specific

64
Q

Persistent infections, hypersensitivity diseases, and prolonged exposure to toxic agents and foreign material can cause ___ inflammation.

A

Chronic

65
Q

The _____ is the dominant cell in most chronic inflammatory reactions. It ingests and eliminates microbes, and dead tissue. Peak activity is 2 to 3 days after inflammation begins.

A

Macrophage

66
Q

Macrophages, secrete cytokines such as ___, ___, ___, and others that initiate inflammatory reactions. Macrophages also display ____ and respond to signals from T cells.

A

TNF
IL-1
Chemokines
Antigens

67
Q

Macrophage development occurs in the bone marrow starting with a ___ stem cell. In the blood, it is a ____ which gets activated into a macrophage by inflammation.

A

Hematopoietic
Monocyte

68
Q

In the fetal liver, there is a ___ in the yolk sac which turns into a resident tissue ___.

A

Progenitor
Macrophage

69
Q

Picture of monocytes and activated macrophages:

A
70
Q

Diagram of classically activated versus alternatively activated macrophage:

A
71
Q

____ refers to classically activated macrophage and ___ refers to alternatively activated macrophage.

A

M1
M2

72
Q

Microbes and other antigens activate T & B lymphocytes. They amplify and propagate ___ ___. They generate ___ cells, allowing for persistent and severe reactions.

A

Chronic inflammation
Memory

73
Q

_____ T lymphocytes promote, and influence the nature of the inflammatory reaction.

A

CD4+

74
Q

____ cells secrete INF-gamma which activate macrophages by the classical pathway

A

Th1

75
Q

____ cells secrete IL-4, IL-5, IL-13 which recruit and activate eosinophils and are responsible for the alternative pathway of macrophage activation

A

TH2

76
Q

Diagram:

A
77
Q

____ cells produce IL-17 which induces the secretion of chemokines responsible for recruiting neutrophils and monocytes into the reaction

A

Th17

78
Q

____ is a cytokine produced by dendritic cells and macrophages. It increases production of INF-gamma

A

IL-12

79
Q

____ is a cytokine that is produced by T lymphocytes and natural killer cells. It activates macrophages.

A

INF-gamma

80
Q

Picture of plasma B cells in chronic inflammation:

A
81
Q

Granulomatous inflammation:
A pattern of chronic inflammation induced by persistent ___ ___ in some infections, immune mediated diseases, and foreign bodies

A

T-cell response

82
Q

Composition of granulomatous: Aggregates of activated ___ with abundant pink cytoplasm, peripheral lymphocytes, multinucleated giant cells (fusion of numerous ___), and sometimes central necrosis

A

Macrophages
Macrophages

83
Q

____ plays a crucial role in evolution of macrophages to epithelioid cells and giant cells. ___ ___ therapy can cause granulomatous to break down. This could make a previously contained infection such as TB disseminate

A

TNF
Anti TNF

84
Q

Picture of peripheral lymphocytes

A
85
Q

Conditions with granulomas:
TB, bartonella henselae, listeria, treponema pallidum (tertiary syphilis)
Fungal: histoplasmosis
Parasitic: schistosomiasis

A
86
Q

Conditions with granulomas non-infectious:

A

Sarcoidosis, crohn disease, primary biliary cholangitis, Churg-Strauss, giant cell arteritis, Takayasu arteritis, foreign body

87
Q

____ is used when the predominating disease state is inflammation. If inflammation is not the main disease state, do not use the term ___.

A

-itis
-itis