Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

AMP GPP > Inflammation > Flashcards

Inflammation Flashcards

1
Q

Define inflammation

A

Inflammation is a response of vascularized tissues to infections and damaged tissues that bring cells and molecules of host defense from the circulation to the sites where they are needed, in order to eliminate the offending agents.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What does the process of inflammation do to the damaged tissue

A

•The process of inflammation delivers phagocytic leukocytes and proteins (antibodies and complement proteins) to damaged or necrotic tissues and foreign invaders, such as microbes,
•Then activates recruited cells and molecules, which then function to get rid of the harmful or unwanted substances.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What happens in the absence of inflammation

A

infections would go unchecked, wounds would never heal, and injured tissues might remain permanent festering sores.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What else provides first response to infection apart from leukocytes

A

• The components of innate immunity which include natural killer cells, dendritic cells, and epithelial cells, as well as soluble factors such as the proteins of the complement system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the steps of the typical inflammatory reaction

A

• The offending agent, which is located in extravascular tissues, is recognized by host cells and molecules.
• Leukocytes and plasma proteins are recruited from the
circulation to the site where the offending agent is located.
• The leukocytes and proteins are activated; together they destroy and eliminate the offending substance.
• The reaction is controlled and terminated. • The damaged tissue is repaired.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What’s the sequence of events for inflammation of an epithelium cut buy a pin with pathogen on it

A

•Chemical signals released by the activated macrophage and mast cells at the injury site cause nearby capillaries to expand and become more permeable
•Fluid, clotting elements and anti microbial agents move from the blood to the site and clotting begins
•chemokines released by various kinds of cells attract more phagocytes from blood to injury site
•Neutrophils and macrophages phagocytose pathogens and cell debris at the site, and the tissue heals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What types of cells are most abundant in acute and chronic nflammatory site

A

Neutrophils - acute inflammation
Lymphocytes and macrophages- chronic inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What type of cell causes Acute respiratory distress syndrome -

A

Neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What Acute Diseases are Caused by Inflammatory Reactions

A

•Acute respiratory distress syndrome -
•Asthma
•Glomerulonephritis
•Septic shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What chronic Diseases are Caused by Inflammatory Reactions

A

•Arthritis
•Asthma
•Atherosclerosis
•Pulmonary fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What cell or molecule is involved in acute respiratory distress syndrome

A

Neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What kind of cell causes asthma

A

Eosinophils;
IgE antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What kind of cell causes glomerulonephritis

A

Antibodies and complement; neutrophils, monocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What kind of cells cause septic shock

A

Cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What kind of cells cause arthritis

A

Lymphocytes,
macrophages;
antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What kind of cells cause atherosclerotis

A

Macrophages;
lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What kind of cells cause pulmonary fibrosis

A

Macrophages;
fibroblasts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is acute inflammation

A

The initial, rapid response to infections and tissue damage
•develops within minutes or hours and is of short duration, lasting for several hours or a few days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What’s the main characteristic of acute inflammation

A

It’s main characteristics are the exudation of fluid and plasma proteins (edema) and the emigration of leukocytes, predominantly neutrophils (also called polymorphonuclear leukocytes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What happens if the acute inflammation fails to clear the stimulus

A

the reaction can progress to a protracted phase (chronic inflammation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is chronic inflammation

A

It is an inflammation of longer duration, slower in onset than acute inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the things associated with chronic inflammation

A

• more tissue destruction,
• the presence of lymphocytes and macrophages,
• proliferation of blood vessels, and the deposition of connective tissue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the cardinal signs of inflammation

A

• rubor (redness),
• tumor (swelling),
• calor (heat),
• dolor (pain).
• functio laesa (loss of function)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the causes of inflammation

A

• Infections - (bacterial, viral, fungal, parasitic) and microbial toxins are among the most common and medically important causes of inflammation.
• Tissue necrosis - ischemia (reduced blood flow, the cause of myocardial infarction), trauma, and physical and chemical injury (e.g., thermal injury, as in burns or frostbite; irradiation; exposure to some environmental chemicals).
• Foreign bodies - splinters, dirt, sutures.
• Deposition of endogenous substances – harmful when large amounts are deposited in tissues; such substances include urate crystals (in the disease gout), cholesterol crystals (in atherosclerosis), and lipids (in obesity-associated metabolic syndrome).
•Immune reactions (also called hypersensitivity) - The injurious immune responses may be directed against self antigens, causing autoimmune diseases, or may be inappropriate reactions against environmental substances, as in allergies, or against microbes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the 3 major components of acute inflammation

A

•dilation of small vessels leading to an increase in blood flow,
•increased permeability of the microvasculature enabling plasma proteins and leukocytes to leave the circulation, and
•emigration of the leukocytes from the microcirculation, their accumulation in the focus of injury, and their activation to eliminate the offending agent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the 2 vascular changes seen in acute inflammation

A

•changes in the flow of blood and
•the permeability of vessels,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is exudation

A

The escape of fluid, proteins, and blood cells from the vascular system into the interstitial tissue or body cavities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is an exudate

A

extravascular fluid that has a high protein concentration and contains cellular debris.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is a transudate

A

a fluid with low protein content (most of which is albumin), little or no cellular material, and low specific gravity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

When is a transudate produced

A

Transudate is essentially an ultrafiltrate of blood plasma that is produced as a result of osmotic or hydrostatic imbalance across the vessel wall without an increase in vascular permeability.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What’s the difference between an exudate and a transudate

A

Exudate occurs due to increased vessel permeability in acute inflammation while transudate occurs due to osmotic imbalance and no increased permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is edema

A

denotes an excess of fluid in the interstitial tissue or serous cavities; it can be either an exudate or a transudate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is pus

A

a purulent exudate, is an inflammatory exudate rich in leukocytes (mostly neutrophils), the debris of dead cells and, in many cases, microbes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

When does change in vascular flow and caliber occur

A

early after injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What does change in vascular flow and caliber consist of

A

I. Vasodilation induced by the action of several mediators, notably histamine, on vascular smooth muscle.

II. Vasodilation is quickly followed by increased permeability of the microvasculature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is one of the earliest manifestations of acute inflammation

A

Vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What vessels are dilated in acute inflammation

A

Vasodilation first involves the arterioles and then leads to
opening of new capillary beds in the area.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What causes heat and redness at the site of inflammation

A

increased blood flow due to vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What happens when there’s increased permeability of the micro vasculature

A

There is outpouring of protein-rich fluid into the extravascular tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What Does The loss of fluid and increased vessel diameter lead to in acute inflammation

A

slower blood flow, concentration of red cells in small vessels, and increased viscosity of the blood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is stasis

A

engorgement of small vessels with slowly moving red cells ( due to loss of protein filled fluid leaving the vessels in inflammation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

How is stasis seen

A

vascular congestion and localized redness of the involved tissue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What happens as stasis develops

A

blood leukocytes, principally neutrophils, accumulate along the vascular endothelium.

(Endothelial cells are activated)

Leukocytes then adhere to the endothelium, and soon afterward they migrate through the vascular wall into the interstitial tissue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

How are endothelial cells activated

A

• endothelial cells are activated by mediators produced at sites of infection and tissue damage
• The endothelial cells express increased levels of adhesion molecules.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What are the mechanisms responsible for the increased permeability of postcapillary venules

A

a. Contraction of endothelial cells resulting in increased inter- endothelial spaces is the most common mechanism of vascular leakage.

b..Endothelial injury, resulting in endothelial cell necrosis and detachment

c. Increased transport of fluids and proteins, called transcytosis, through the endothelial cell.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What elicits contraction of endothelial cells

A

histamine,
bradykinin,
leukotrienes, and other chemical mediators

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Why is contraction of endothelial cells called the immediate transient response

A

because it occurs rapidly after exposure to the mediator and is usually short- lived (15 to 30 minutes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is vascular leakage

A

Increased vascular permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

How does vascular leakage occur in mild injury

A

In some forms of mild injury (e.g., after burns, irradiation or ultraviolet radiation, and exposure to certain bacterial toxins), vascular leakage begins after a delay of 2 to 12 hours and lasts for several hours or even days;

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What causes delayed prolonged leakage in mild injury

A

caused by contraction of endothelial cells or mild endothelial damage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Example of delayed prolonged leakage

A

Late appearing sunburn

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What causes direct damage to the endothelium that leads to vascular leakage

A

Direct damage to the endothelium is encountered in severe injuries, for example, in burns, or is induced by the actions of microbes and microbial toxins that target endothelial cells.

Neutrophils that adhere to the endothelium during inflammation may also injure the endothelial cells and thus amplify the reaction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

When does vascular leakage occur

A

n most instances leakage starts immediately after injury and is sustained for several hours until the damaged vessels are thrombosed or repaired.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What is transcytosis

A

Increased transport of fluids and proteins, through the endothelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What does transcytosis involve

A

This process may involve intracellular channels that may be stimulated by certain factors, such as vascular endothelial growth factor (VEGF).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Im what vessel does contraction of endothelial cells cause leakage and induced by what

A

Mostly venules
Induced by histamine, NO, leukotrienes, bradykinin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

In what vessels do endothelial injury causes leakage and what causes it

A

Arterioles, capillaries, venules
Causes- burns, microbial toxins etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

In what vessels do leukocytes mediated vessel injury cause leakage and when does it occur

A

Venules, pulmonary capillaries
Late stages of inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

In what vessels does increases transcytosis occur and what induces it

A

Venules
Induces by VEGF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What’s the duration of contraction derived vascular leakage

A

Rapid and short lived (minutes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What’s the duration of endothelial damage derived vascular leakage

A

Rapid and May be long lived (hours to days)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What’s the duration of leukocyte mediated endothelial damage

A

Long lived

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What’s the response of lymphatic vessels and lymph nodes to inflammation

A

• Lymph flow is increased and helps drain edema fluid
• Also leukocytes and cell debris, as well as microbes, may find
their way into lymph.
• Lymphatic vessels, like blood vessels, proliferate during inflammatory reactions to handle the increased load.
• The lymphatics may become secondarily inflamed (lymphangitis), as may the draining lymph nodes (lymphadenitis).
• Inflamed lymph nodes are often enlarged due to hyperplasia of the lymphoid follicles.
• This constellation of pathologic changes is termed reactive, or inflammatory lymphadenitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What is the constellation of pathologic changes in lymphatic vessels and lymph nodes in response to inflammation

A

reactive, or inflammatory lymphadenitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Why do Lymphatic vessels, like blood vessels, proliferate during inflammatory reactions

A

to handle the increased load.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What is lymphangitis

A

When the lymphatics become secondarily inflamed as a result of inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What is lymphadenitis

A

When the draining lymph nodes become secondary inflamed as a result of inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

How does inflamed lymph nodes (lymphadenitis) occur

A

enlarged due to hyperplasia of the lymphoid follicles.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What leukocytes are most important for inflammation

A

Cells capable of phagocytes
Neutrophil and macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What is The changes in blood flow and vascular permeability quickly followed by

A

Influx of leukocytes into the tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What’s the function of leukocytes in inflammation

A

•perform the key function of eliminating the offending agents

• These leukocytes ingest and destroy bacteria and other microbes, as well as necrotic tissue and foreign substances.
• Leukocytes also produce growth factors that aid in repair.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What mediates and controls the journey of leukocytes from the vessel lumen to the tissue

A

It is mediated and controlled by adhesion molecules and cytokines called chemokines.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What are the three sequential phases in the journey of the leukocyte from the vessel Limen to the tissue

A

I. In the lumen: margination, rolling, and adhesion to endothelium.
II. Migration across the endothelium and vessel wall
III. Migration in the tissues toward a chemotactic stimulus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Since Vascular endothelium normally does not bind circulating cells or impede their passage, how do leukocytes adhere to the endothelium

A

In inflammation, the endothelium is activated and can bind leukocytes as a prelude to their exit from the blood vessels. (This occurs after the change in blood flow to stasis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

How do leukocytes migrate out of the vessel lumen after adhesion

A

Insert pseudopods into endothelial cell junction and squeeze through

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What’s is the process of adhesion and transmigration dependent on

A

Binding of adhesion molecules on leukocytes and endothelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

In normal flowing venule, where are the red cells and leukocytes arranged

A

In normally flowing blood in venules, red cells are confined to a central axial column, displacing the leukocytes toward the wall of the vessel.

Due to slow blood flow (stasis) and hemodynamic conditions change (wall shear stress decreases), more white cells assume a peripheral position along the endothelial surface.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What is margination

A

Due to slow blood flow (stasis) and hemodynamic conditions change (wall shear stress decreases), more white cells assume a peripheral position along the endothelial surface.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What occurs to leukocytes after margination

A

Subsequently, leukocytes adhere transiently to the endothelium,
detach and bind again, thus rolling on the vessel wall.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What do leukocytes resemble when they adhere firmly to the endothelial cells

A

resemble pebbles over which a stream runs without disturbing them

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What mediates the adherence of leukocytes on endothelium

A

The attachment of leukocytes to endothelial cells is mediated by complementary adhesion molecules (selectin and integrins) on the two cell types whose expression is enhanced by cytokines.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

How are cytokines secreted

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What are The two major families of molecules involved in leukocyte adhesion and migration and where are they expressed

A

selectins and integrins, and their ligands.

Expressed on leukocytes and endothelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What’s the function of cytokines in adhesion

A

This ensures that leukocytes are recruited to the tissues where these stimuli are present.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What mediates the leukocytes rolling interaction

A

Selectins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What are he three types of selectins

A

• L-selectin – expressed on leukocytes,
• E-selectin – expressed on endothelium, and
• P-selectin - platelets and on endothelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What are the ligands for selectins

A

sialylated oligosaccharides bound to mucin- like glycoprotein backbones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What regulates the expression of selectins and their ligands

A

Cytokins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

How do Tissue macrophages, mast cells, and endothelial cells that encounter microbes and dead tissues respond

A

respond by secreting several cytokines, including tumor necrosis factor (TNF), IL-1, and chemokines (chemoattractant cytokines).

90
Q

What does TNF and IL-1 act on

A

act on the endothelial cells of postcapillary venules adjacent to the infection and induce the coordinate expression of numerous adhesion molecules.

91
Q

How long before the endothelial cells begin to secrete E selectin

A

Within 1 to 2 hours

92
Q

What is the normal intracellular stores in endothelial cell granules for P selectin called

A

Weibel-Palade bodies)

93
Q

What stimulates redistribution of p selectin from Weibel-Palade bodies to cell surface

A

Other mediators such as histamine and thrombin, stimulate the redistribution of P-selectin from its normal intracellular stores in endothelial cell granules (called Weibel-Palade bodies) to the cell surface.

94
Q

Where do leukocytes express L selectin

A

At the tip of their microvilli

95
Q

What selectins do leukocytes contain

A

L selectin
And ligands for E and P selectins

96
Q

What kind of interaction is between the leukocytes that adheres it’s selectin to the endothelium

A

low-affinity interactions with a fast off rate

97
Q

What happens as a result of the low-affinity interactions with a fast off rate between leukocytes and endothelium

A

• As a result, the bound leukocytes bind, detach, and bind again, and thus begin to roll along the endothelial surface.

98
Q

What effect does the rolling interaction have on the leukocytes

A

Slows down the leukocytes

99
Q

What mediates firm adhesion of leukocytes to endothelium

A

mediated by a family of heterodimeric leukocyte surface proteins called integrins

100
Q

What induces endothelial expression of ligands for integrin

A

TNF and IL-1 induce endothelial expression of ligands for integrins, mainly vascular cell adhesion molecule 1 (VCAM-1, the ligand for the β1 integrin VLA-4) and intercellular adhesion molecule-1 (ICAM-1, the ligand for the β2 integrins LFA-1 and Mac-1).

101
Q

What’s the ligand for β1 integrin VLA-4

A

vascular cell adhesion molecule 1 (VCAM-1)

102
Q

What’s the ligand for β2 integrins LFA-1 and Mac-1).

A

intercellular adhesion molecule-1 (ICAM-1)

103
Q

At what state do leukocytes normally express integrins

A

In a low affinity state

104
Q

What do chemokines bind to on the endothelial cells

A

Endothelial cell proteoglycan

105
Q

What binds to and activate rolling leukocytes

A

Chemokines

106
Q

At what con are cytokines present on the endothelial surface

A

At a high concentration

107
Q

Consequences of activation of rolling leukocytes by cytokines

A

One of the consequences of activation is the conversion of VLA-4 (β1 integrin) and LFA-1 (β2 integrins) integrins on the leukocytes to a high-affinity state.

108
Q

When the cytokines activate the rolling leukocytes, it converts the integrin on the leukocytes to high affinity
What does this lead to

A

The combination of cytokine-induced expression of integrin ligands on the endothelium and increased integrin affinity on the leukocytes results in firm integrin-mediated binding of the leukocytes to the endothelium at the site of inflammation.

* The leukocytes stop rolling, their cytoskeleton is reorganized, and they spread out on the endothelial surface.*

109
Q

What does the firm integrin-mediated binding of the leukocytes to the endothelium at the site of inflammation (caused by activation of rolling leukocytes) cause

A

The leukocytes stop rolling, their cytoskeleton is reorganized, and they spread out on the endothelial surface

110
Q

What’s another name for transmigration of the leukocyte through the endothelium

A

diapedesis

111
Q

What kind of vessels does transmigration of leukocytes occur mainly

A

postcapillary venules.

112
Q

What acts on the adherent leukocytes and stimulate the cells to migrate

A

Chemokines

113
Q

Where do the leukocytes migrate through and to

A

through inter endothelial spaces toward the chemical concentration gradient.

114
Q

Other than chemokines, what’s involved in the migration of leukocytes.

A

Several adhesion molecules present in the intercellular junctions between endothelial cells

115
Q

Examples of adhesion molecules present in the intercellular junctions between endothelial cells

A

include a member of the immunoglobulin superfamily called CD31 or PECAM-1 (platelet endothelial cell adhesion molecule).

116
Q

What happens after leukocytes traverse the endothelium

A

After traversing the endothelium, leukocytes pierce the basement membrane, probably by secreting collagenases, and enter the extravascular tissue

117
Q

What creates the chemotactic gradient

A

chemokines and other chemoattractants

118
Q

What does the leukocytes do after crossing the basement membrane to the extra vascular tissue

A

The cells then migrate toward the chemotactic gradient created by chemokines and other chemoattractants and accumulate in the extravascular site

119
Q

What’s the The most telling proof of the importance of leukocyte adhesion molecules

A

is the existence of genetic deficiencies in these molecules that result in recurrent bacterial

120
Q

What does chemotoxis mean

A

Chemotaxis is defined as locomotion of leukocytes along a chemical gradient towards the site of injury.

121
Q

What kind of substances act as chemoattractants

A

Both exogenous and endogenous substances

122
Q

What are the most common exogenous agents as chemoattractants

A

bacterial products and some
lipids.

123
Q

Examples of Endogenous chemoattractants

A

include several chemical mediators:

 cytokines, particularly those of the chemokine family (e.g., IL-8);
 components of the complement system, particularly C5a; and
 arachidonic acid (AA) metabolites, mainly leukotriene B4 (LTB4).

124
Q

Where do chemotactic agents bind on the surface of the leukocyte

A

All these chemotactic agents bind to specific seven transmembrane G protein-coupled receptors on the surface of leukocytes.

125
Q

What kind of signal is elicited from the receptor chemotactic agents bind to on the leukocyte

A

Signals initiated from these receptors result in activation of second messengers that increase cytosolic calcium and activate small guanosine triphosphatases of the Rac/Rho/cdc42 family as well as numerous kinases.

This induce polymerization of actin at the leading edge of the cell and localization of myosin filaments at the back.

126
Q

What does polymerization of actin at the leading edge of the cell and localization of myosin filaments at the back. (A result of binding of chemotactic agents to GCPR receptors on leukocytes)

A

• The leukocyte moves by extending filopodia that pull the back of the cell in the direction of extension.
• The net result is that leukocytes migrate toward the inflammatory stimulus in the direction of the locally produced chemoattractants.

127
Q

What does the nature of the leukocyte infiltrate vary upon with example

A

varies with the age of the inflammatory response and the type of stimulus.

Eg In acute inflammation, neutrophils predominate in the inflammatory infiltrate during the first 6 to 24 hours and are replaced by monocytes in 24 to 48 hours.

128
Q

Why are neutrophils replaced from the inflamed tissues after 24 hours

A

After entering tissues, neutrophils are short-lived; they undergo apoptosis and disappear within 24 to 48 hours.

129
Q

What leukocytes are dominant in prolonged inflammatory reactions and why

A

• Monocytes survive longer and also proliferate in the tissues, and thus they become the dominant population in prolonged inflammatory reaction

130
Q

What are the exceptions to the normal stereotypical pattern of cellular infiltration. (Neutrophils - 6-24 hrs, monocytes - 24-48 hrs)

A

• Pseudomonas bacteria - the cellular infiltrate is dominated by continuously recruited neutrophils for several days;
• viral infections - lymphocytes may be the first cells to arrive;
• some hypersensitivity reactions are dominated by activated lymphocytes, macrophages, and plasma cells (reflecting the immune response);
• Allergic reactions - eosinophils may be the main cell type.

131
Q

One example of the most successful therapeutics ever developed for chronic inflammatory diseases

A

Agents that block TNF, one of the major cytokines in leukocyte recruitment,

132
Q

What is leukocyte activation

A

Recognition of microbes or dead cells induces several responses in leukocytes that are collectively called leukocyte activation.

133
Q

How does leukocyte’s activation come about

A

results from signaling pathways that are triggered in leukocytes, resulting in increases in cytosolic Ca2+ and activation of enzymes such as protein kinase C and phospholipase A2.

134
Q

What functional responses
are most important for destruction of microbes and other offender

A

phagocytosis and intracellular killing.

135
Q

What are the 3 sequential steps in phagocytosis

A

• recognition and attachment of the particle to be ingested by the leukocyte;
• engulfment, with subsequent formation of a phagocytic vacuole; and
• killing or degradation of the ingested material.

136
Q

Examples of phagocytic receptors

A

Mannose receptors,
scavenger receptors,
and receptors for various opsonins bind and ingest microbes.

137
Q

What is the macrophage mannose receptor

A

The macrophage mannose receptor is a lectin that binds terminal mannose and fucose residues of glycoproteins and glycolipids.

138
Q

What do the macrophage mannose receptor recognize

A

The mannose receptor recognizes microbes and not host cells

139
Q

What else can bind microbes for phagocytosis

A

Macrophage integrins notably Mac-1 (CD11b/CD18),

140
Q

What enhances the efficiency of phagocytes

A

The efficiency of phagocytosis is greatly enhanced when microbes are opsonized by specific proteins (opsonins) for which the phagocytes express high affinity receptors.

141
Q

What are the major opsonized

A

• IgG antibodies,
• the C3b breakdown product of complement, and
• Certain plasma lectins, notably mannose-binding lectin.

142
Q

What is engulfment

A

After a particle is bound to phagocyte receptors, extensions of the cytoplasm (pseudopods) flow around it, and the plasma membrane pinches off to form a vesicle (phagosome) that encloses the particle.

143
Q

What is a phagolysosome

A

• The phagosome fuses with a lysosomal granule, resulting in phagolysosome

144
Q

What kind of process is phagocytosis

A

The process of phagocytosis is complex and involves the integration of many receptor-initiated signals that lead to membrane remodeling and cytoskeletal changes.

145
Q

What is phagocytosis dependent on

A

• Phagocytosis is dependent on polymerization of actin filaments;

146
Q

The killing of microbes is accomplished by what

A

 reactive oxygen species (ROS, also called reactive oxygen
intermediates),
 reactive nitrogen species, mainly derived from nitric oxide
(NO),
 lysosomal enzymes that destroy phagocytosed debris.

147
Q

What is the final step in the elimination of infectious agents and necrotic cells.

A

Intracellular destruction of microbes and debris

148
Q

When does the killing and degradation of microbes and dead cell debris within neutrophils and macrophages occur most efficiently

A

after activation of the phagocytes.

149
Q

Where are all the killing mechanisms normally sequestered

A

• All these killing mechanisms are normally sequestered in lysosomes, to which phagocytosed materials are brought.

150
Q

How are ROS produced

A

ROS are produced by the rapid assembly and activation of a multicomponent oxidase, NADPH oxidase (also called phagocyte oxidase), which oxidizes NADPH (reduced nicotinamide-adenine dinucleotide phosphate) and, in the process, reduces oxygen to superoxide anion.

151
Q

In neutrophils, what triggers the formation of ROS

A

In neutrophils, this oxidative reaction is triggered by activating signals and accompanies phagocytosis, and is called the respiratory burst.

152
Q

What is respiratory burst

A

The formation of ROS in neutrophils during phagocytosis

153
Q

Where are ROS produced in the cell

A

ROS are produced within the lysosome and phagolysosome, where they can act on ingested particles without damaging the host cell.

154
Q

What happens after the respiratory burst (production of ROS for phagocytosis)

A

• O2 is then converted into hydrogen peroxide H2O2
• Enzyme myeloperoxidase (MPO) in the presence of a halide such as Cl−, converts H2O2 to hypochlorite (OCl2)
• The H2O2-MPO-halide system is the most efficient bactericidal system of neutrophils.

155
Q

What is the most efficient bactericidal system of neutrophils.

A

The H2O2-MPO-halide system

156
Q

What is NO

A

• NO, a soluble gas produced from arginine by the action of nitric oxide synthase (NOS), also participates in microbial killing

157
Q

What are the 3 types of Nitric Oxide Synthase

A

 endothelial (eNOS),
 neuronal (nNOS), and
 Inducible (iNOS).

158
Q

Characteristics of eNOS and nNOS

A

constitutively expressed at low levels and the NO they generate functions to maintain vascular tone and as a neurotransmitter, respectively.

159
Q

Which of the NOS produces NO used in microbial killing

A

iNOS

160
Q

Characterized of iNOS

A

the type that is involved in microbial killing, is induced when macrophages and neutrophils are activated by cytokines (e.g., IFN- γ) or microbial products.

161
Q

What does NO react with in macrophages, and to produce what

A

In macrophages, NO reacts with superoxide (O2 • ) to generate the highly reactive free radical peroxynitrite (ONOO−).

162
Q

How are Reactive Nitrogen Species produced

A

NO reacts with superoxide (O2 • ) to generate the highly reactive free radical peroxynitrite (ONOO−).

163
Q

What are the 2 main types of granules contained in the lysosome

A

• The smaller (or secondary) granules
• The larger azurophil (or primary) granules

164
Q

What enzymes are contained in the smaller (secondary) lysosome granule

A

lysozyme, collagenase, gelatinase, lactoferrin, plasminogen activator, histaminase, and alkaline phosphatase.

165
Q

What enzymes are contained in the larger azurophil (primary) lysosome granule

A

myeloperoxidase, bactericidal factors (lysozyme, defensins), acid hydrolases, and a variety of neutral proteases (elastase, cathepsin G, nonspecific collagenases, proteinase 3).

166
Q

What granule of lysosome fuses with the engulfed material

A

Both types of granules can fuse with phagocytic vacuoles containing engulfed material, or the granule contents can be released into the extracellular space.

167
Q

What’s the function of acid proteases in the granule of lysosomes

A

degrade bacteria and debris within the phagolysosomes,

168
Q

Function of neutral proteases in the larger granules of lysosome

A

capable of degrading various extracellular components, such as collagen, basement membrane, fibrin, elastin, and cartilage, resulting in the tissue destruction that accompanies inflammatory processes.

It can also cleave C3 and C5

169
Q

What controls the harmful proteases in the lysosome

A

These harmful proteases, however, are normally controlled by a system of antiproteases in the serum and tissue fluids.

170
Q

Give examples of antiproteases in the tissue and body fluid that regulates the proteases

A

• Foremost among these is α1-antitrypsin, which is the major inhibitor of neutrophil elastase. A deficiency of these inhibitors may lead to sustained action of leukocyte proteases as is the case in patients with α1-antitrypsin deficiency
• α2-Macroglobulin is another antiprotease found in serum and various secretions.

171
Q

What does α1-antitrypsin inhibit

A

major inhibitor of neutrophil elastase

172
Q

What are Neutrophil extracellular traps (NETs).

A

They are extracellular fibrillar networks that provide a high concentration of antimicrobial substances at sites of infection and prevent the spread of the microbes by trapping them in the fibrils

173
Q

When are Neutrophil Extracellular Traps produced

A

They are produced by neutrophils in response to infectious pathogens (mainly bacteria and fungi) and inflammatory mediators (e.g., chemokines, cytokines [mainly interferons], complement proteins, and ROS).

174
Q

What does the extracellular traps in NETs consist of

A

The extracellular traps consist of a viscous meshwork of nuclear chromatin that binds and concentrates granule proteins such as antimicrobial peptides and enzymes.

175
Q

When can the leukocyte cause injury to normal cell and tissue (leukocyte mediated injury)

A

• In some infections that are difficult to eradicate, such as tuberculosis and certain viral diseases, the prolonged host response contributes more to the pathology than does the microbe itself

The inflammatory response is inappropriately directed against host tissues, as in certain autoimmune diseases.

176
Q

How does the host react to environmental substances in leukocytes mediated tissue injury

A

• The host reacts excessively against usually harmless environmental substances, as in allergic diseases, including asthma.

177
Q

In leukocyte mediated tissue injury, what mechanism does the leukocyte use

A

• In all these situations, the mechanisms by which leukocytes damage normal tissues are the same as the mechanisms involved in antimicrobial defense,
• The contents of lysosomal granules are secreted by leukocytes into the extracellular milieu by several mechanisms.

178
Q

How does inflammation come to an end

A

• Neutrophils also have short half-lives in tissues and die by apoptosis within a few hours after leaving the blood.
• In addition, as inflammation develops, the process itself triggers a variety of stop signals that actively terminate the reaction.

179
Q

What are active termination mechanism that are triggered by inflammation to stop it

A

• a switch in the type of arachidonic acid metabolite produced, from proinflammatory leukotrienes to antiinflammatory lipoxins
• liberation of anti-inflammatory cytokines, including transforming growth factor-β (TGF-β) and IL-10.

180
Q

Which inflammation cardinal signs are as a result of vasodilation

A

Rubor and Calor

181
Q

Which cardinal sign is as a result of vascular permeability

A

Tumor

182
Q

Of the chemicals responsible for vasodilation, which is preformed and which is synthesized

A

Histamine is preformed
Prostaglandin E2 is synthesized

183
Q

What are prostaglandin and leukotrienes gotten from

A

Lipid in membrane—- Arachidonic acid —— Leukotrienes and Prostaglandins

184
Q

What are the types of leukotrienes

A

LTB4 LTC4 LTD4

185
Q

What are the types of prostaglandins

A

PGF2
FGF2
PGK2

186
Q

What converts lipid in membrane (in leukocytes) to arachidonic acid

A

Phospholipase A2

187
Q

What’s the function of Bradykinine

A

Vasodilation
Increases vascular permeability
Pajn

188
Q

How is Bradykinin gotten

A

Factor 12—- Prekalikreine—-Kalikreine—-Bradykinin

189
Q

How is Bradykinin degraded

A

ACE

190
Q

What’s a side effect of Bradykinin

A

Angioedema

191
Q

What vessel undergoes vascular permeability

A

Post capillary venules

192
Q

What causes endothelial contractions

A

Bradykinin, prostaglandins, Histermine

193
Q

What vessel does fluid leak from

A

Post capillary venules

194
Q

What causes transudate leak

A

Low protein and specific gravity

195
Q

What are examples of things that cause fever in inflammation

A

They are pyrogenes
LPS
IL1
TNF
Prostaglandin E2

196
Q

What are acute phase reactants

A

inflammation markers that exhibit significant changes in serum concentration during inflammation (produced in the liver)

197
Q

Examples of acute phase reactants

A

C reactive proteins
Serum amyloid A
Ferritin
Hepsidin
Fibrinogen

198
Q

Why is there increased ESR in inflammation

A

Increased acute phase reactants

199
Q

What type of inflammation in part of innate immunity

A

Acute inflammation

200
Q

What are the signaling tags on the inflammation

A

DAMPS( Damage associated molecular pattern) and PAMPS(pathogen associated molecular pattern)

201
Q

Which of the signaling tags is present in human being

A

DAMPS

202
Q

Example of PAMPS

A

LPS

203
Q

What receptors do macrophages use to bind to DAMP and PAMP

A

Toll like receptors called pattern recognition receptors (cell membrane and endosome)

204
Q

How long do neutrophils circulate for

A

5 days

205
Q

How do neutrophils exit vascular system

A

At post capillary venules

206
Q

Where are Evselectin and P selectin found

A

Endothelium

207
Q

What does E selectin bind to

A

WEAKLY binds to Sialyl Lewis x on neutrophil

208
Q

What mediates firm adhesion

A

VCAM and ICAM

209
Q

What binds to VCAM and ICAM for strong adhesion

A

Integrins

210
Q

What IL mediates integrin action

A

IL8

211
Q

What’s another name for neutrophil transmigrations

A

Diapedesis

212
Q

What mediates diapedesis

A

PECAM- CD31
(Platelets endothelial cell adhesion molecule)

213
Q

What are chemotactic factors

A

Direct neutrophils to site of damage
Eg C5A IL8 Leukotrienes

214
Q

Examples of opsonin

A

C5A
C3B
IGG

215
Q

What mediates respiratory burst

A

NADPH oxidase

216
Q

Describe the pathway that leads to bacteria killing

A

O3
|NADPH oxidase
|
O2
|superoxide dismal taste
|
H2O2
|myeloperoxidase
|
HOCl

217
Q

What causes chronic granulomatos

A

A defect in the enzymes that cause bacterial kill (superoxide dismultase, myeloperoxidase)

218
Q

What is LAD1

A

Leukocytes adhesion disorder
Problem with integrins

219
Q

LAD2

A

Problem with Sialyl Lewis x

220
Q

What’s CHEDIAK HEGASHI syndrome

A

Failure to form pahgolysosome
(Problem with mucrotubles)

AMP GPP (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions