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Inflammation 1 Flashcards

1
Q

Inflammation is a response of _________ to ______ and ______ tissues that bring cells and molecules of _______ from the _______ to the sites where they are needed, in order to eliminate the offending agents.

A

vascularized tissues

infections

damaged

host defense

Circulation

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2
Q

The process of inflammation delivers __________ and proteins (_______ and ______) 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.

A

phagocytic leukocytes

antibodies and complement proteins

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3
Q

Without inflammation, infections would go _______, wounds would ______, and injured tissues might remain __________

A

unchecked

never heal

permanent festering sores.

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4
Q

The components of innate immunity which include ______ cells, _____ cells, and _______ cells, as well as (soluble or insoluble?) factors such as the proteins of the complement system provide first response to infection apart from leukocytes.

A

natural killer

dendritic

epithelial

Insoluble

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5
Q

The typical inflammatory reaction develops through a series of sequential steps:

• The offending agent, which is located in (intra or extra?) vascular tissues, is ________
•________ and ____ are recruited from the circulation to the site where the offending agent is located.

• The _______ are ______; together they destroy and eliminate the offending substance.

The damaged tissue is _____.

A

Extra; recognized by host cells and molecules.

Leukocytes and plasma proteins

leukocytes and proteins ; activated

repaired

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6
Q

Inflammation reaction is controlled and terminated at a point

T/F

A

T

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7
Q

Mention the cells and molecule involved in the injury

Acute respiratory distress syndrome

A

Neutrophils

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8
Q

Mention the cells and molecule involved in the injury

Acute asthma

A

Eosinophils

Ig E antibodies

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9
Q

Mention the cells and molecule involved in the injury

Glomerulonephritis

A

Antibodies
Complement proteins
Neutrophils
Monocytes

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10
Q

Mention the cells and molecule involved in the injury

Septic shock

A

Cytokines

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11
Q

Mention the cells and molecule involved in the injury

Chronic arthritis

A

Lymphocytes
Macrophages
Antibodies

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12
Q

Mention the cells and molecule involved in the injury

Chronic asthma

A

Eosinophils
Ig E antibodies

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13
Q

Mention the cells and molecule involved in the injury

Atherosclerosis

A

Macrophages
Lymphocytes

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14
Q

Mention the cells and molecule involved in the injury

Pulmonary fibrosis

A

Macrophages
Fibroblasts

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15
Q

Acute inflammation.
• The initial, (slow or rapid?) response to infections and tissue damage.
• It typically develops within ______ or _____ and is of (short or long?) duration, lasting for ________ or _______;

A

Rapid

minutes or hours; short; several hours or a few days

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16
Q

Acute inflammation

Its main characteristics are the ________ and ______ and the emigration of ______, predominantly _______

A

exudation of fluid and plasma proteins (edema)

leukocytes

neutrophils

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17
Q

neutrophils also called ______ leukocytes

A

polymorphonuclear

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18
Q

Chronic inflammation.
• It is of (shorter or longer?) duration, (slow or rapid ?) in onset

A

Longer; slow

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19
Q

Chronic inflammation.

It is associated with –
• more _______
• the presence of ___________
• proliferation of _______, and the deposition of _________

A

tissue destruction

lymphocytes and macrophages

blood vessels; connective tissue

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20
Q

Cardinal signs of inflammation
•______ (______),
• ______ (_____),
• _____ (_____),
• _____ (_____).
• _____(_________)

A

rubor; redness
Tumor; swelling
Calor; heat
Dolor; pain
Function laesa; loss of function

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21
Q

Causes of Inflammation:
• ______

• Tissue ________

• _______

• Deposition of ______- substances

•———- reactions (also called _______)

A

Infections

necrosis - ischemia

Foreign bodies

endogenous

Immune; hypersensitivity

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22
Q

Causes of Inflammation:

• Deposition of endogenous substances – harmful when (small or large?) amounts are deposited in tissues; such substances include _____ (in the disease gout), _______ (in atherosclerosis), and _____ (in obesity-associated metabolic syndrome).

A

Large

urate crystals; cholesterol crystals; lipids

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23
Q

Causes of Inflammation:

• Immune reactions - The injurious immune responses may be directed against ________, causing _______, or may be inappropriate reactions against environmental substances, as in _______, or against microbes.

A

self antigens ; autoimmune diseases

allergies

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24
Q

ACUTE INFLAMMATION
Acute inflammation has three major components:

_________ leading to __________

increased ______of the microvasculature enabling _____ and ________ to leave the circulation, and

___________ from the microcirculation, their accumulation in the focus of injury, and their activation to eliminate the offending agent

A

dilation of small vessels; an increase in blood flow

permeability ; plasma proteins and leukocytes

emigration of the leukocytes

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25
Q

Reactions of Blood Vessels in Acute Inflammation
The vascular reactions of acute inflammation consist of

-changes in the _______ and
-the _______ of vessels,

both of the above is designed to maximize the movement of _____ and ______ out of the circulation and into the site of infection or injury.

A

flow of blood

permeability

plasma proteins and leukocytes

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26
Q

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

A

exudation

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27
Q

An exudate is an _____vascular fluid that has a high _____ concentration and contains _______

A

extra

protein

cellular debris.

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28
Q

a transudate is a fluid with (high or low?) protein content (most of which is _______), ______ cellular material, and ( low or high?) specific gravity.

A

Low

albumin

little or no

Low

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29
Q

Transudate is essentially an ultrafiltrate of blood plasma that is produced as a result of _____ or _____ imbalance across the vessel wall without ______

A

osmotic or hydrostatic

an increase in vascular permeability.

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30
Q

Edema is exudate

T/F

A

F

it can be either an exudate or a transudate.

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31
Q

Pus, a purulent (exudate or transudate?) , is an inflammatory _____, rich in ______ (mostly _____), the debris of dead cells and, in many cases, microbes

A

exudate; exudate

leukocytes; neutrophils

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32
Q

• Changes in vascular flow and caliber begin early after injury
• It consist of the following:
I. Vaso______ induced by the action of several mediators, notably ______, on vascular smooth muscle.

• It first involves the _____ and then leads to _________ in the area.
• The result is _______, which is the cause of ______ and _____ at the site of inflammation.

A

dilation; histamine

arterioles; opening of new capillary beds

increased blood flow

heat and redness

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33
Q

one of the earliest manifestations of acute inflammation is ???

A

Vasodilation

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34
Q

Changes in vascular flow and caliber begin early after injury
• It consist of the following:

II. Vasodilation is quickly followed by _________ of the microvasculature
• There is outpouring of ____-rich fluid into the _____vascular tissues.

A

increased permeability

protein

Extra

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35
Q

In acute inflammation, The loss of fluid and increased vessel diameter lead to _____ blood flow, concentration of red cells in small vessels, and increased ______ of the blood.
• These changes result in engorgement of small vessels with _____ moving red cells, a condition termed ______, which is seen as ________ and localized _____ of the involved tissue.

A

slower

viscosity; slowly; stasis

vascular congestion ; redness

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36
Q

• As stasis develops, blood _____, principally _____, accumulate along the vascular endothelium.
• Also endothelial cells are activated by mediators produced at _________
• The endothelial cells express increased levels of ________
• ______ then adhere to the endothelium, and soon afterward they migrate through the _______ into the interstitial tissue.

A

leukocytes; neutrophils

sites of infection and tissue damage

adhesion molecules.

Leukocytes; vascular wall

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37
Q

Increased Vascular Permeability (Vascular Leakage)
• Several mechanisms are responsible for the increased permeability of postcapillary venules, a hallmark of _____ inflammation

A

acute

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38
Q

Increased Vascular Permeability (Vascular Leakage)

a. (Contraction or dilatation?) of endothelial cells resulting in increased __________ is the most common mechanism of vascular leakage.
• It is elicited by _____,______,_______, and other chemical mediators.
• It is called the ______ response because it occurs (slowly or rapidly?) after exposure to the mediator and is usually (short or long?)- lived (______).

A

Contraction

inter- endothelial spaces

histamine, bradykinin, leukotrienes

immediate transient

Rapidly; short; 15-30 minutes

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39
Q

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 ____________ and lasts for _______

A

2 to 12 hours

several hours or even days;

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40
Q

This delayed and prolonged vascular leakage may be caused by ____________ or ___________
___________ is a good example of this type of leakage.

A

contraction of endothelial cells or mild endothelial damage.

Late-appearing sunburns

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41
Q

Several mechanisms are responsible for the increased permeability of postcapillary venules

_________, resulting in _________ and detachment

•____ 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.
• _____ that adhere to the endothelium during inflammation may also injure the endothelial cells and thus amplify the reaction.
• In most instances leakage starts ____ after injury and is sustained for _______ until the damaged vessels are thrombosed or repaired.

A

Endothelial injury

endothelial cell necrosis; Direct

Neutrophils

immediately; several hoursm

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42
Q

Neutrophils that adhere to the endothelium during inflammation may also injure the endothelial cells

T/F

A

T

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43
Q

Several mechanisms are responsible for the increased permeability of postcapillary venules

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

•This process may involve intracellular channels that may be stimulated by certain factors, such as _________

A

transcytosis

vascular endothelial growth factor (VEGF).

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44
Q

Responses of Lymphatic Vessels and Lymph Nodes

• Lymph flow is ___eased and helps drain _____
• Also ______ and ______ , as well as _____, may find their way into lymph.
• Lymphatic vessels, like blood vessels, _______ during inflammatory reactions to __________

A

Incr; edema fluid

leukocytes and cell debris; microbes

proliferate; handle the increased load.

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45
Q

Responses of Lymphatic Vessels and Lymph Nodes

• The lymphatics may become secondarily inflamed (_______), as may the draining lymph nodes ( _______ ).
• Inflamed lymph nodes are often ____- due to ______ of the lymphoid follicles.
• This constellation of pathologic changes is termed —, or inflammatory lymphadenitis

A

lymphangitis: lymphadenitis

Enlarged; hyperplasia

reactive

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46
Q

Leukocyte Recruitment to Sites of Inflammation

• The changes in _____ and ______ are quickly followed by an influx of leukocytes into the tissue.
• These leukocytes perform the key function of ___________
• The most important leukocytes are the ones capable of ————-, namely _______ and ______
• These leukocytes _____ and destroy bacteria and other microbes, as well as necrotic tissue and foreign substances.
• Leukocytes also produce _____ that aid in repair.

A

blood flow and vascular permeability

eliminating the offending agents.

phagocytosis; neutrophils and macrophages.

ingest

growth factors; repair

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47
Q

The journey of leukocytes from the vessel lumen to the tissue is a multistep process

It is mediated and controlled by _______ molecules and ______ called _______.

• This process can be divided into sequential phases:
I. In the lumen: _____,_____, and ____ to endothelium.

II. Migration ___________

III. Migration in the _____ toward a ______

A

adhesion; cytokines; chemokines

margination, rolling, and adhesion

across the endothelium and vessel wall

tissues; chemotactic stimulus

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48
Q

The journey of leukocytes from the vessel lumen to the tissue is a multistep process

• This process can be divided into sequential phases:
I. In the lumen: margination, rolling, and adhesion to endothelium.

Vascular endothelium normally does not __________ or _______

In inflammation, the endothelium is ________ and can bind leukocytes as a prelude to their exit from the blood vessels.

A

bind circulating cells or impede their passage.

activated

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49
Q

Leukocyte Adhesion to Endothelium
• In normally flowing blood in venules, red cells are confined to a __________, displacing the leukocytes toward the ____ of the vessel.
• Due to slow blood flow (_____) and hemodynamic conditions change (wall _____ ____eases), more white cells assume a peripheral position along the endothelial surface.
• This process of leukocyte redistribution is called ______.
• Subsequently, leukocytes adhere ______ to the endothelium,____ and ______ again, thus ______ on the vessel wall.
• The cells finally come to rest where they adhere (weakly or firmly?) (resembling pebbles over which a stream runs without disturbing them).
• The attachment of leukocytes to endothelial cells is mediated by _________ molecules on the two cell types whose expression is enhanced by cytokines.

A

central axial column; wall

stasis; shear stress decr

margination; transiently ; detach and bind

rolling; firmly

complementary adhesion

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50
Q

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

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

A

sentinel; leukocytes

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51
Q

The two major families of molecules involved in leukocyte adhesion and migration are the ______ and ____, and their ligands.

They are expressed on ______ and _______ cells.

A

selectins and integrins

leukocytes and endothelial

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52
Q

Leukocytes adhesion to endothelia cells

The initial rolling interactions are mediated by a family of proteins called
_______.

A

selectins

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53
Q

There are three types of selectins:

•__-selectin – expressed on ______,
• __-selectin – expressed on ______
• __-selectin - expressed on _____________

A

L; leukocytes
E; endothelium
P; platelets and on endothelium

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54
Q

The ligands for selectins are __________ bound to _____- like ______ backbones.

A

sialylated oligosaccharides

mucin; glycoprotein

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55
Q

The expression of selectins and their ligands is regulated by _______ produced in response to infection and injury.

A

cytokines

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56
Q

Tissue macrophages, mast cells, and endothelial cells that encounter microbes and dead tissues respond by secreting several _____, including ________,____ and ______

A

cytokines

tumor necrosis factor (TNF)

IL-1, chemokines (chemoattractant cytokines).

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57
Q

TNF and IL-1 act on the _____ cells of postcapillary venules adjacent to the infection and induce the _______ of numerous adhesion molecules.
• Within _______ hours the endothelial cells begin to expres ___-selectin and the ____ for __-selectin.
• Other mediators such as ____ and ______, stimulate the redistribution of __-selectin from its normal ___cellular stores in _____ cell granules to the cell surface.

A

endothelial; coordinate expression

1 to 2 ; E; ligands; L

histamine and thrombin

P; intra; endothelial

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58
Q

P-selectin intracellular stores is called _______ bodies

A

Weibel-Palade

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59
Q

Leukocytes express ___-selectin at the ___ of their _____ and also express _____ for _______-selectins, all of which bind to the complementary molecules on the endothelial cells.

A

L; tips; micovilli

ligands; E- and P

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60
Q

Selectins are (low or high?) -affinity interactions with a (slow or fast?) off rate.

A

Low

Fast

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61
Q

These weak rolling interactions ____ the leukocytes.

A

slow down

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62
Q

Firm adhesion is mediated by a family of __________ leukocyte surface proteins called _______.

A

heterodimeric

integrins

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63
Q

___________ induce endothelial expression of ligands for integrins, mainly (______, the ligand for the β1 integrin VLA-4) and _____, the ligand for the β2 integrins LFA-1 and Mac-1).

A

TNF and IL-1

VCAM-1

ICAM-1

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64
Q

Full meaning of VCAM

Full meaning of ICAM

A

vascular cell adhesion molecule

intercellular adhesion molecule

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65
Q

Leukocytes normally express integrins in a (low or high?) affinity state.

A

Low

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66
Q

Chemokines that were produced at the site of injury bind to endothelial cell _____, and are displayed at (low or high?) concentrations on the endothelial surface.

A

proteoglycans; high

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67
Q

chemokines bound on the endothelial wall bind to and activate the rolling leukocytes.

T/F

A

T

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68
Q

One of the consequences of activation of leukocytes is the conversion of _____ and _______ on the leukocytes to a (low or high?) -affinity state.

A

VLA-4 and LFA-1 integrins

High

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69
Q

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

A

endothelium

leukocytes

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70
Q

After firm adhesion by integrins, The leukocytes stop rolling, their ______ is reorganized, and they spread out on the ______

A

cytoskeleton

endothelial surface.

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71
Q

Leukocyte migration through endothelium
• The migration of the leukocytes through the endothelium is called _______ or ______

A

transmigration or diapedesis.

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72
Q

Transmigration of leukocytes occurs mainly in ________

A

postcapillary venules.

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73
Q

• Chemokines act on the ____ leukocytes and stimulate the cells to migrate through inter endothelial spaces toward the chemical concentration gradient.
• Several _________ present in the intercellular junctions between endothelial cells are involved in the migration of leukocytes.
• These molecules include a member of the _________ called __________________

A

adherent

adhesion molecules

immunoglobulin superfamily

CD31 or PECAM-1

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74
Q

Full meaning of PECAM

A

platelet endothelial cell adhesion molecule

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75
Q

After traversing the endothelium, leukocytes pierce the _______, probably by secreting ______, and enter the _______ tissue.

The cells then migrate toward the ______ created by ______ and other _____ and accumulate in the extravascular site.

A

basement membrane

collagenases; extravascular

chemotactic gradient; chemokines; chemoattractants

76
Q

The most telling proof of the importance of leukocyte adhesion molecules is the existence of ________ in these molecules that result in recurrent bacterial infections

A

genetic deficiencies

77
Q

Chemotaxis of Leukocytes

• Chemotaxis is defined as ______ of ________ along a _______ towards the site of injury.

A

locomotion of leukocytes

chemical gradient

78
Q

Only endogenous substances can act as chemoattractants.

T/F

A

F

Both exogenous and endogenous substances can act as chemoattractants.

79
Q

The most common exogenous agents are _____ products and some ____.

A

bacterial
Lipids

80
Q

Endogenous chemoattractants include several chemical mediators:

 ______, particularly those of the ____ family (e.g., IL-8);
 components of the ______, particularly ___; and
_________ metabolites, mainly ________

A

cytokines; chemokine

complement system; C5a

arachidonic acid (AA); leukotriene B4 (LTB4).

81
Q

these chemotactic agents bind to specific _______ receptors on the surface of leukocytes.

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

A

seven transmembrane G protein-coupled

Rac/Rho/cdc42

82
Q

The leukocyte moves by extending _____ that pull the (front or back?) of the cell in the direction of _____.

• The net result is that leukocytes migrate toward the ______ in the direction of the ___________

A

filopodia

Back

Extension

inflammatory stimulus

locally produced chemoattractants.

83
Q

• The nature of the leukocyte infiltrate varies with the ____________ and ______

A

age of the inflammatory response and the type of stimulus.

84
Q

In most forms of acute inflammation ____ predominate in inflammatory infiltrate during the first 6 to 24 hours and are replaced by _____ in 24 to 48 hours

A

neutrophils

monocytes

85
Q

After entering tissues, neutrophils are (short or long?) -lived; they undergo ______ and disappear within __________

A

Short ; apoptosis

24 to 48 hours.

86
Q

Monocytes survive (shorter or longer?) than neutrophils and also proliferate in the tissues, and thus they become the dominant population in prolonged inflammatory reactions.

A

Longer

87
Q

There are, however, exceptions to this stereotypic pattern of cellular infiltration.
• ________ bacteria - the cellular infiltrate is dominated by continuously recruited neutrophils for several days;
• viral infections -______ may be the first cells to arrive;
• some hypersensitivity reactions are dominated by activated ______,_______, and _________ (reflecting the immune response);
• Allergic reactions - ________ may be the main cell type.

A

Pseudomonas

lymphocytes

lymphocytes, macrophages, and plasma cells

eosinophils

88
Q

• Agents that block ___, one of the major cytokines in leukocyte recruitment, are among the most successful therapeutics ever developed for chronic inflammatory diseases

A

TNF

89
Q

Phagocytosis and clearance of the offending agent

• Recognition of microbes or dead cells induces several responses in leukocytes that are collectively called _______
• Activation results from signaling pathways that are triggered in leukocytes, resulting in increases in cytosolic ___ and activation of enzymes such as ____________ and ________

A

leukocyte activation.

Ca2+

protein kinase C and phospholipase A2.

90
Q

The functional responses that are most important for destruction of microbes and other offenders are ________ and ______

A

phagocytosis and intracellular killing.

91
Q

Phagocytosis
• Phagocytosis involves three sequential steps:

•________ and _____ of the particle to be ingested by the leukocyte;
• _______, with subsequent formation of a ___________; and
• ________ or _________ of the ingested material.

A

recognition and attachment

engulfment; phagocytic vacuole

killing or degradation

92
Q

Phagocytic Receptors
•______ receptors, ______ receptors, and receptors for various ______ bind and ingest microbes.

A

Mannose; scavenger; opsonins

93
Q

The macrophage mannose receptor is a _____ that binds terminal ______ and ——— residues of glycoproteins and glycolipids.

• The mannose receptor recognizes ______ and not ____ cells.

A

lectin

mannose and fucose

microbes; host cells

94
Q

mannose receptor recognizes host cells

T/F

A

F

95
Q

Macrophage integrins notably Mac-1 (CD11b/CD18), can not bind
microbes for phagocytosis.

T/F

A

F

It can

96
Q

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

A

opsonized

High

97
Q

The major opsonins are:
•__________,
• the ______________ of complement, and
• Certain ________, notably ______

A

IgG antibodies

C3b breakdown product

plasma lectins

mannose-binding lectin.

98
Q

Engulfment
• After a particle is bound to phagocyte receptors, extensions of the cytoplasm (______) flow around it, and the plasma membrane pinches off to form a vesicle (_____) that encloses the particle which then fuses with a ______, resulting in _______

A

pseudopods

phagosome

lysosomal granule; phagolysosome

99
Q

Phagocytosis is independent of polymerization of actin filaments

T/F

A

F

It’s dependent on

100
Q

Intracellular destruction of microbes and debris

• Killing of microbes is accomplished by
 _______________
 ___________, mainly derived from ______,
_______ enzymes that destroy phagocytosed debris.
• This is the final step in the elimination of infectious agents and necrotic cells.
• The killing and degradation of microbes and dead cell debris within neutrophils and macrophages occur most efficiently after activation of the phagocytes.
• All these killing mechanisms are normally sequestered in ____, to which phagocytosed materials are brought.

A

reactive oxygen species (ROS)

reactive nitrogen species,

nitric oxide((NO)

lysosomal; lysosomes

101
Q

Reactive Oxygen Species.
• ROS are produced by the rapid assembly and activation of a multicomponent oxidase, _______ (also called _______), which (oxidizes or reduces)_______ and, in the process, reduces oxygen to superoxide anion.
• In neutrophils, this oxidative reaction is triggered by activating signals and accompanies phagocytosis, and is called the _______

A

NADPH oxidase; phagocyte oxidase

NADPH

respiratory burst.

102
Q

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

A

lysosome and phagolysosome

103
Q

Enzyme ________ in the presence of a _____ such as Cl−, converts H2O2 to hypochlorite (OCl2)

A

myeloperoxidase (MPO)

Halide

104
Q

The ___-___-____ system is the most efficient bactericidal system of neutrophils.

A

H2O2-MPO-halide

105
Q

Nitric Oxide.
• NO, a (soluble or insoluble ?) gas produced from _____ by the action of _____________, also participates in microbial killing.

A

Soluble ; arginine

nitric oxide synthase (NOS)

106
Q

• There are three different types of NOS:
 ______ (_NOS),
 _______(_NOS), and
 _________(_NOS).

A

endothelial (e
neuronal (n
Inducible (i

107
Q

• eNOS and nNOS are constitutively expressed at (low or high?) levels and the NO they generate functions to ______ and as a ________, respectively.

A

Low

maintain vascular tone

neurotransmitter

108
Q

__NOS, 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.

A

i

109
Q

In macrophages, NO reacts with _________ to generate the highly reactive free radical _________

A

superoxide (O2 • )

peroxynitrite (ONOO−).

110
Q

Lysosomal Enzymes and Other Lysosomal Proteins.

• Neutrophils have two main types of granules.
• The ———(___) granules contain lysozyme, collagenase, gelatinase, lactoferrin, plasminogen activator, histaminase, and alkaline phosphatase.

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

A

smaller (or secondary)

larger azurophil (or primary)

111
Q

The 2 types of granules In neutrophils can __________________, or the ___________

A

fuse with phagocytic vacuoles containing engulfed material

granule contents can be released into the extracellular space.

112
Q

Acid proteases degrade ___ and _____ within the phagolysosomes,

A

bacteria and debris

113
Q

Neutral proteases are capable of degrading various ___cellular components, such as ____,______, fibrin, elastin, and cartilage, resulting in the __________ that accompanies inflammatory processes.

A

Extra

collagen, basement membrane

tissue destruction

114
Q

Neutral proteases can also cleave ____ and ___

A

C3 and C5

115
Q

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

A

antiproteases

116
Q

Foremost among these is ______, 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

A

α1-antitrypsin

117
Q

•________ is another (besides α1-antitrypsin ) antiprotease found in serum and various secretions.

A

α2-Macroglobulin

118
Q

Neutrophil Extracellular Traps
• Neutrophil extracellular traps (NETs) are extracellular ____ networks that provide a high concentration of ______ substances at sites of infection and prevent the spread of the microbes by _____________.
• They are produced by neutrophils in response to infectious pathogens (mainly _____ and _____) and inflammatory mediators (e.g., ____,___ [mainly _____], _____,_____).

A

fibrillar; antimicrobial

trapping them in the fibrils

bacteria and fungi

chemokines, cytokines; interferons

complement proteins, and ROS

119
Q

The extracellular traps consist of a _______ of _______ that binds and concentrates granule proteins such as ________ and ______.

A

viscous meshwork

nuclear chromatin

antimicrobial peptides and enzymes

120
Q

Leukocyte-Mediated Tissue Injury
• Leukocytes are important causes of injury to normal cells and tissues under several circumstances:
• In some infections that are _______, such as _______ and certain _____ diseases, the prolonged host response contributes more to the pathology than does the microbe itself.
• The inflammatory response is inappropriately directed against __ tissues, as in certain _____ diseases.
• The host reacts excessively against usually _____ environmental substances, as in _____ diseases, including _____.

A

Difficult to eradicate

tuberculosis

viral

host; autoimmune
Harmless; allergic; asthma

121
Q

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 ______ are secreted by leukocytes into the _______ by several mechanisms.

A

lysosomal granules

extracellular milieu

122
Q

Termination of inflammation
• 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.
• These active termination mechanisms include
• a switch in the type of ____________ produced, from ___________ to _________
• liberation of _____________, including ____________ factor-β (TGF-β) and _____

A

arachidonic acid metabolite

proinflammatory leukotrienes to antiinflammatory lipoxins

anti-inflammatory cytokines

transforming growth

IL-10.

123
Q

Acute inflammation has limited specificity

T/F

A

T

124
Q

Innate immunity includes

______ cells
______ secreted by cells
_______ systems
Some cells like ___ cells, _____,_____

A

Epithelial

Mucus

Complement

mast, macrophages , the granulocytes

125
Q

Neutrophils is under _____ immunity

A

Innate

126
Q

Full meaning of TLRs

A

Toll -like receptors

127
Q

TLR is present on cells of _____ immune system (_____ and ____)

A

Innate

Macrophages and dendritic cells

128
Q

TLRs have the ability to recognize _____

A

PAMPs

129
Q

Full meaning of PAMPs

A

pathogen associates molecular pattern

130
Q

Examples of TLRs

A

CD14

131
Q

Example of a PAMP

A

Lps on gram negative bacteria

132
Q

TLR activation results in upregulation of ______

A

NF-kappa B

133
Q

TLR also plays a role in adaptive immunity

T/F

A

T

134
Q

TLR does not play a role in chronic inflammation

T/F

A

F

It does

135
Q

Cyclopxygenases act on arachidonic acid to produce _____ like ___,—-,___ that mediate ____

A

Prostaglandins

PGI2, PGD2, PGE2

Vasodilation and increased vascular permeability

136
Q

PG___ also mediates fever and pain

A

E2

137
Q

Acute inflammation

Vasodilation is to _____ as increased vascular permeability is to _____

A

Arterioles

Post capillary venules

138
Q

4 key mediators that actually attract and activate neutrophils?

A

LTB4
C5a
IL-8
Bacterial products

139
Q

Lipooxygenase act on arachidonic acid to form _______ like ___,___,____,____

A

Leukotrienes

LTB4, LTC4, LTD4, LTE4

140
Q

LT__ attracts and actuvates neutrophils

A

B4

141
Q

Function of LTC4, LTD4, LTE4

A

Mediate Vasoconstriction , bronchospasm and increased vascular permeability

142
Q

Mast cells are activated by :

1)_______
2)______ proteins ___ and ___
3) cross linking of cell surface __ by antigen

A

Tissue trauma

Complement ; C3a ; C5a

IgE

143
Q

Once mast cell gets activated, it undergoes an immediate response of _____ that mediate vasodilation and increased vascular permeability

The delayed response of the mast cells is the production of _______ , particularly _____

A

Dumping histamine granules

Arachidonic acid metabolites

Leukotrienes

144
Q

Complement proteins are a group of (pro or anti ?) inflammatory serum proteins that ______ inflammation and circulate as (active or inactive?) precursors

A

Pro

Complement

Inactive

145
Q

Activation of complement proteins

______
______
_______

A

Classical pathways
Alternative pathway
Mannose-binding lectin pathway

146
Q

Classical pathway of Activating complement proteins

____ binds to ___ or ___ that is bound to ____

A

C1

IgG or IgM

Antigen

147
Q

Alternative pathway of Activating complement proteins

The ______ directly activate the complement

A

Microbial products

148
Q

Mannose-binding lectin pathway pathway of Activating complement proteins

______ binds ______ on _____ and activates complement

A

MBL

Mannose

Microorganisms

149
Q

Result of pathways of activating complement system

C3 convertase converts __ to __ and ___ which helps to produce _______ that coverts ___ to _____ and ____ which complexes with __________ to produce the ______

A

C3; c3a; c3b; c5 convertase; c5a; c5b

C6-C9

Membrane attack complex

150
Q

Complement system key product functions

_____ trigger mast cell degranulation
——— is a chemotactic for neutrophils
_____ is an opsonin for phagocytosis
_____lyses microbes by creating holes in their membranes

A

C3a and C5a

C5a

C3b

MAC

151
Q

Hageman factor

-an inactive (anti or pro?) inflammatory protein produced in the ____
-activated upon exposure to ______ or _____

A

pro; liver

subendothelial or tissue collagen

152
Q

Activated Hageman factor cleaves _____ to ____ which mediates ___,____, and _____

A

High molecular weight kinninogen(HMWK)

Bradykinin

Vasodilation, increased vascular permeability, and pain

153
Q

Key mediators of redness and calor in acute inflammation??

A

Bradykinin
Prostaglandins
Histamine

154
Q

Key mediators of swelling in acute inflammation??

A

Histamine
Tissue damage

155
Q

Key mediators of pain in acute inflammation??

A

Bradykinin

PGE2

156
Q

Fever is a cardinal sign of acute inflammation

T/F

A

T

157
Q

Fever is mediated by ____ and ___ released by ____ to increase ____ activity in _____ cells of the _____ thereby increasing ____ which increases the temperature

A

IL1 and TNF
Macrophages
COX
Perivascular cells
Hypothalamus

PGE2

158
Q

P- selectin is mediated by _____
E-selectin is induced by ______

A

Histamine

IL1, TNF

159
Q

Cellular adhesion molecules are up regulated on ———- by ________

Integrins are upregulated on ______ by _______

A

Endothelium; TNF and IL1

Leukocytes; C5a and LTB4

160
Q

Leukocyte adhesion deficiency

Autosomal recessive defect of _______ subunit

A

Integrins
CD18

161
Q

Pus is basically dead ______ sitting in fluid

A

Neutrophils

162
Q

Chediak-Higashi syndrome

________ defect

Characterized by impaired ______ formation

A

Protein trafficking

Phagolysosome

163
Q

Neutrophils granules are produced by the _____

A

Golgi apparatus

164
Q

______ are the managers of the acute inflammatory process

A

Macrophages

165
Q

Excessive inflammation ( _____ )

A

sepsis

166
Q

Bradykinin is degraded by ______

A

ACE

167
Q

___ inhibitors can raise bradykinin levels

A

ACE

168
Q

Dangerous side effect of too much bradykinin is _____

A

angioedema

169
Q

Bradykinin is Also degraded by ________ (complement system) and its deficiency causes ________

A

C1 inhibitor

hereditary angioedema

170
Q

Bacterial infections:______
Viral infections: _______
fungal and parasitic infections: _________

A

neutrophils (neutrophilia)

lymphocytes (lymphocytosis)

Eosinophils

171
Q

Acute phase reactants

Are _______
Levels (rise or fall?) with inflammation (acute or chronic)
Mostly produced by ____
Synthesis increased by cytokines often ___

A

Serum proteins

Rise

liver; IL-6

172
Q

Mention 5 APRs

A

C-reactive protein
Serum amyloid A
Ferritin
Hepcidin
Fibrinogen

173
Q

C- reactive protein

Liver synthesis in response to ___(___)
Binds _____ polysaccharides
Activates ______ system

A

IL-6 (macrophages)

bacterial

complement

174
Q

There is Diagnosis of iron deficiency during infection

T/F

A

T

175
Q

Hepcidin

________ properties
Inhibits ____ transport

Contributes to _____ of chronic disease

A

Anti-bacterial

iron

anemia

176
Q

Hepcidin

Binds to ______ in enterocytes and ———to prevent iron release
Iron trapped in cells as ______

A

ferroportin; macrophages

ferritin

177
Q

ESR is decreased by APRs in inflammation

T/F

A

F

Increased

178
Q

RBC is ______tively charged

A

Negative

179
Q

ESR

Determined by balance of factors

Pro-sedimentation: ____, especially ____ (sticky)
Anti-sedimentation: ______

A

APRs

fibrinogen; negative charge of RBC

180
Q

Some APRs are inhibited by cytokines and their levels (rise or fall?) in inflammation

List them

A

Fall

Albumin
Transferrin
Transthyretin

181
Q

Neutrophils circulate for approximately _____ days then die unless activated

A

5 days

182
Q

Normally, the fluid portion of the blood is in the _______ while the cellular portion is in the ________

A

Periphery

Central

183
Q

Functions of TNF and IL-1

A

CAM expression
E selectin expression
Fever

184
Q

Chemokines include???

A

IL8
PGD2
LTB4
C5a
5-HETE

185
Q

List 2 antiproteases

A

Alpha 1- antitrypsin
AlphA2- macroglobulin

186
Q

anti-inflammatory cytokines, including

A

transforming growth factor-β (TGF-β)

IL-10.

187
Q

List 5 things from mast cells

A

Histamine
Serotonin (in rodents, not humans)
Prostaglandins
Leukotrienes
Platelet activating factor

House AMP (64 decks)

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