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Block 4 week 2 Dani > Hunter: inflammation > Flashcards

Hunter: inflammation Flashcards

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1
Q

(blank) is a component of the innate immune response to pathogenic microorganisms, tissue injury, physical and chemical insults.

A

Inflammation

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2
Q

What would happen if you didnt have inflammation?

A

pathogenic microbes would overwhelm us and injured tissue would never heal

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3
Q

Why is it important to understand inflammation?

A

because it sometimes is inappropriately triggered or poorly controlled and is thus the cause of tissue injury in many disorders

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4
Q

what are the five cardinal signals of inflammation?

A

redness, swelling, heat, pain, loss of function.

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5
Q

Is inflammation a disease?

A

no, it is a nonspecific response that can be both protective and harmful to the host

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6
Q

Do leukocytes crawl out of arteries or veins?

A

VEINS!

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7
Q

(blank) creates almost all cell types that are involved in the immune system.

A

bone marrow

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8
Q

The bone marrow gives rise to 2 lineages, what are they?

A

the myeloid and lymphoid line

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9
Q

the myeloid cells leave the bone marrow to become (blank)

A

granulocytes

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10
Q

What are the 2 most important granulocytes?

A

neutrophils and monocytes

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11
Q

Where do macrophages come from?

A

monocytes :)

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12
Q

What lineage do these cells come from:

neutrophils, eosinophils, basophils, monocytes, mast cell precursors, macrophages, mast cells, dendritic cells

A

myeloid lineage

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13
Q

What lineage do these cells come from:

B cells, T cells, NK cells, plasma cells

A

lymphoid lineage

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14
Q

What is Dr. Hunters favorite cell?

A

macrophage

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15
Q

Where are mast cells found?

A

everywhere (blood and tissues)

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16
Q

What 2 cells can recognize cell and tissue injury and can directly recognize microbes because they have fancy receptors?

A

mast cells and macrophages

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17
Q

What does this:
elimination of microbes, dead tissue
source of mediators (cytokines, others)
role in immune response

A

macrophages

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18
Q

What do polymorphonuclear leukocytes (neutrophils) do?

A

eliminate microbes and dead tissue

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19
Q

What are these:
complement; mediators of inflammation, elimination of microbes
clotting factors and kininogens; mediators of inflammation

A

Plasma proteins

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20
Q

What cells release NO, cytokines and other mediators?

A

endothelial cells

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21
Q

Walk me through a splinter in the hand

A

splinter goes in hand-> causes trauma and carries some microbes into the skin-> macrophages and mast cells recognize the components of tissue damage and microbes and orchestrate the process of inflammation. The macrophage is the orchestrator and releases mediators that causes all sorts of changes. The ultimate goal is to get a variety of hematopoietic cells (we primarily want neutrophils) and increased blood flow.

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22
Q

(blank) of inflammation can be exogenous signals (e.g. pathogens and toxins) or endogenous signals (e.g. ATP or urate crystals) that report on tissue stress, injury, or malfunction (“danger signals”)

A

inducers

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23
Q

(blank), such as tissue-resident macrophages and mast cells, detect inducers with specific receptors and respond by producing specific inflammatory mediatiors.

A

sensor cells

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24
Q

(blank) act on target tissues and alter their functional states, promoting elimination of the inducers, adaptation to the noxious state, and restoration of tissue homeostasis.

A

Inflammatory mediators

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25
Q

What are some mediators in the inflammatory process?

A

Cytokines, chemokines, eicosanoids, amines

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26
Q

(blank) cells play a critical role in inflammation.

A

endothelial

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27
Q

If a macrophage encounters a microbe, what is the first thing it does?

A

it communicates with the endothelial cells so that they can change the vasculature of that area (increase permeability to allow for cells and blood to enter)

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28
Q

What is Dr Hunters favorite molecule?

A

TNF alpha

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29
Q

Although (blank) are the primary effector cells of inflammation, endothelial cells also play a critical role.

A

leukocytes

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30
Q

The (blank) to an inflammatory focus is modified by various mediators like tumor necrosis factor-a (TNF-alpha) to attract leukocytes and to allow them to pass into the tissues.

A

endothelium ADJACENT

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31
Q

What are some stimuli for inflammation?

A

infections
tissue necrosis
hypersensitivity

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32
Q

(blank) is when the normally protective immune system damages cells and tissues. This is seen with autoimmune diseases and allergies

A

Hypersensitivity reactions or immunopathology

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33
Q

Explain how to activate phagocytic cells via pathogens

A

Pathogen with danger signals AKA PAMPs (pathogen associated molecular patterns) -> binds to PRR (pattern recognition receptors) on phagocytic cells-> triggers INTRAcellular signaling cascades that activate phagocytic cells and inflammatory mediators are expressed-> immune response/destruction of pathogen

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34
Q

Recognition of (blank) promotes phagocytosis of the pathogens, while simultaneously causing production of inflammatory mediators.

A

PAMPS by PRR receptors on phagocytic cells

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35
Q

What are very famous PRR receptors and are they intracellular or extracellular?

A

TLR (toll-like receptors)

both

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36
Q

What is a PRR that recognizes beta glucans which is a molecular motif that triggers immune response to fungi?

A

Dectin-1

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37
Q

Does apoptosis have inflammation?

A

no, just necrosis

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38
Q

Explain how to create inflammation via cell and tissue injury (necrosis)

A

Injured cells release or express DAMP (damage associated molecular patterns AKA alarmins)-> phagocytic cells recognize via DAMP receptors-> activation of intracellular signaling pathways-> inflammation-> tissue regeneration/repair

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39
Q

(blank) orchestrates the processes of tissue regeneration and repair

A

mediators

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40
Q

What is this:

when normal tissue gets damaged by inflammation process that destroys foreign invaders and removes necrotic tissue

A

collateral damage

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41
Q

The inflammatory response is closely aligned with the process of tissue repair (wound healing). Repair begins (blank) inflammation.

A

During (but usually reaches completion after the injurious agent has been neutralized)

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42
Q

How is injured tissue replaced?

A

regeneration of parenchymal cells
and
filling with fibrous tissue (scarring)

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43
Q

(blank) inflammation is rapid in onset (minutes), and usually short in duration (hours or a few days)
(blanK) inflammation may follow acute inflammation or be insidious in onset. It is of longer duration (days to months or longer)

A

Acute (like sun burn)
Chronic (like psoriasis)

Moral booster question lol**

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44
Q

How does inflammation get terminated?

A

offending agent is eliminated
mediators are broken down
neutrophils die (only live 1-2 days)
anti-inflammatory mediators

random note, macrophages live for a while**

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45
Q

What am I talking about:

In some cases the stimulus arises from immune responses to self tissues, and these inflammatory responses are protracted

A

(autoimmune diseases)

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46
Q

Describe how you get acute inflammation

A

rapid host reponse->deliver luekocytes and plasma proteins (complement) to site of infection/injury-> vasodilation (stasis)-> increased vascular permeability-> recruitment, adhesion, and transmigration of leukocytes across BV-> chemotaxis of leukocyte to site of infection/injury-> phagoytosis and destruction of pathogen or dead cells

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47
Q

What is stasis?

A

vasodilation resulting in increased blood flow but decreased blood velocity

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48
Q

So tell me about vasodilation

A

its often preceded by vasoconstriction
caused by mediators released from phagocytes
result of relaxation of SM via histamine or NO
arterioles, capillaries and venules do it
stasis occurs
shows vascular congestion

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49
Q

What mediators make vasodilation occur?

What vessels undergo vasodilation?

A

histamine and NO

arterioles, venules, capillaries

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50
Q

SO tell me about vascular permeability

A

contract endothelial cells (create vascular leakage-> short lived 15-30 min) Via histamine, NO, Leukotrienes

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51
Q

What can burns or some microbial toxins do?

A

increase vascular permeability by injurying endothelial cells (rapid or long lived i.e. hours to days)

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52
Q

How can you get leukocyte-mediated vascular injury that increases vascular permeability?

A

in venules or pulmonary capillaries, neutrophils adhere to endothelium during late stages of inflammation and injuries it and AMPLIFIES the inflammation…… darn it

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53
Q

A (blank) is a fluid with low protein content, with little or no cellular material. It is essentially an ultrafiltrate of blood plasma that results from osmotic or hydrostatic imbalance across the vessel wall without an increase in vascular permeability

A

transudate

54
Q

An (blank) is an extravascular fluid that has a high protein concentration, and contains cells and cellular debris. Its presence implies an increase in the normal permeability of small blood vessels in an area of injury and, therefore, an inflammatory reaction

A

exudate

55
Q

Why do you get swollen lymph nodes when you are sick?

A

microbes get into lymph and lymph nodes and cause inflamation (lymphangitis and lymphadenitis)-> hyperplasia of lymph follicles due to increased number of lymphocytes and macrophages

56
Q

What do red streaks near a skin wound tell us?

A

infection of the wound, these streaks follow the course of the lymphatic channel

57
Q

How does the body recruit leukocytes to the site of injury

A

via chemokines (produced by macrophages)

58
Q

The movement of leukocytes from the vessel lumen to the interstitial tissue is called (blank)

A

extravasion

59
Q

How do you extravate a leukocyte?

A

margination, rolling and adhesion to endothelium

60
Q

How do we get leukocytes to bind during inflammation?

A

the endothelium gets activated and binds leukocytes via adhesion molecules

61
Q

Migration of leukocytes across the endothelium and vessel wall is called (blank)

A

diapedesis

62
Q

Migration of leukocytes in the tisssues towards the inflammatory stimulus is called (blank).

A

chemotaxis

63
Q

(blank) are immune system hormones that have the ability to attract particular cell types like CXCL8 (interlukin 8 ) which calls neutrophils to a particular locus.

A

chemokines

64
Q

What do adhesion molecules do and how do they come around?

A

they bind leukocytes to endothelial. They are upregulated by cytokines (released by macrophages) when damage has ensued.

65
Q

What are the four groups of adhesion molecules?

A

selectins, vascular addressins, integrins, immunoglobulin superfamily proteins

66
Q

What adhesion molecule binds tightly to a rolling leukocyte to keep it from rolling any further?
Does this happen in veins or arteries?

A

ICAM-1 (intracellular adhesion molecule 1)

Veins!

67
Q

Leukocytes enter the extravascular tissue by secreting (blank) hat break down basesment membrane

A

collagenase

68
Q

Can endogenous or exogenous substances act as chemoattractants?

A

both :)

69
Q

(blank) chemoattractants include several chemical mediators like chemokines, components of the complement system, and leukotrienes

A

endogenous

70
Q

The most common (blank) agents are bacterial products, including peptides that possess an N-formylmethionine terminal amino acid and some lipids

A

exogenous

71
Q

What are these:

things that are released that allow the neutrophil to hunt down something

A

chemoattractant

72
Q

Once (blank) have been recruited to the site of inflammation and activated, they recognize and remove pathogen and/or necrotic tissue

A

leukocytes (typically phagocytes)

73
Q

What are the three sequential steps that take place for phagocytosis?

A

1) recognition and attachment of the particle to be ingested by leukocyte
2) engulfment of the particle with formation of phagosome
3) fusion of phagosome w/ lysosomes to form phagolysosomes.

74
Q

The (blank) is a complex of proteins that assembles at the phagolysosome membrane and generates a hostile microenvironment that leads to killing and degredation of ingested material.

A

NADPH oxidase

75
Q

What is this:

limited tissue injury and return to normal function

A

resolution

76
Q

What is this:

significnt tissue injury and loss of some function

A

healing by fibrosis

77
Q

Can you have chronic inflammation w/out having acute?

A

yes

78
Q

Acute inflammation is characterized by vascular changes, edema, and a predominantly (blank) infiltration

A

neutrophilic infiltration

79
Q

Chronic inflammation, involves a (blank) infiltration which include macrophages, lymphocyte, and plasma cells.

A

monocytic infiltration

80
Q

(blank) inflammation is characterized by CT replacement of damaged tissue, accomplished by proliferation of small blood vessels (angiogenesis) and fibrosis

A

chronic

81
Q

What are ways you can get chronic inflammation?

A

delayed type hypersensitivity
autoimmune disease
allergic diseases
prolonged exposure to toxic exogenous or endogenous agents

82
Q

blood monocytes emigrate into extravascular tissues in a manner similiar to neutrophils and when they reach the extravascular tissue, it undergoes transformation into a larger tissue (blank)

A

macrophage

83
Q

Can you get healing without macrophages?

A

no, they are essential to the repair process

84
Q

If you see multi-nucleated giant cells and epithelioid cells, then what kind of inflammation is occuring?

A

chronic

85
Q

Why are mediators considered the “checks and balances” of inlammation?

A

because they are released when damage ensues and trigger inflammation, but they only last a short while so as not to keep producing an inflammatory signal

86
Q

Some cell-derived (blank) are sequestered in intracellular granules and can be rapidly secreted by granule exocytosis (e.g., histamine in mast cell granules)
Some are synthesized de novo (e.g., prostaglandins, cytokines) and secreted in response to a stimulus

A

mediators

87
Q

What are the major cell types that produce mediators of acute inflammation?

A

platelets, neutrophils, monocytes or macrophages, and mast cells
(mesenchymal cells and epithelia can too)

88
Q

Can you derive mediators from plasma proteins?

A

yes!

89
Q

What do mast cells, basophils and platelets secrete that results in vasodilation, increased vascular permeability, and endothelial activation?

A

histamine

90
Q

What do platelets secrete that allows for increased vascular permeability and vasodilation?

A

serotonin

91
Q

What do mast cells and leukocytes secrete that results in increased vascular permeability, chemotaxis, leukocyte adhesion, and vasoconstriction?

A

prostaglandins

92
Q

What do leukocytes and mast cells secrete that results in vasodilation, increased vascular permeability, leukocyte adhesion, chemotaxis, degranulation and respiratory burst?

A

platelet-activating factor

93
Q

What does the endothelium and macrophages secrete that results in vascular smooth muscle relaxation and microbial killing?

A

NO

94
Q

What do macrophages, endotheilal cells and mast cells secrete that results in local endothelial activation (expression of adhesion molecules, fever, pain, anorexia, hypotension, and decreased vascular resistance?

A

cytokines (TNF alpha, IL-1)

95
Q

What do leukocytes and activated macrophages secrete that results in chemotaxis and leukocyte activation?

A

chemokines

96
Q

What are the three plasma protein derived mediators?

A

complement, kinins, coagulation pathway proteases

97
Q

What plasma proteins derived mediators results in leukocyte chemotaxis and activation, and vasodilation via mast cell stimulation?

A

complement

98
Q

What plasma protein derived mediator results in increased vascular permeability, smooth muscle contraction, vasodilation and pain?

A

kinins (bradykinin)

99
Q

What plasma protein derived mediator results in endothelial activation and leukocyte recruitment?

A

coagulation pathway proteases

100
Q

What happens if you activate a complement?

A

you get inflammation, phagocytosis and lysis of a microbe

101
Q

(blank) and (blank) are stored in cellular granules as preformed molecules are among the first mediators to be released during inflammation (within minutes)

A

histamine and serotonin

102
Q

(blank) is abundant in mast cells found in CT adjacent to blood vessels. Some is found in basophils and platelets.

A

histamine

103
Q

Where do you mostly find seritonin?

A

in platelets

104
Q

How do you release histamine?

A

via mast cell degranulation in response to stimuli such as physical injury, antibodies, complements, or cytokines

105
Q

How does histamine cause vasodilation of arterioles and increased permeability of venules?

A

it binds to H1 receptors on microvascular endothelial cells causing dilation of arterioles and increased permeability of venules

106
Q

What is the principal mediator of the immediate transient phase of increased vascular permeability?

A

histamine

107
Q

Which releases mediators more quickly, macrophages or mast cells?

A

mast cells!

108
Q

Mechanical, chemical, and physical stimuli or other endogenous mediators release (blank) from membrane phospholipids through the action of cellular phospholipases, mainly phospholipase A2

A

arachidonic acid (AA)

109
Q

What are arachidonic acid derived mediators? How are they synthesized?

A

eicosanoids
COX-> prostaglandins and thromboxanes
LOX-> leukotrienes and lipoxins

110
Q

(blank) bind to G protein-coupled receptors on many cell types and can mediate virtually every step of inflammation.

A

eicosanoids

111
Q

(blank) blocks leucotriene receptors.

A

monteleukast

112
Q

(blank) blocks 5LOX

A

zilutron

113
Q

(blank) inhibits phospholipases

A

steroids

114
Q

What is this:
Phospholipid-derived mediator initially shown to induce platelet aggregation, but now known to have multiple inflammatory effects
Produced by a variety of cells including platelets themselves, basophils, mast cells, neutrophils, macrophages, and endothelial cells
Induces vasodilation and increased vascular permeability at extremely low concentrations with a potency 100 to 10,000 times greater than that of histamine

A

platelet activating factor (PAF)

115
Q

What does this:
increases leukocyte adhesion to endothelium, chemotaxis, degranulation, and the oxidative burst, and boosts the synthesis of other mediators, particularly eicosanoids

A

PAF (platelet activating factor)

116
Q

What does lots of stuff and is super potent?

A

PAF

117
Q

Where do we get superoxide anions (O2-) hydrogen peroxide (H2O2), and hydroxyl radical (OH-) ?
Why?
Whats a problem with this?

A

from leukocytes and NADPH oxidase activation
to destroy microbes
can hurt the host

118
Q

What is a soluble as produced by endothelial cells, macrophages and some neurons in the brain. It only lasts a few seconds so it can only act on nearby cells?

A

Nitric Oxide (NO)

119
Q

NO and its derivatives (peroxynitrite) are (blank) and thus NO is a mediator of host defense against infection/

A

microbicdal

120
Q

(blank) is produced when macrophages and other cells are activated by cytokines (TNF alpha) or microbial products.

A

inducible nitric oxide (iNOS)

121
Q

What are NO’s functions in inflammation?

A

promots vasodilation
reduced platelet aggregation and adhesion
inhibits mast cell-induced inflammation
inhibits leukocyte recruitment

122
Q

Because of the inhibitor actions, production of NO is thought to be a (blank) mechanism for controlling inflammatory responses

A

endogenous

123
Q

What is this:
Produced by many cell types (principally activated lymphocytes and macrophages, but also endothelial, epithelial, and connective tissue cells); modulate the functions of other cell types

A

proinflammatory cytokines

124
Q

(blank X 3), three of the major cytokines that mediate inflammation, are produced mainly by activated macrophages.
How can you get secretion of these?

A

TNF-a, interleukin 1 (IL-1), and IL-6

by micrbial products, immune complexes, physical injury and inflammatory stimuli

125
Q

What do cytokines affect the most locally?

What do they trigger here?

A

endothelium, leukocytes, fibroblasts

acute-phase reactions

126
Q

What mediates endothelial activation; including increased adhesion molecules, increased chemical mediators, increased enzymes ass. w/ matrix remodeling, increased surface thrombogenicity of the endothelium?

A

proinflammatory cytokines

127
Q

Problem with some of these mediators-> when you have a systemic bacterial infection, your mediators can release too much stuff and you will go into (blank) .

A

sepsis

128
Q

Do cytokines cause coagulation or anticoagulation?

A

coagulation

129
Q

Do cytokines repair or destroy?

A

repair

130
Q

WHen you see the word TB what should immediately come to mind?

A

caseous necrosis

Block 4 week 2 Dani (8 decks)

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