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Block 4; Week 2-Michelle > Inflammation-Hunter > Flashcards

Inflammation-Hunter Flashcards

1
Q

What is the purpose of inflammation?

A

it is an innate immune response to deal w/ microbes & necrosis (from any cause). Need to get rid of pathogens & need to heal.

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2
Q

T/F Inflammation can be both good & bad–>it is a double edged sword.

A

TRUE

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3
Q

What are some examples where inflammation is good & an example where inflammation is bad?

A

Good inflammation: impetigo in response to streptococcus pyogenes; function of vaccines requires inflammation w/ exposure
Bad inflammation: rheumatoid arthritis

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4
Q

What are the features of inflammation that were recognized long ago?

A 
Redness (Rubor)
Swelling (Tumor)
Heat (Calor)
Pain (Dolor)
Loss of Function (functio laesa)
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5
Q

T/F Inflammation is in itself a disease.

A

FALSE. It is a nonspecific response that can be helpful or harmful.

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6
Q

Where is the “mama” of the immune system located? How does this relate to inflammation?

A

Bone marrow: “mama” of the immune system
produces a bunch of the cells involved in inflammation
Pluripotent hematopoietic stem cells give rise to 2 lineages.
Lymphoid & Myeloid.
Myeloid is our focus. These are released into the blood.
Most important cell of this lineage: neutrophil
Other important cell: monocyte–>differentiates into macrophages!
Mast cells also found here.

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7
Q

What is another name for neutrophils?

A

polymorphonuclear leukocyte

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8
Q

Where are mast cells usu found?

A

usu found in the tissues. Often found in CT & lining blood vessels. Less often found in the blood.

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9
Q

What are the primary sensors of acute inflammation? What do these cells do?

A

mast cells & macrophages (main guy)
these cells recognize tissue damage (from a variety of causes) & can recognize specific microbes (b/c they have receptors on their surface).
They then release mediators & orchestrate the inflammation response.

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10
Q

When the mast cells & macrophages (main guy) orchestrate the acute inflammatory immune response…which players do they get in the game?

A 
hematopoietic cell types
neutrophils!
plasma proteins (complement)
endothelial cells lining blood vessels (to release stuff)
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11
Q

Describe the order of the inflammatory process in general terms.

A

Inducer damages tissue.
Sensors recognize the damage & release mediators.
Mediators go to the target tissue & eliminate inducers & try to achieve homeostasis.

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12
Q

What are inducers?

A

exogenous or endogenous signals that report tissue damage, injury, or malfunction
could be trauma, burn, pathogens, toxins, ATP, urate crystals etc.
**they start the inflammatory process b/c they cause the problem

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13
Q

What are sensors?

A

tissue resident macrophages & mast cells that detect inducers w/ their specific receptors & release mediators for the inflammatory response.

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14
Q

In addition to macrophages & mast cells, what is another sensor?

A

dendritic cell

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15
Q

What are some examples of mediators & their classes?

A

cytokines: TNF, IL-1, IL-6
chemokines: CCL2, CXCL8
Vasoactive amines: histamine, bradykinin
Eicosanoids: includes prostaglandins

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16
Q

Direct Activation of a Sensor produces? Indirect activation of a sensor produces?

A

Direct Activation: good inflammation, get rid of a pathogen

Indirect Activation: bad inflammation, collateral damage of tissue

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17
Q

So, a macrophage senses a pathogen. What does it release to communicate to the endothelial cells lining blood vessels? Why is it important to communicate to these endothelial cells?

A

Among other things, it releases TNF alpha.
TNF alpha goes to the endothelial cells & says “hey, join the inflammation team!”
Endothelium attracts leukocytes, including neutrophils, & lets them pass into injured tissue.
It also becomes permeable to plasma & lets antibodies & fluid into the damaged tissue.

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18
Q

We have said that the main causes of inflammation (as sensed by macrophages & mast cells) are pathogens & tissue necrosis. What are some specific infections that can prompt inflammation?

A 
bacterial infection
viral infection
fungal infection
parasitic attack
microbial toxins
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19
Q

We have said that the main causes of inflammation (as sensed by macrophages & mast cells) are pathogens & tissue necrosis. What are some specific causes of tissue necrosis that can cause inflammation?

A

Ischemia (MI)
Physical or Chemical Trauma (thermal injury, irradiation, environment chemicals, foreign bodies)
Hypoxia

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20
Q

An MI produces coagulative ischemic necrosis. What type of inflammation does it produce?

A

sterile inflammation

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21
Q

What are hypersensitivity reactions? What are they also called? What are some examples?

A

Also called immunopathology
normally protective immune system inflammation rxn damages cells & tissues
Ex: autoimmune diseases & allergies

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22
Q

When inducers are pathogenic microorganisms…what signal do they have & how is they recognized such that they trigger inflammation?

A

Inducer: pathogen–>has danger signal/PAMP
Sensors/Phagocytic Cells (macrophages): have PRR that bind PAMP.
Intracellular signaling pathway & activation of macrophages.
They release mediators for inflammation & get goin’ on their phagocytosis.
Then you get rid of the pathogen & you get tissue regeneration & repair.

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23
Q

What does PAMP stand for?

What does PRR stand for?

A

PAMP: pathogen-associated molecular patterns
PRR: pattern recognition receptors

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24
Q

What are some specific examples of PRRs found on sensor cell surfaces?

A 
TLR: toll like receptors
*found on plasma membrane & intracellularly
Ex: TLR-5--sees flagellum. 
Other: 
Dectin-1: recognizes beta glucans. Fights fungi. 
CRD/mannose receptor
Complement Receptor
Scavenger Receptors: SR-A, MARCO
Lipid Receptor: CD36
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25
Q

Describe how inflammation is induced by tissue injury.

A

Danger signals in the form of alarmins or DAMPs come from tissue that has experienced necrosis.
Phagocytic cells have DAMP receptors.
Cells release mediators & get inflammation going
Get tissue regeneration & repair.

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26
Q

What does DAMP stand for? What are some examples of DAMPs?

A 
damage-associated molecular patterns
Ex: 
HMGB-1
S100A8/A9
ATP
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27
Q

T/F Tissue that has experienced apoptosis releases DAMPs.

A

FALSE. Only tissue that has experienced necrosis. Apoptosis does NOT prompt inflammation.

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28
Q

What is collateral damage? What are some examples of this?

A

the bad effects of inflammation
chronic diseases: rheumatoid arthritis, atherosclerosis, lung fibrosis
hypersensitivity to insect bites, drugs, toxins
**have to use anti-inflammatory drugs

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29
Q

So…it seems cyclical: tissue damage–inflammation–collateral damage–inflammation. How is this cycle stopped?

A

stopped via the body’s anti-inflammatory mechanisms
stopped when the microbe or dead tissue is removed.
**trickier w/ autoimmune diseases

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30
Q

What is the trade off of anti-inflammatory medications?

A

more susceptible to infections

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31
Q 
Describe what collateral damage might look like in the following tissues: 
Brain
Lung
Cardiovascular System
Kidney 
Liver
GI
Microcirculation
A 
Brain: confusion
Lung: respiratory distress
Cardiovascular System: shock
Kidney: oliguria, anuria
Liver: excretory failure
GI: loss of fcn, ileus
Microcirculation: capillary leak edema, DIC
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32
Q

Describe a general order to tissue repair. Note: tissue repair peaks after injurious agent has been removed.

A

Inflammation
Granulation Tissue
Wound Contraction
Collagen Accumulation Remodeling.

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33
Q

What is acute inflammation?

A

this is inflammation that has a fast onset & short duration (up to a couple of days)
ends when the offending agent is broken down
when it is over, mediators are broken down
Ex: sunburn

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34
Q

What is chronic inflammation?

A

can sometimes follow acute inflammation
longer duration (more than a few days)
sometimes occurs when the stimulus can’t be removed.
Ex: psoriasis

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35
Q

Which are more short-lived: macrophages or neutrophils?

A

neutrophils!

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36
Q

What accounts for the redness & swelling in acute inflammation?

A

Redness-hyperemia: b/c of vasodilation to arterioles, capillary bed, & venules w/ acute inflammation. More blood flows there.
Swelling-edema: b/c of increased vascular permeability @ capillaries. Fluid, leukocytes, & plasma proteins get out.

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37
Q

Once again, as a result of increased vascular permeability during times of acute inflammation…what substances get into damaged area?

A

leukocytes
plasma proteins (complement)
fluid

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38
Q

In general terms, describe the journey of the leukocyte that is a part of inflammation?

A

In the blood.
Recruited to a capillary bed.
Adheres to the endothelium of the blood vessel.
Transmigrates across the blood vessel into surrounding tissues.
Gets to damaged area via chemotaxis.
May or may not be a part of phagocytosis of bad stuff there.

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39
Q

With acute inflammation, there is vasodilation. But this is often preceded by _______. How does this happen?

A

preceded by vasoconstriction. This is neurogenic response to the acute injury.

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40
Q

How does vasodilation happen?

A

the injured tissue has some macrophages or phagocytic cells that release mediators. Histamine & NO will go to the smooth muscle of the arterioles, capillaries & venules & relax them. Then, these blood vessels will dilate.

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41
Q

What are the tradeoffs of having vasodilation & greater blood volume to an injured area?

A

stasis: the blood doesn’t move as quickly, it kind of just stays there.
Vascular congestion: you have a lot more blood in that area.

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42
Q

There are both good causes & bad causes of increased vascular permeability related to inflammation. What is the good cause?

A

Good Cause:
macrophages @ site of injury release mediators (including NO, histamine & leukotrienes). These target b.v. (esp venules) & contract endothelial cells (increasing inter endothelial spaces). These allows for more vascular leakage.

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43
Q

There are both good causes & bad causes of increased vascular permeability related to inflammation. What are the bad causes?

A

severe injuries that directly hurt the endothelium (burns, microbes)
neutrophils that adhere to the endothelium don’t know what to do & release their contents, causing more collateral damage to the endothelium.

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44
Q

What is the difference b/w transudate & exudate? They both result in edema.

A

transudate: fluid w/ low protein content, ultra filtrate of blood plasma. gets there b/c of imbalance b/w hydrostatic & osmotic pressure–not b/c of inflammation or increased vascular permeability
exudate: fluid w/ high protein conc’n & cells, gets there b/c of inflammation & increased vascular permeability.

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45
Q

What are examples of situations where you would see excess transudate?

A

Too high hydrostatic pressure b/c of congestive heart failure. Too low osmotic pressure b/c of starvation. Results in edema.

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46
Q

If you see a red streak along the site of a wound…what does it likely mean?

A

It means that there is a problem. This is an infection moving across a lymphatic channel. Microbes find their way into the lymph during inflammation.

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47
Q

What is lymphangitis? What is lymphadenitis? Why are lymph nodes enlarged in some of these cases?

A

lymphangitis: secondary inflammation of lymphatics
lymphadenitis: secondary inflammation of draining lymph nodes
* *lymph nodes enlarged b/c of hyperplasia of the lymphoid follicles & increased numbers of lymphocytes & macrophages.

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48
Q

How do macrophages recruit leukocytes to the injury site?

A

Among other things, macrophages release chemokines. This includes CXCL8: interleukin-8. This calls neutrophils.

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49
Q

What is extravasation of leukocytes & what are the sub-steps of this process?

A

extravasation: movement of leukocytes from lumen of blood vessel into interstitial tissue
* margination
* rolling
* adhesion (to endothelium via adhesion molecules)
* diapedesis (migration across vessel walls)
* chemotaxis (migration toward inflammatory stimulus of tissues).

50
Q

How do adhesion molecules get added to endothelial cells of blood vessels?

A

macrophages @ the site of injury release a variety of mediators for the inflammatory response.
One set is cytokines (TNF alpha as an example). These add adhesion molecules to endothelial cells of blood vessels.

51
Q

What are the different types of adhesion molecules & what role do they play in the recruitment of leukocytes?

A

Addressins on leukocytes bind selectins on endothelial cells. These bind w/ a low affinity & allow rolling of the leukocytes along, looking for injury site.
The immunoglobin superfamily adhesion molecules (LFA as an ex) are attached to leukocytes & bind integrins (ICAM as example) on endothelial cells tightly. This stops the leukocytes & tells them to get to that injury site!

52
Q

Once the leukocytes have been stopped in their tracks, what happens?

A

They squeeze thru the inter endothelial spaces that have been created by some of the mediators secreted by macrophages. Note: this is in venules. Called diapedesis.

53
Q

Once the inflammation is done, how do you get rid of the adhesion molecules?

A

once the blood vessels are no longer dilated, the blood flow will increase (no more stasis) & sheer force will get rid of the adhesion molecules.

54
Q

How do the leukocytes get past the basement membrane of the blood vessel?

A

they secrete collagenase: creates a little damage to the blood vessel.

55
Q

What is involved in chemotaxis?

A

leukocytes get to the site of injury by following chemoattractants (going up the conc’n gradient of this, almost chasing a snack)

56
Q

Chemoattractants can be both endogenous & exogenous. What are examples of endogenous chemoattractants?

A

Endogenous:
chemokines (CXCL8)
complement (C5a)
leukotrienes (LTB4)

57
Q

Chemoattractants can be both endogenous & exogenous. What are examples of exogenous chemoattractants?

A

Exogenous:
bacterial products
N-formylmethionine (f-met-leu-phe)
lipids

58
Q

Explain the process of phagocytosis.

A

internalize stuff as a vacuole (called phagosome)
this fuses w/ a lysosome=phagolysosome
Bad stuff digested via NADPH oxidase (creates ROS)
Digested bad stuff is released to external environment via exocytosis.

59
Q

What is the purpose of phagocytosis?

A

to get rid of bad microorganisms & dead & dying tissue

60
Q

What are the 3 stage of histopathology of acute inflammation?

A
  1. Normal tissue
  2. vascular congestion, hyperemia, stasis w/ vasodilation.
  3. leukocytic infiltrate
61
Q

What kinds of leukocytes are mainly involved in acute inflammation?

A

neutrophils.

62
Q

What are some examples of injuries that can cause acute inflammation?

A

trauma
toxins
infarction
bacterial infections

63
Q

What are some examples of injuries that can cause chronic inflammation?

A

viral infections
chronic infections
persistent injuries
autoimmune diseases

64
Q

What are the 2 roads to chronic inflammation?

A

Road #1: acute inflammation that is prolonged

Road #2: a type of injury that immediately produces chronic inflammation

65
Q

What does acute inflammation look like? Where can it go from there?

A 
neutrophils predominant
vascular changes
limited tissue injury
**can resolve & bring tissue back to normal
**can form an abscess
66
Q

How does an abscess heal? What do it look like?

A

has pus formation

heals via fibrosis (tissue injury, collagen deposition & some loss of function)

67
Q

What are the features of chronic inflammation & how does it heal?

A 
angiogenesis
mononuclear infiltrate
fibrosis
progressive tissue injury
**heals by permanently changing the tissue, probably fibrosis
68
Q

What is found in the mononuclear infiltrate found in chronic inflammation?

A

mainly macrophages & lymphocytes, not as many neutrophils. plasma cells also present

69
Q

What is another name for neutrophils? What does this mean?

A

polymorphonuclear leukocytes
**means that their nuclei have multiple lobes.
You see a bunch of cells w/ multiple lobar nuclei that are neutrophils. You are looking @ acute inflammation.

70
Q

What are some pathogens that can lead to chronic inflammation?

A

mycobacteria (TB)

some persistent viruses, fungi, parasites

71
Q

The pathogens that cause chronic inflammation often display ______________.

A

delayed type hypersensitivity.
Ex: TB skin test, mycobacteria if present will show delayed hypersensitivity & you will see a bump on your skin w/i 72 hours.

72
Q

What are some triggers of chronic inflammation that only cause collateral damage, have no good components?

A

autoimmune diseases

allergic diseases

73
Q

Prolonged exposure to what can lead to chronic inflammation?

A

toxic exogenous agents: silica–silicosis

toxic endogenous agents: plasma lipids–atherosclerosis

74
Q

What are the macrophages in the brain called? In the liver? Where do macrophages come from?

A

Brain: microglia
Liver: Kupffer cell
*bone marrow releases monocytes into the blood.
monocytes go from the blood into the tissues where they become macrophages.

75
Q

How do macrophages get into the surrounding tissues?

A

via adhesion molecules & chemotaxis

**predominant around 2 days

76
Q

What cell type mainly secretes things to activate macrophages in tissues? What types of things activate macrophages?

A

sensitized T lymphocytes secrete things

Thing: microbial products, cytokines (IFN gamma)

77
Q

Macrophages once they are activated secrete things. What types of things & what is their effect?

A 
Tissue Injury/Inflammation when they secrete:
ROS
proteases
cytokines
coagulation factors
arachidonic acid metabolites
Tissue Repair when they secrete:
growth factors
fibrinogenic cytokines
angiogenic factors
remodelling collagenases
78
Q

If you are looking @ a slide of tuberculous granuloma…what process is at play & what do you see?

A

chronic inflammation w/ delayed type hypersensitivity
see mononuclear infiltrate: lymphocytes, macrophages
Macrophages becoming 2 things: multinucleate giant cells & epithelioid cells

79
Q

T/F The mediators of inflammation are long-lived so that you assure the pathogen has been removed.

A

FALSE. the mediators are short-lived & potent.

80
Q

What are the 2 ways that cells produce/release mediators?

A
  1. some mediators are already made & sequestered in granules in the cell ready for exocytosis
    Ex: histamine in mast cell granules.
  2. some mediators are synthesized from nothing when they are needed & secreted in response to a stimulus
    Ex: prostaglandins, cytokines
81
Q

T/F Some mediators are derived from plasma proteins.

A

True.

82
Q

What are cells that can release mediators?

A 
platelets
neutrophils
monocytes/macrophages
mast cells
mesenchymal cells (smooth muscle cells, endothelial cells, fibroblasts)
83
Q

Histamine comes from what cell type?

A

mast cells
basophils
platelets

84
Q

What is the action of histamine?

A

vasodilation
increased vascular permeability
endothelial activation

85
Q

Serotonin comes from what cell type?

A

platelets

86
Q

What is the action of serotonin?

A

vasodilation

increased vascular permeability

87
Q

Leukotrienes & prostaglandins are both:

A

eicosanoids

88
Q

Leukotrienes come from what cell type?

A

mast cells

leukocytes

89
Q

What are the actions of leukotrienes?

A

increased vascular permeability
chemotaxis
leukocyte adhesion
vasoconstriction

90
Q

Prostaglandins come from what cell type?

A

mast cells

leukocytes

91
Q

What are the actions of prostaglandins?

A

vasodilation
pain
fever

92
Q

Platelet activating factor is very potent & comes from what cell type?

A 
platelets
leukocytes
basophils
mast cells
neutrophils
macrophages
endothelial cells
93
Q

What are the actions of platelet activating factor?

A 
vasodilation
increased vascular permeability
leukocyte adhesion
chemotaxis
degranulation
oxidative burst
boost the synthesis of other mediators, esp eicosanoids
94
Q

ROS come from what cell type?

A

leukocytes

95
Q

What are the actions of ROS?

A

killing microbes

tissue damage

96
Q

NO comes from what cell type?

A

endothelium

macrophages

97
Q

What is the action of NO?

A

vascular smooth muscle relaxation

microbial killing

98
Q

What are some examples of cytokines? What cell types do they come from?

A 
Ex: TNF alpha, IL-1
Come from:
macrophages
endothelial cells
mast cells
99
Q

What are the actions of cytokines?

A 
local endothelial activation (to express adhesion molecules)
fever
pain
anorexia
hypotension
decreased vascular resistance
100
Q

Chemokines come from what cell type?

A

leukocytes

activated macrophages

101
Q

What are the actions of chemokines?

A

chemotaxis

leukocyte activation

102
Q

What are the 3 categories of plasma protein-derived mediators?

A

Complement
kinins
coagulation pathway proteases

103
Q

What are some examples of cells of the complement? Where do they come from?

A

Ex: C5a, C3a, C4a
Come from:
plasma (produced in the liver)

104
Q

What are the actions of cells of the complement?

A

leukocyte chemotaxis & activation

vasodilation (thru mast cell activation)

105
Q

What are some examples of cells that are kinins? Where do they come from?

A

Ex: bradykinin

Come from: plasma (produced in the liver)

106
Q

What are the actions of the kinins?

A

increased vascular permeability
smooth muscle contraction
vasodilation
pain

107
Q

Where do coagulation pathway proteases come from?

A

plasma (produced in the liver)

108
Q

What are the actions of coagulation pathway proteases?

A

endothelial activation

leukocyte recruitment

109
Q

What are the 2 vasoactive amine mediators?

A

histamine

serotonin

110
Q

How are vasoactive amines released?

A

they are pre-produced & stored in intracellular granules. They are released via exocytosis. Histamine: mast cell degranulation. **they are the first responders b/c they are pre-produced.

111
Q

Histamine is the principle mediator of what?

A

immediate transient phase of increased vascular permeability

112
Q

Mast cell degranulation occurs, releasing histamine, in response to what stimuli?

A

Physical Injury: trauma, thermal
Allergic Rxn: antibodies bound to mast cell
Complement anaphylatoxins
Cytokines

113
Q

Endogenous mediators prompt release of arachidonic acid from _______, mainly via the enzyme: _________. This produces a class of actors called______.

A

membrane phospholipids
phospholipase A2
Eicosanoids

114
Q

Eicosanoids can be modified via 2 enzymes that produce different end substances. Describe these 2 pathways.

A 
Pathway #1: cyclooxygenase
-prostaglandins
-thromboxanes
Pathway #2: lipooxygenase
-leukotrienes
-lipoxin
115
Q

Eicosanoids can mediate almost every step of the inflammation pathway. What communication pathway do they use?

A

G protein coupled receptors on cells.

116
Q

What is platelet activating factor derived from?

A

phospholipids

117
Q

T/F Platelet activating factor is more potent than histamine.

A

TRUE! This is why it is such an important drug target. It has a huge role in inflammation.

118
Q

What produces ROS? What is their fcn? What is the downside?

A

NADPH oxidase system produces them

fcn: these radicals are toxic to microorganisms
downside: collateral damage if released into host tissue

119
Q

T/F NO has a long half life.

A

False. Super short half life. Seconds it is a gas! It works on only nearby cells.

120
Q

Describe how NO comes to be. What is its effect?

A

Cytokines go to a macrophage or something & it then produce NO via inducible nitric oxide synthase (iNOS). This then causes vasodilation & is microbicidal.

121
Q

Aside from vasodilation & its microbicidal effects, what are the counterintuitive effects of NO?

A 
anti-inflammatory effects:
reduces platelet aggregation
reduces platelet adhesion
reduces mast-cell inflammation
reduces leukocyte recruitment
122
Q

If you have too much TNFalpha what happens?

If you have too little TNFalpha what happens?

A

You die-sepsis.

Block 4; Week 2-Michelle (8 decks)

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