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Pathology > Chapter 3: Acute inflammation > Flashcards

Chapter 3: Acute inflammation Flashcards

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1
Q

The typical inflammatory reaction develops through a
series of sequential steps. Describe in five simple steps what happens to an offending agent when it arrives at a certain tissue.

A
  • The offending agent is recognized by host cells and molecules.
  • Leukocytes and plasma proteins are recruited from the blood circulation to the site of infection.
  • Leukocytes and proteins are activated and work together to destroy and eliminate the offending agent.
  • This reaction is eventually terminated.
  • The damages tissue is repaired.
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2
Q

What are characteristics of acute inflammation?

A
  • It’s of short duration (few hours-few days)
  • Exudation of fluid and plasma proteins.
  • Emigration of leukocytes (neutrophils).
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3
Q

What happens when the reaction of acute inflammation progresses?

A

It becomes a chronic inflammation.

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4
Q

What are five clinical manifestations of an inflammation?

A

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

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5
Q

What sort of inflammation can cause a disease/illness?

A

Excessive inflammation and defective inflammation.

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6
Q

Wat are the differences between acute and chronic inflammation (name difference in onset, cellular infiltrates, how bad tissue injury)?

A

Onset: acute inflammation is fast (minutes-hours), chronic inflammation is slow (days).
Cellular infiltrate: in acute inflammation mainly neutrophils, in chronic infl. monocytes/macrophages and lymphocytes.

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7
Q

Arrange the following diseases in either acute or chronic inflammation:
arthritis, pulmonary fibrosis, glomerulonephritis, septic shock, asthma, acute respiratory distress syndrome, atherosclerosis.

A

Acute inflammation: acute respiratory distress syndrome, asthma, glomerulonephritis, septic shock.
Chronic inflammation: arthritis, asthma, atherosclerosis and pulmonary fibrosis.

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8
Q

Why is inflammation terminated when the offending agent is eliminated?

A

When the offending agent is eliminated, cells are no longer stimulated to produce mediators like cytokines and so can no longer activate and stimulate other cells like leukocytes. The cells that still surround the injured tissue will be broken down and cells like leukocytes die because of their short lifespan. Also, there are anti-inflammatory mechanisms that are activated when the offending agent is eliminated.

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9
Q

Why are anti-inflammatory mechanisms important?

A

Because they control the respons and prevent it from causing excessive damage to the host.

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10
Q

What happens when the tissue is being repaired?

A

Here injured tissue is replaced through regeneration of surviving cells and where there are no more effective cells it’s replaced with connective tissue (scarring).

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11
Q

Name four causes of inflammation.

A

Infections (bacterial, viral, fungal, parasitic), tissue necrosis, foreign bodies, immune reactions.

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12
Q

Is there always inflammation during tissue necrosis? Or does it depend on the cause of cell death?

A

No it doesn’t depend on the cause of cell death. Regardless of this, it always elicits inflammation.

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13
Q

Where are Toll-like receptors located in cells and what do they recognize/bind?

A

The ones located on the plasma membranes recognize bacterial product (e.g. LPS). The ones located in endosomes recognize viral and bacterial DNA/RNA.

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14
Q

What happens when a Toll-like receptor is activated through binding of a pathogen?

A

It activates transcription factors for stimulation and expression of membrane proteins. These proteins are mediators of inflammation, (anti-viral) cytokines and proteins that promote lymphocyte activation.

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15
Q

Where are NOD-like receptors located and what do they recognize?

A

They’re located in the cytosol. They recognize products of necrotic cells (uric acid and ATP), ion disturbances (loss of K+) and some microbial products.

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16
Q

What is the inflammasome?

A

A protein complex that is activated through a NOD-like receptor, which in turn activates caspase-1.

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17
Q

What happens when a NOD-like receptor is activated?

A

It activates the inflammasome, which in turn activates caspase-1. Caspase-1 activates IL-1.

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18
Q

What does IL-1 do?

A

It’s a mediator of inlammation, recruits leukocytes and induces fever.

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19
Q

In which type of inflammation does the inflammasome play a role in?

A

In chronic disorders with chronic inflammation.

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20
Q

Where are C-type lectin receptors located, what do they recognize and what do they do upon recognition?

A

They’re located on the plasma membranes of macrophages and dendritic cells. They recognize fungal glycans and create an inflammatory respons against it.

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21
Q

What are the two cytosolic receptors called, what do they recognize and what do they do upon recognition?

A

RIG-I and cytosolic DNA sensor. They recognize nucleic acids of virusses (respectively RNA and DNA) and stimulate the prodction of anti-viral cytokines.

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22
Q

Where are G protein-coupled receptors located, what do they recognize and what do they do upon recognition?

A

They’re located on leukocytes like neutrophils and macrophages and recognize bacterial peptides (N-formylmethionyl residuen). They stimulate a chemotactic respons.

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23
Q

What do mannose receptors recognize and what do they do upon recognition?

A

They recognize microbial sugars (mannose and fucose) and induce phagocytosis

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24
Q

What is exudation and what is typical for an exudate?

A

Fluid, proteins and blood cells leave the bloodvessel into interstitial tissues. An exudate has a high concentration proteins and cell debris.

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25
What clue gives the presence of an exudate us?
The blood vessels' permeability has increased.
26
What is a transudate and how does it arise?
Fluid with a low concentration of proteins or cell debris. It arises due to an osmotic or hydrostatic imbalans.
27
Did the permeability of the blood vessel change if there's a transudate present?
No.
28
Is edema transudate of exudate?
It can be either exudate or transudate.
29
What is the definition of pus?
It's an inflammatory exudate with a high concentration leukocytes and cell- and microbe debris.
30
What are the first few steps during the start of inflammation?
Due to the inflammation different mediators are produced which cause vasodilation of vascular smooth muscle -> increased bloodflow -> increased permeability -> fluid from blood vessel goes into extravascular tissue (forms an exudate) -> combination of vasodilation and loss of fluid causes a decrease in bloodflow and an increased viscosity -> stasis bloodflow and congestion of red blood cells -> accumulation of neutrophils and production of mediators -> leukocytes will bind to the endothelium and leaves the blood vessel
31
What are factors that are responsible for an increase in permeability during inflammation?
Retraction of endothelium, endothelial injury and transcytosis.
32
Does retraction of endothelium happen in every vein/artery?
No, it occurs mostly in post-capillary venules.
33
Name examples of mediators that stimulate endothelial retraction.
Histamin, NO, bradykinin, leukotrienes
34
What is meant by endothelial injury?
This is necrosis and detachment of endothelial cells.
35
What is meant by transcytosis?
Increased transport of fluids and proteins. It's probably caused by factors like VEGF, channels are formed that stimulate vascular leakage.
36
What is the function of lymphatic vessels and nodes during an inflammation?
They drain accumulated oedema.
37
Why can inflammation result in lymphangitis or lymphadenitis?
Like blood vessels, lymphatic vessels proliferate to keep up with the increased workload. This can result in inflammation of the lymphatic vessels or nodes.
38
Which blood cells move in the center of a blood vessel and which blood cells move more outwards during circulation? Why?
Red blood cells are light-weighted and smaller and so tend to move faster than the larger white cells. Therefore red cells are confined to the central axial column and white cells are pushed out toward the wall of the vessel.
39
Why can't white blood cells bind to the endothelium when they're so close to it?
The fast bloodflow prevents them from binding.
40
What is the definition of margination?
Redistribution of leukocytes to a more peripheral position.
41
What makes margination possible?
During inflammation bloodflow decreases (stasis) and hemodynamic conditions change (wall shear stress decreases).
42
E-selectin/CD62E P-selectin/CD62P L-selectin/CD62L Where are these selectins located?
E-selectin is located on endothelial cells P-selectin is located on platelets and endothelial cells. L-selectin is located on leukocytes.
43
Why are the selectins on endothelial cells only expressed at low levels or not at all (only upon stimulation)?
So that binding of leukocytes is restricted to the endothelium at sites of infection or tissue injury.
44
Why do the leukocytes have low-affinity L-selectin on their membranes?
Because the bloodflow constantly interrupts binding, thus the leukocyte rolls over the endothelium.
45
P-selectin is located in Weibel-Palade bodies. What mediators stimulate the redistribution of P-selectin to the surface?
Histamine and thrombin.
46
Transmembrane glycoproteins that help adhere leukocytes to the endothelium so that they can leave the blood vessel. Are these selectins or integrins?
Integrins
47
Leukocytes express integrins with a low affinity towards endothelial cells. What induces a higher affinity towards endothelial cells?
When leukocytes are activated by chemokines.
48
Which chemokines stimulate the expression of which intregin ligands?
Chemokines TNF and IL-10 stimulate endothelial cells to express ICAM-1, Mac-1 and VCAM-1.
49
What is it called when leukocytes leave the blood vessel through intracellular junctions and enter the infected tissue?
Transmigration or diapedesis.
50
What are the ligands of these integrins? Integrins: ICAM-1, Mac-1, VCAM-1, Ligands: VLA-4, LFA-1,
LFA-1 binds to ICAM-1 | VLA-4 binds to Mac-1 and VCAM-1.
51
What does the adhesion molecule PECAM-1/CD31 do during transmigration?
It resides on endothelial cells and leukocytes and it helps leukocytes moving through the blood vessel wall.
52
Why does transmigration occur mostly in post-capillary venules?
Because they contain the least amount of endothelial cells.
53
How does a leukocyte move towards its destination?
A chemotaxic gradient pulls the leukocyte toward its destination.
54
Which chemoattractants are responsible for a chemotaxic gradient?
Bacterial products, cytokines (IL-8), complement-factor 5a (C5a) and leukotriene B4.
55
What happens when chemoattractants are produced? To what cells do they bind and what happens then?
They bind to G protein-coupled receptor on leukocytes, this causes a growth of actin- and myosin filaments on the leukocytes so that they can move towards the infection.
56
Why do neutrophils dominate in the first 6-24 hours of infection? And why don't they after 24-48 hours?
There are far more circulating neutrophils than there are leukocytes, they react faster to chemokines than leukocytes and bind more strongly to adhesion molecules on endothelial cells. After 24-48 hours neutrophils undergo apoptosis, after this leukocytes dominate the infection.
57
What are exceptions of the fact that in the first 6-24 hours neutrophils dominate the infection?
Pseudomonas bacteria (neutrophils dominate), viral infections (lymphocytes arrive first), hypersensitivity (lymphocytes, macrophages and plasma cells dominate), allergie (eosinophils dominate).
58
What are phagocytic receptors?
Mannose and Scavenger receptors
59
What do Scavenger receptors recognize?
LDL-particles and some microbes.
60
What are opsonins (name examples as well)?
Phagocytosis is optimized when proteins named opsonins cover the pathogen. Phagocytes have higher affinity towards opsonins. Examples are IgG, C3b and some lectines.
61
What happens after binding of the pathogen to its receptor? What can happen during this process?
It's engulfed into the phagocyt. The phagosome fuses with lysosomes and forms a phagolysosome. During this process the phagocyte also may release some granule contents into the extracellular space, thereby damaging innocent bystander normal cells.
62
Why is it important that a pathogen is fused into a phago(lyso)some?
So that the pathogen is seperated from the cytoplasm en nucleus.
63
How is the killing of microbes accomplished?
Through production of ROS, reactive nitrogen species and lysosomal enzymes.
64
What is needed to form reactive oxygen?
NADPH needs to be converted into NADP+. For this reaction NADPH oxidase is needed, the subunits of this enzyme are scattered around the cytosol. Activating stimuli cause translocation and arrangement of these subunits. When NADPH is converted into NADP+, reactive oxygen is formed.
65
What happens to the reactive oxygen after it is produced?
It is converted into H2O2.
66
H2O2 can't do much on its own and needs to be converted into hypochlorite before being able to do damage. How is this accomplished?
Certain neutrophils contain azurophilic granules, these granules contain the enzyme MPO which can convert H2O2 into hypochlorite in the presence of a halide (CI-).
67
Through which processes can hypochlorite help with phagocytosis?
Through halogenation (the halide binds to microbe residues) or oxidation of proteins and lipids.
68
In what molecule can H2O2 be converted besides hypochlorite? And what's the function of this molecule?
Hydroxy (OH-) radical, they bind en modify lipids, proteins, nucleic acids.
69
Serum, tissue fluid and host cells possess anti-oxidant mechanisms that protect against these potentially harmful oxygen-derived radicals. What are the names of these enzymes?
Superoxide dismutase (present in a lot of cells) and glutathion peroxidase and catalase (both detoxify H2O2).
70
How is NO formed?
It is formed from arginine with the help of the enzyme NOS.
71
There are three types of NOS: endothelial (e)NOS, neuronal (n)NOS and inducable (i)NOS. Which NOS is used for what?
eNOS and nNOS are always present in low concentrations and are important for vascularisation and neurotransmission. iNOS is used for killing microbes and is only present when induced by cytokines like IFN-y or microbial products.
72
Neutrophils contain smaller/secondary granules and bigger/azurophilic/primary granules. Down here some enzymes are named that are located in one of these granules. Order them by granule: non-specific collagenase, hydrolase, type IV collagenase, phospholipase A2, myeloperoxidase, lactoferrin, MPO, lysozyme, alkaline phosphatase, acid hydrolase, leukocyte adhesion molecules.
Smaller/secondary granules: lactoferrin, lysozyme, alkaline phosphatase , type IV collagenase, leukocyte adhesion molecules, phospholipase A2. Azurophilic granules: MPO, myeloperoxidase, lysozyme, acid hydrolase, elastase, non-specific collagenase, phospholipase A2.
73
What do acid proteases do?
They digest bacteria and cell debris in phagolysosomes.
74
What do neutral proteases do?
They digest extracellular parts (collagen, basement membrane, fibrin, elastin and cartilage) which results in the typical tissue destruction during inflammation.
75
More tissue damage can be caused when the initial leukocytic infiltration goes unchecked. How is this process controlled (so that this doesn't happen)?
This process is controlled by a system of anti-proteases in serum and tissue fluids. An important anti-protease is a1-anti-trypsin (elastase inhibitor).
76
What is a1-anti-trypsin?
An elastase inhibitor
77
What are Neutrophil Extracellular Traps?
NETs are extracellular fibrillar networks that concentrate anti-microbial substances at sites of infection and prevent the spread of the microbes by trapping them in the fibrils.
78
When and how are Neutrophil Extracellular Traps produced?
NETs are producerd when a pathogen or inflammatory mediator is present. The neutrophil stretches out its nuclear chromatin as a trap and binds granule proteins (e.g. anti-microbial peptides and enzymes), while doing this the nuclei of the neutrophils are lost. This leads to death of the cells.
79
What is NETosis?
Cell death affecting neutrophils as a consequence of losing their nuclei.
80
The nuclear chromatin in the NETs, which includes histones and associated DNA, may be a source of nuclear antigens in systemic autoimmune diseases. Which disease in particular?
Lupus
81
NETs are formed when pathogens are present near the neutrophil. Which pathogens in particular?
Bacteria or fungi
82
What is meant by frustrated phagocytosis?
This happens when a phagocyte encounter a material that cannot be digested easily. The phagocyte becomes 'frustrated' which triggers a strong activation. Granules are then released extracellularly, which can be harmful to the surrounding tissue.
83
What is another important function of leukocytes except phagocytosis?
They produce cytokines and growthfactors and so play an important role over the course of chronic inflammation and tissue repair.
84
What other cells play an important role during (acute) inflammation? What do they produce (among others)?
T-lymphocytes, they produce cytokines like IL-17. Production of cytokines induces the secretion of chemokines that recruit other leukocytes.
85
What happens if you miss the IL-17 respons?
You are then more susceptible to fungal and bacterial infections. When infected -> cold abcesses develop, lacking the classic features of acute inflammation, such as warmth and redness.
86
What else happens when a pathogen is destroyed and most immune cells have died?
A variety of stop signals are triggered that actively terminate the reaction.
87
What are these kinds of stop signals that terminate inflammation reactions?
A switch in the type of arachidonic acid metabolite produced, from proinflammatory leukotrienes to anti-inflammatory lipoxins and the liberation of anti-inflammatory cytokines (TGF-B and IL-10).
88
What are characteristics of a serous inflammation?
It is marked by the exudation of fluid with no/few cells, proteins or debris into body cavities. Typically, the fluid is not infected by destructive organisms and exudation can be caused by e.g. burn blisters.
89
What is the definition of effusion?
Accumulation of fluid in body cavities.
90
What are characteristics of a fibrinous inflammation?
It is marked by the exudation of fluid with cells, proteins or debris into body cavities. Vascular leaks are large and therefore higher-molecular-weight proteins such as fibrinogen pass out of the blood. Fibrin is formed and extracellularly deposited.
91
What happens if the fibrin is not dissolved by fibrinolysis and cleared by macrophages during a fibrinous inflammation?
It then stimulates the ingrowth of fibroblasts and blood vessels which leads to scarring (organization).
92
What are characteristics of a purulent inflammation?
It is marked by the exudation of fluid with a high concentration of immune cells (like neutrophils), the liquefied debris of necrotic cells and edema fluid.
93
In what sort of infection does purulent inflammation occur the most?
In infections with bacteria that cause liquefactive tissue necrosis.
94
What is meant by a pyogenic bacteria?
A pus-producing bacteria (that induces purulent inflammation).
95
How can abcesses be described and identified?
Abcesses are localized collections of pus. They are produced by seeding of pyogenic bacteria into a tissue. Abcesses have a central region that appears as a mass of necrotic leukocytes and tissue cells, this region may be surrounded by preserved neutrophils. In time abcesses may become walled off and replaced by connective tissue.
96
What is the definition of an ulcer?
An ulcer is a local defect/cavity (excavation) on the surface of an organ or tissue. It results from the shedding of inflamed necrotic tissue.
97
Can ulceration occur everywhere? If no, where can it occur?
Ulceration can occur only when tissue necrosis and resultant | inflammation exist on or near a surface.
98
What are the three possible outcomes of acute inflammation?
Complete resolution (complete healing of the inflammation), healing by connective tissue replacement (scarring/fibrosis) or chronic inflammation.
99
When is complete resolution possible? What is needed to restore everything?
When the injury is limited or short-lived or when there has been little tissue destruction and the damaged parenchymal cells can regenerate. It involves removal of cellular debris and microbes by macrophages and resorption of edema fluid by lymphatics.
100
When does healing by connective tissue replacement occur?
. This occurs after substantial tissue destruction, when the inflammatory injury involves tissues that are incapable of regeneration, or when there is abundant fibrin exudation in tissue or in serous cavities (pleura, peritoneum) that cannot be adequately cleared.
101
When progresses acute inflammation into chronic inflammation?
When acute inflammation cannot be resolved as a result of either the persistence of the injurious agent or some interference with the normal process of healing

Pathology (28 decks)

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