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0V015 Biology & Pathology > Acute Inflamation L03 > Flashcards

Acute Inflamation L03 Flashcards

1
Q

What is inflammation?

A

A response of vascularised tissue

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2
Q

What can inflammation be caused by?

A

Tissue Necrosis
Foreign Bodies
Immune reactions

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3
Q

What can tissue necrosis be caused by?

A

Chemical agents
Cold, Heat
Trauma
Ischemia

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4
Q

What is ischemia?

A

Inadequate blood supply

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5
Q

What is the purpose of inflammation?

A

It serves to destroy, dilute or wall off the infectious agent
as well as rid you of both the initial cause of injury and to clean up the area.

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6
Q

What does inflammation induce?

A

Repair ( wound healing)

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7
Q

What is chronic inflammation?

A

Chronic inflammation is where the inflammatory response is uncontrolled and thus harmful

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8
Q

What are the two types of inflammation?

A

Acute and Chronic

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9
Q

What type of inflammation occurs initially?

A

Acute inflammation

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10
Q

How do we distinguish between acute inflammation and chronic inflammation?

A

By the Duration and type of inflammatory cells

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11
Q

Is acute inflammation a long or short process?

A

Short - it can normally resolve itself in one to two days.

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12
Q

What type of cells are involved in chronic inflammation?

A

monocytes/macrophages and lymphocytes

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13
Q

What are the cardinal signs of infection?

A 
Rubor = Redness
Tumor= Swelling 
Calor= Heat 
Dolor= Pain
Functio lasea = Loss of function
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14
Q

What are some of the mediators of acute inflammation?

A

Phagocytic leukocytes i.e neutrophils and resident macrophages
Plasma proteins
Mast cells - which are sentinel cells.

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15
Q

What is the first step of acute inflammation?

A

The foreign agent must be recognised by host cells/molecules

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16
Q

What are examples of chemical signalling molecules in acute inflammation?

A

Amines & cytokines

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17
Q

What is the second step of acute inflammation? - i.e. the step after the foreign agent has been recognised.

A

The recruitment of leukocytes and plasma proteins from circulation to the site of the agent.

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18
Q

What happens in acute inflammation once leukocytes have been released into the bloodstream to the site of the foreign agent?

A

The leukocytes and proteins work in harmony to eliminate the causative agent.

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19
Q

What happens in acute inflammation once the leukocytes and proteins have worked together and successfully eliminated the causative agent?

A

The reaction is controlled and wound repair responses are stimulated.

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20
Q

How does the body recognise the offending agent?

A 
Using: 
Cellular Receptors
Sensors of cell damage 
Antibodies and complement proteins 
Circulating proteins
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21
Q

How does the body use cellular receptors to identify offending agents?

A

These will be present as integral proteins in the plasma membrane.
These can also be present as toll-like receptors.
These can be present on cells that come into contact with foreign microbes.

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22
Q

What are toll-like receptors

A

These are membrane-spanning receptors usually on macrophages or dendritic cells.

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23
Q

How do sensors of cell damage help identify offending agents?

A

Before necrosis of the cell occurs, the cell releases chemicals such as ATP or interleukin 1 (IL1) which causes an inflammatory response.

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24
Q

How do antibodies and complement proteins help identify offending agents?

A

They are able to bind to microbes or anything that shouldnt be there thus acting as flag markers for macrophages to ingest the material. This is the process of opsonisation.

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25
Q

How do circulating proteins help identify offending agents?

A

As part of the complement system.

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26
Q

What happens once a cellular receptor on a phagocyte/macrophage detects an offending agent?

A

The cell tries to phagocytose the offending agent.

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27
Q

How do mast cells respond to an offending agent?

A

They degranulate

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28
Q

What is degranulation?

A

Degranulation is a cellular process that releases antimicrobial cytotoxic or other molecules from secretory vesicles called granules found inside some cells.

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29
Q

How do dendritic cells respond to an offending agent?

A

They release chemicals like the mast cells which act as signals to prompt the immune system

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30
Q

What signals are released?

A

Cytokines
Lipid messengers
Other mediators

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31
Q

Where to mediators travel to from the site of the offending agent?

A

To blood vessels

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32
Q

How do mediators affect blood vessels?

A

They induce a vascular response

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33
Q

In acute inflammation what is the first thing that happens to blood vessels as a result of contact with a mediator?

A

Alteration of vascular calibre - eg. there is a very brief period of vasoconstriction which lasts seconds before vasodilation.

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34
Q

What does vasodilation in acute inflammation lead to?

A

Blood Pooling, Redness and Warmth

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35
Q

Why does vasodilation lead to blood pooling?

A

Because you have a larger surface area for blood to be n you get pooling.

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36
Q

What signs of inflammation are caused by vasodilation?

A

Rubor (Redness) & Calor (Heat)

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37
Q

What happens to blood vessels upon contact of a mediator during acute inflammation as well as the alteration of vascular calibre?

A

Changes to microvasculature and emigration of leukocytes from microcirculation

38
Q

What is vascular calibre?

A

Calibre means/relates to the diameter and vascular refers to blood vessels i.e. the diameter of blood vessels.

39
Q

What changes of microvasculature are experienced in acute inflammation after vessels have come into contact with mediators?

A

Endothelium cells that line blood vessels produce little gaps between themselves creating ‘holes’ which increases the permeability of the blood vessels of water and plasma proteins. This allows water from the plasma, and plasma proteins to seep out causing localised swelling (tumor).

40
Q

What happens to the concentration and speed of blood flow near a point of swelling?

A

At a point of swelling water has been lost from blood vessels as a result the concentration of red blood cells per unit of blood at that point increases. The speed of blood actually decreases as there’s less fluid to carry it swiftly on, as a result, white blood cells move to the corners of the vessel near the epithelium and their rate of movement slows down. This is called stasis.

41
Q

What is stasis?

A

Stasis is the slowing or pooling of blood.

42
Q

How does stasis lead onto the emigration of leukocytes from blood vessels?

A

White blood cells start binding to endothelium cells. The endothelium cells send out signals indicating that the leukocytes is needed ( activates the leukocyte). The white blood cells then migrate out of the vessel towards the offending agent.

43
Q

what is oedema?

A

Excessive fluid in tissues

44
Q

What are the two processes that can cause oedema?

A

Transudate & Exudate

45
Q

What is tumor (swelling) a result of?

A

Oedema ( excessive fluid in tissues)

46
Q

What is the formation of a transudate typically due to in the body?

A

Blood vessels are normally intact however there is probably an increase in blood pressure over time which leads to a hydrostatic imbalance ( or osmotic imbalance). This is going to force water (only) out of circulation i.e. into surrounding tissues producing a fluid known as an ‘ultrafiltrate of plasma’ as it has a high water concentration but a low protein concentration.

47
Q

Why is the fluid of a transudate refered to as an ultrafiltrate of plasma?

A

Because it has a high concentration of water but a low protein concentration.

48
Q

What is a transudate?

A

An extravascular fluid ( i.e. a fluid outside of blood vessels) with a low protein concentration.

49
Q

In Acute inflammation does exudation occur or transudation?

A

Exudation

50
Q

What does the oedema of exudation contain?

A

High water and protein content

51
Q

Why does exudate contain high protein content?

A

This is due to the increased interendothelial spaces which increase the vascular permeability thus allowing proteins to pass through.

52
Q

Why do we have leaky blood vessels?

A

Vascular permeability allows leukocytes to leave blood vessels and enter the site of injury in order to clear microbes and debris which is incredibly beneficial for us.

53
Q

What is leukocyte extravasation?

A

The process of leukocytes leaving blood vessels and going out into tissues.

54
Q

What is the sequence of events involved in leukocyte extravasation?

A 
Margination,
Rolling,
Adhesion,
Transmigration ( diapedesis),
Migration.
55
Q

What two types of reactions does an inflammatory response invoke?

A

Vascular and cellular reactions

56
Q

What does TNF-a stand for?

A

TNF alpha ( Tumor necrosis factor-alpha)

57
Q

What are both TNF-a and IL1 examples of?

A

Mediators

58
Q

What is a mediator?

A

Molecules that not only initiate the inflammatory response but also regulate the inflammatory response.

59
Q

What cells may release mediators?

A

Macrophages

60
Q

How do endothelial cells of blood vessels respond to chemical mediators?

A

By opening up gaps between themselves and by shuttling proteins to their surface called E selectin and P selectin as well as secreting more chemical messengers into the bloodstream.

61
Q

What are the names of proteins that are shuttled to the surface of endothelial cells when they come into contact with mediators?

A

E selectin and P selectin

62
Q

As a result of gaps opening between endothelial cells what happens?

A

Water and plasma is lost out into extravascular tissue thus stasis occurs and neutrophils/leukocytes move close to the endothelial cells.

63
Q

What is margination?

A

A phenomenon that occurs during the relatively early phases of inflammation; as a result of dilation of capillaries and slowing of the bloodstream, leukocytes tend to occupy the periphery of the cross-sectional lumen and adhere to the endothelial cells that line the vessels.

64
Q

How do neutrophils inside the blood vessels respond to the chemical signals as it is moving closer to the endothelial cells (in margination)?

A

It expresses proteins such as L selectin on its plasma membrane.

65
Q

What happens in rolling?

A

The L selectin on the surface of neutrophils starts interacting with glycoproteins sticking up on endothelial cells and thus they bind.

The E and P selectin on the surface of the endothelial cell starts to bind to glycoproteins on the surface of the neutrophil.

Once attached to the endothelial cell the neutrophil ends up ‘rolling’ across the endothelial cells due to the flow of blood.

66
Q

What are glycoproteins?

A

Proteins bound to a sugar on the cell surface membrane.

67
Q

Do Selectins bind to each other?

A

No, they bind to glycoproteins on opposite surfaces.

68
Q

When does rolling stop?

A

When the neutrophil reaches a patch of endothelial cells where there is the highest amount of chemical mediators ( i.e. its closest to the site of injury).

69
Q

Define Rolling

A

Transient binding to endothelial cells as a result of the push of blood flow

70
Q

Define Transient

A

Lasting only for a short time; impermanent

71
Q

At the site of the highest concentration of chemical mediators (still within the blood) what other proteins are being expressed on the endothelial cells?

A

ICAM 1

72
Q

At the site of the highest concentration of chemical mediators (still within the blood) what other proteins are being expressed on the neutrophils?

A

B-integrins ( Beta integrins)

73
Q

What is the process of adhesion?

A

B-intergrins and ICAM1 bind tightly thus making the neutrophil stationary.

74
Q

What is adhesion?

A

When leukocytes stop rolling and bind via integrins

75
Q

What are the conditions for transmigration/diapedesis to occur?

A

The leukocyte must be stationary.

76
Q

What is transmigration?

A

Migration of leukocytes from between endothelial cells from blood into tissues.

77
Q

What protein is transmigration triggered by?

A

PECAM1

78
Q

How do leukocytes get to the site of injury after having left the blood vessels?

A

They migrate across a chemotactic gradient until they reach the site with the highest concentration of chemical signals/mediators i.e. the exact site of injury.

( key idea to remember here is as you get further from the site of injury their are less chemical mediators nearby as you get closer to site of injury they are more)

79
Q

What is a chemotactic gradient?

A

A gradient where you have a variable concenrtation of a chemical.

80
Q

what is chemotaxis?

A

movement of a motile cell or organism, or part of one, in a direction corresponding to a gradient of increasing or decreasing concentration of a particular substance.

81
Q

Where is P selectin found?

A

on platelets and Endothelium

82
Q

Where is E selectin found?

A

On endothium cells

83
Q

Where is L selectin found?

A

On leukocytes

84
Q

Once a leukocyte has encountered the source of the inflammation i.e. the microbe or foreign body, what happens?

A

They become activated as a result of toll-like receptors and phagocytose.

85
Q

How do phagocytes identify foreign bodies?

A

Using toll-like receptors as well as identifying the roughness and charge of the molecule or substance.

86
Q

What are the three distinct steps of phagocytosis?

A

Recognition and attachment
Engulfment and fusion of phagosome and lysosome
Killing and degradation of ingested material

87
Q

What are the three mechanisms of intracellular destruction of microbes and debris?

A

Free radical formation through the production of reactive oxygen species

Free radical formation through the production of reactive nitrogen species.

Lysosomal enzymes

88
Q

What do free radicals have the ability to do?

A

Pull apart other molecules

89
Q

What mechanisms of intracellular destruction are microbes killed by?

A

Free radical formation through the production of reactive oxygen species

Free radical formation through the production of reactive nitrogen species.

90
Q

What mechanism is debris cleared through via intracellualr destruction?

A

All three mechanisms i.e.
Free radical formation through the production of reactive oxygen species

Free radical formation through the production of reactive nitrogen species.

Lysosomal enzymes

0V015 Biology & Pathology (57 decks)

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