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Pathology I: Test 1 > Lecture 4: Inflammation 1 > Flashcards

Lecture 4: Inflammation 1 Flashcards

1
Q

What is inflammation?

A

It is the tissues response to injury or infection and is the body’s way of healing and repairing tissue, or defending itself against pathogens

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2
Q

What are the usual four sequences of events of inflammation?

A

1) Acute inflammation
2) Resolution/regeneration/restitution
3) Healing by repair
4) Chronic inflammation

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3
Q

Is acute inflammation early or late stage response to tissue damage?

A

Early tissue response

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4
Q

Acute inflammation: What are its main features?

A
  • Non-specific pattern of reaction
  • Always the initial response to damage
  • Named with suffix –itis
  • Lasts from a few hours to a few days
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5
Q

5 aetiological agents of acute inflammation. What are they and give an example of each

A

Physical agents:
Trauma, ionising radiation, heat, cold

Chemicals:
Corrosives, acids, alkalis, bacterial toxins

Hypersensitivity reactions:
Parasites, tubercle (granuloma) bacilli

Microorganisms:
Pyogenic (pus inducing bacteria)

Tissue necrosis:
Infarction

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6
Q

What are the 5 Latin terms used to describe clinical signs pointing to an inflammatory response?

A

<b><i> rubor</i> redness </b>
Increased dilatation of small blood vessels in damaged area

<b><i> calor</i> heat </b>
Hyperaemia (increased blood flow) and continued vascular dilatation

<b><i> dolor</i> pain </b>
Oedema and pus formation causing pain through stretching and distortion of tissues and chemical mediators being liberated from damaged tissues which trigger nerve endings.

<b><i> tumor</i> swelling </b>
Due to accumulation of fluid in extravascular space as part of fluid exudate – called oedema

<b><i> functio laesa</i> Loss of function/movement</b>
because of the pain and swelling

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7
Q

What does the acute inflammatory response do? What is its purpose (3)?

A
  • To carry fluids, proteins and cells in the form of fluid exudate for mediation of local defences
  • To eliminate and destroy the infective aetiological agent
  • To break down and remove damaged tissue through liquefaction
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8
Q

What do chemical messengers control?

A

Chemical messengers control the acute inflammatory process once they are produced and diffused

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9
Q

Where do chemical messengers come from?

A

Chemical messengers are liberated from damaged tissues or released from circulation as acute inflammatory exudate.

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10
Q

What are the two stages of acute inflammation called and what do they involve?

A

They are early stage and late stage acute inflammation.

Both involve vascular and cellular activity.

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11
Q

Briefly describe what early stage acute inflammation involves:

A

Early-stage acute inflammation involves acute inflammatory exudate (oedema fluid, fibrin and neutrophil polymorphs) outpouring from the blood vessels and accumulating into extracellular spaces of damaged tissue

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12
Q

What are the three vascular and cellular processes involved in early stage acute inflammatory reaction?

A

1) Changes in <u>vascular calibre</u> and therefore flow
2) Increased <u>vascular permeability</u> causing vascular leakage of fluid to extravascular spaces, forming fluid exudate
3) Formation of <u>cellular component</u> – emigration of cells, mostly neutrophil polymorphs, into extravascular space

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13
Q

Describe all steps involved with changes to vascular calibre in acute inflammatory reaction.

A

Initially, there is <u>vasoconstriction</u> that lasts a few seconds. Next, <u>vasodilation</u> will occur - called active hyperaemia it lasts from 15 minutes to several hours which will depend on injury severity. Due to vasodilation, there is an <u>increase in blood flow</u> which may be up to 10x.
Next, there will be <u>increased vascular permeability</u> and leakage of plasma proteins into tissues, however because blood cells remain within vessels it will cause blood viscosity to increase and <u>blood flow to decrease.</u>
At this point, there is stasis, in which these small blood vessels are dilated still but they are packed with RBCs, which flow near to vessel wall causing blood flow to slow down even more.

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14
Q

Which comes first: vasoconstriction or vasodilation?

A

Vasoconstriction

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15
Q

How long does vasoconstriction last versus vasodilation?

A

vasoconstriction: a few seconds
vasodilation: 15 minutes to several hours depending on tissue severity

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16
Q

Why does blood viscosity increase in early stage acute inflammation?

A

It increases because as the plasma proteins exit the cell along with fluid as exudate, red cells remain in the blood vessels. This decreases blood flow and increases blood viscosity.

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17
Q

Describe the normal circumstances of fluid movement through the capillaries

A

Under normal circumstances, capillary hydrostatic pressure increases at the arteriolar end of capillaries forcing fluid out into extravascular space and returns at the venous end of capillaries as hydrostatic pressure decreases. Increased colloid osmotic pressure also favours fluid return.

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18
Q

Describe the abnormal circumstances due to acute inflammation acting on vascular and extravascular pressure.

A

Under abnormal circumstances ie. acute inflammation more fluid leaves the blood vessels than returns:
capillary hydrostatic pressure continues to rise and protein-rich fluid is pushed out into the extravascular space

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19
Q

What are the two mechanisms of vascular leakage into the tissues, that occur during acute inflammation?

A
  1. <b> Non-mediated leakage </b>
    Leakage due to toxins/physical agents causing cell necrosis and the vascular endothelium lining the cells is compromised.
2.<b> Mediated vascular leakage </b>
Dead tissue (excluding vascular endothelium) triggers release of chemical mediators which produce persistent vasodilatation and loss of axial flow which causes endothelial cell swelling and separation, plus increased permeability and consequently exudation from plasma into damaged area which then leads to tissue swelling (oedema).
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20
Q

Where does acute inflammatory exudate come from?

A

It is derived from local blood vessels

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21
Q

What is acute inflammatory exudate made of?

A

Fluid: salts and water
Small proteins: immunoglobulins and fibrinogen
Cells: neutrophil polymorphs, few macrophages and few lymphocytes

22
Q

What is the normal fluid flow in the body like?

A

It is constantly circulating, going from local vessels to extracellular space of damaged tissues to being drained and reabsorbed by lymphatics/local nodes.

23
Q

Why is fluid so important to the acute inflammatory process?

A

Important because:
1. It allows foreign antigens to be presented to immune system to help the development of a specific immune response.

  1. Lowers concentration of locally produced toxins in area of damage through fluid dilution and salts buffers.
  2. Supports and provides macrophages in the area with nutrients e.g. glucose/O2.
  3. Allows diffusion of mediators (e.g. plasma derived precursors) of inflammatory process into area of damage.
  4. Ig (in exudate) act as opsonins for phagocytosis.
24
Q

What role does fibrin play in acute inflammatory response?

A

Fibrin or specifically a network of fibrin threads joining together will try to localise the damage by preventing migration of micro-organisms. It also produces scaffolds to assist movement of neutrophil polymorphs and macrophages through the damaged area.

25
Q

How does fibrinogen polymerise to fibrin?

A

Fibrin is a long filamentous insoluble protein formed by polymerisation of fibrinogen.
Fibrinogen leaks from blood vessels in acute inflammation along with fluids and salts. Once fibrinogen is outside the vessel lumen and makes contact with extravascular tissue it polymerises into insoluble fibrin threads through activation of the blood coagulation cascade.

26
Q

Roles of endothelium

A

-

27
Q

What secreted factors control regional blood flow?

A

The balance of secreted factors control regional blood flow. The balance can be changed by increasing synthesis of PAF (platelet activating factor) and NO. PAF increases vascular permeability and NO promotes vascular dilatation.

28
Q

What secreted factors promote cell adhesion molecules?

A

Secreted factors IL-1, TNF, chemokines promote cell adhesion molecules (which bind with neutrophil polymorphs).

29
Q

Describe neutrophil margination

A

It is the 3 stages of the effects of cell adhesion mechanisms on neutrophil polymorphs (NP).

30
Q

What are the three stages of neutrophil margination in acute inflammation?

A

1) Rolling: where the NP is in close contact with endothelium rolls along surface
2) Adhesion: NP adhere firmly to endothelium
3) Aggregation: “holding hands” adjacent NP adhere to each other and undergo shape changes

31
Q

Emigration refers to emigration of what cell?

A

the neutrophil polymorphs

32
Q

Where do these cells migrate to?

A

neutrophil polymorphs migrate through vessel membrane into area of tissue damage by passing between the endothelial cells

33
Q

How do chemotactic factors mediate this movement?

A

By chemotactic factor’s concentration gradient, which diffuse from area of tissue damage by chemotaxis.

34
Q

Late stage acute inflammation is mainly to do with?

A

It is to do with chemical mediators, macrophages neutrophil polymorphs and their role in acute inflammation.

35
Q

Where are chemical mediators derived from

A

Chemical mediators can be plasma-derived or cell-derived: they can come from plasma or cells.

36
Q

Chemical mediators are present in plasma as what form?

A

Plasma-derived chemical mediators are present as precursor forms in the plasma.

37
Q

Chemical mediators:
How are they activated?
How long do they stay in tissues?
How are they inactivated?

A

A series of proteolytic cleavages activates the factors to allow them to acquire biologic properties such as complement. However, they have short half-lives and once in tissues they are inactivated by enzymatic/scavenging systems.

38
Q

How do the plasma-derived chemical mediators enter the area of damage?

A

By being secreted in inflammatory exudate

39
Q

Where in the cells are the chemical mediators sequestered?

A

in intracellular granules that are then secreted from these cells: platelets, neutrophil polymorphs, macrophages, endothelium, mast cells, smooth muscle, fibroblasts.

40
Q

What cells synthesise chemical-mediators?

A

platelets, neutrophil polymorphs, macrophages, endothelium, mast cells, smooth muscle, fibroblasts.

41
Q

Are cell-derived chemical mediators synthesised all the time?

A

No - only when needed (de novo) and in response to stimulus

42
Q

List the sequence of their (cell-derived mediators) biological activity

A

Their biological activity starts from binding to their target cells’ specific receptors, further directing enzymatic activity (lysosomal proteases) and then mediating oxidative damage (O2 metabolites).

43
Q

How long do chemical mediators stay in the body?

A

Not long - they are short-lived and quickly decayed, inactivated by enzymes, scavenged and inhibited

44
Q

What are secondary mediators?

A

Chemical mediators that are derived from the target cells stimulated by cell-derived chemical mediators

45
Q

Give 3 examples of chemical mediators, their source and their role in acute inflammation.

A

PLASMA-DERIVED:
1. Bradykinin; from plasma substrate; triggers vascular leakage and pain, NOT chemotaxis

CELL-DERIVED:
2. O2 metabolites; from leukocytes; triggers vascular leakage, endothelial damage and tissue damage, NOT chemotaxis

  1. NO; found in macrophages, endothelium; triggers vascular leakage, vasodilatation, cytotoxicity, and chemotaxis
46
Q

T/F: macrophages play a large role in acute inflammation.

A

False - more important in chronic. Here they are a minor component of inflammatory exudate.

47
Q

Which enters damaged area first: neutrophil polymorphs or macrophages?

A

neutrophil polymorphs

48
Q

When do macrophages enter the damaged area?

A

They enter the damaged area later than neutrophil polymorphs do, and increase in number after a time to facilitate phagocytosis of dead material.

49
Q

What are some features of macrophages

A

Other features of macrophages are that they have a larger capacity than NPs for oxidative metabolism and therefore survive longer, they secrete growth factors and cytokines, and are major scavenging cleaning cells that assist in repair following tissue damage.

50
Q

Survivability of NPs?

A

they only survive for a few hours once in the tissues.

Pathology I: Test 1 (11 decks)

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