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PoM > MBC - Inflammation > Flashcards

MBC - Inflammation Flashcards

1
Q

What is inflammation?

A

Biological process designed to remove damaged cells and clear threats such as infections or toxins.

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2
Q

Where does inflammation occur?

A

Can occur in any vascularised tissue and can involve many other cells as well as those at the site of damage.

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3
Q

How is inflammation initiated?

A

When cells in damaged tissue release DAMPS or PAMPS

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4
Q

What type of cells are recruited first in inflammation?

A

Innate immune cells

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5
Q

Why do we have immune cell recruitment in inflammation?

A

Get rid of the inflammatory signal by repairing the damaged tissue.

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6
Q

What innate immune cell do we see especially in inflammation?

A

Neutrophils

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7
Q

How would you describe the first immune response?

A

Acute with a rapid onset.

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8
Q

What happens if innate immune cells cannot get rid of the inflammatory signal?

A

Adaptive immune cells are recruited to induce a state of chronic inflammation

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9
Q

What is the difference between acute and chronic inflammation in terms of damage?

A

Acute rarely causes damage to tissue.

Chronic can cause repetitive rounds of inflammation and thus tissue damage and repair, leading to scarring.

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10
Q

What are the 4 cardinal features of inflammation?

A

Heat (calor)
Pain (dolor)
Swelling (tumor)
Redness (Rubor)

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11
Q

What are some of the other features of inflammation?

A 
Non specific response to cellular injury
Designed to remove cause + consequence of injury
Essential for healing wounds/infection
Complex and tightly regulated
Can occur anywhere in the body.
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12
Q

How is inflammation a universal process?

A

It is seen everywhere in all cells of then body and associated with so many different types of cell injury and deaths

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13
Q

How do we get redness and swelling with inflammation?

A

There is a change to local blood flow due to a change in microvascular structure.

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14
Q

Why do we get redness and swelling with inflammation?

A

This causes an accumulation of protein in the fluid and thus the recruitment of immune cells.

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15
Q

What are the 3 phases of acute inflammation?

A
  1. Steady state
  2. Damage
  3. Immune cell recruitment
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16
Q

In the steady state, what cells do we see in the interstitial layer?

A

Mast cells and macrophages

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17
Q

In the steady state, what cells do we see in the blood vessels?

A

Leukocytes and neutrophils

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18
Q

In the damage phase, what is step 1?

A

Inflammatory signals (PAMPS/DAMPS) from cell death activates the immune response in both tissue and vasculature. There is now a detection of foreign material.

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19
Q

In the damage phase, what is step 2?

A

Vasodilators (histamine and nitric oxide) are released from immune cells such as mast cells, increasing permeability, vasodilation, reduced blood flow and plasma leakage.

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20
Q

In the damage phase, what is step 3?

A

Increased permeability and leakage increase antibody recruitment to site of inflammation in hopes to remove damage signal

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21
Q

In the damage phase, what is step 4?

A

Increased protein leaking into tissue increases repair of tissue and activation of more immune cells

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22
Q

In the damage phase, what is step 5?

A

Increased recruitment of leukocytes as well as the formation of a protective physical barrier.

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23
Q

What other soluble mediators are involved in acute inflammation?

A

Prostaglandins
Cytokines e.g. TNF
Chemokines

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24
Q

What are prostaglandins responsible for?

A

Pain

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25
Q

What are cytokines such as TNF responsible for?

A

Fever, pain and anorexia

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26
Q

What is exudate?

A

Fluid that seeps out of blood vessels into tissue

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27
Q

What does exudate contain?

A

Proteins and cells

28
Q

What is the purpose of exudate?

A

Forms a separating barrier between inflamed and healthy tissue to form a barrier between healthy and inflamed tissue to prevent pathogens from migrating to healthy tissue

29
Q

Why does immune cell recruitment take place?

A

Due to inflammatory signals form immune cells at the site of inflammation

30
Q

In immune cell recruitment, what is step 1?

A

Chemokine diffuse out of site to the nearby vasculature to form a gradient- they also act on endothelial cells themselves to promote cell recruitment

31
Q

In immune cell recruitment, what is step 2?

A

Leukocytes within the vasculature express complementary chemokine receptors, allowing them to migrate towards the chemokine source which is the site of inflammation.

32
Q

What is an example of chemokine receptors in immune cell recruitment.

A

Chemokine CXCL8 (IL-8) has the G-coupled receptors CXCR1 and CXCR2 which are expressed by neutrophils. This results in the early recruitment of neutrophils to the site of inflammation

33
Q

What are the 4 steps of neutrophil extravasation?

A
  1. Chemo-attraction
  2. Rolling adhesion
  3. Tight adhesion
  4. Transmigration
34
Q

What occurs in chemo-attraction?

A

Production of cytokines and chemokine at the site of inflammation that act on the endothelial layer to promote up regulation of adhesion molecules such as selectins

35
Q

What occurs in rolling adhesion?

A

Carbohydrate ligands in a low affinity state on neutrophils bind to these selectins on the endothelial layer gently.

36
Q

What occurs in tight adhesion?

A

Chemokine promote a switch from low to high affinity binding in integrins LFA-1, enhancing the binding of neutrophils to the endothelial layer.

37
Q

What occurs in transmigration?

A

Cytoskeletal arrangement and extension of pseudopodia mediated by PECAM molecules of both the endothelial side and the neutrophil side of the interaction.

38
Q

What do neutrophils do?

A
  • Identify pathogens with innate receptors to recognise lipopolysaccharides.
  • Kill bacteria via phagocytosis or netosis
  • Cytokine secretion into inflamed tissue to amplify immune cell recruitment/activation
39
Q

What happens if neutrophils can contain infection and clear damaged tissue?

A
  • Neutrophils will die very rapidly due to their short lifespan.
  • Inflammatory mediators are rapidly degraded.
  • Recruited macrophages clear apoptotic cells and produce anti-inflammatory mediators
40
Q

What happens if neutrophils cannot contain infection and clear damaged tissue?

A

Chronic inflammation will proceed

41
Q

What is an antigen?

A

Any molecule or molecular structure that can be recognised by an antibody or the adaptive immune system.

42
Q

What are the different types of antigen?

A

Foreign
Self
Immunogen (independently drives immune response)
Hapten - only acts as an antigen when bound to a larger molecule

43
Q

What is the difference between acute and chronic inflammation with respect to antigenic stimulation?

A

Acute: doesn’t always involve it but sometimes will

Chronic (/granulomatous): involve antigenic stimulation

44
Q

What conditions are associated with chronic inflammation?

A 
Rheumatoid arthritis 
Asthma 
Inflammatory bowel disease
MS
Hepatitis
45
Q

What conditions are associated with granulomatous inflammation?

A

TB
Leprosy
Tumour reactions
Crohn’s disease

46
Q

How does chronic inflammation differ to acute in its progression?

A

Chronic is very similar to acute in the initial phases, however there is persistence of inflammatory stimuli in chronic inflammation.

47
Q

What does the cell infiltrate from chronic inflammation contain?

A

T cells, inflammatory macrophages and antibody secreting plasma to get rid of signal.

48
Q

How can chronic inflammation give off a ‘vicious cycle’?

A

No clearance of inflammatory agent leads to bystander destruction and concurrent tissue repair

49
Q

What is the benefit of macrophages in inflammation?

A

Recruited from vasculature as monocytes. They are phagocytic so clear apoptotic cell bodies and can be cytotoxic to mediate cell death.

50
Q

What is the disadvantage of macrophages in inflammation?

A

They produce inflammatory molecules and are inflammatory themselves - promote recruitment of more immune cells to inflamed site if left unchecked. They are also pro-fibrotic and can cause the excess formation of collagen

51
Q

How are T cells pro-inflammatory?

A

Can be pro-inflammtory and are very cytotoxic and regulatory.

52
Q

Are B cells anti or pro inflammatory?

A

Both as they generate plasma cells to clear infection but can operate remotely by secreting antibodies to inflammatory site via lymph nodes.

53
Q

What is granulomatous inflammation?

A

Chronic inflammation with distance pattern of granuloma formation - disruption of surrounding tissue with clear scarring.

54
Q

What is a granuloma?

A

Aggregation of activated macrophages to act as a barrier for clearance.

55
Q

How is granulomatous inflammation triggered?

A

By strong T cell responses

56
Q

What’s the difference between acute and chronic inflammation with respect to onset?

A

Acute: immediate - lasts a few days
Chronic: Delayed onset - weeks to years

57
Q

What’s the difference between acute and chronic inflammation with respect to initial effects?

A

Acute: vasodilation, vascular permeability, leukocyte response
Chronic: persistent inflammation, ongoing tissue injury, attempts at healing

58
Q

What’s the difference between acute and chronic inflammation with respect to immune cell population?

A

Acute: Neutrophils predominate
Chronic: Monocytes/ macrophages predominate

59
Q

What’s the difference between acute and chronic inflammation with respect to mediator release?

A

Acute: Histamine release
Chronic: Ongoing cytokine release

60
Q

What’s the difference between acute and chronic inflammation with respect to necrosis/scarring?

A

Acute: Prominent necrosis
Chronic: Prominent scarring

61
Q

What’s the difference between acute and chronic inflammation with respect to their outcomes?

A

Acute: Complete resolution, progression to chronic
Chronic: Scarring, loss of function

62
Q

What determines the sequelae of inflammation?

A

Tissue site, type and length of inflammation

63
Q

What are some of the sequelae of acute inflammation?

A
  • Cleared quickly mostly
  • Sometimes leads to puss/abscess formation
  • Restoration of normal tissue function
64
Q

How may we get organ failure from acute inflammation?

A

May be a progression of changes and angiogenesis and fibrosis of tissue leading to a fibrotic scar tissue deposition or vascular alternation, these may hinder function and potentially lead to organ failure

65
Q

How may inflammation cause scarring?

A

Wound healing may lead to collagen deposition - the issue can arise when it’s difficult to remove the collagen that’s been deposited in the ECM which leads to scarring.

66
Q

What can scarring (collagen deposition) of the airways lead to?

A

Broncho-pneumonia or interstitial pneumonia.

67
Q

What else can scarring lead to?

A

Hinderance of motility, and scarring on the heart muscle can cause loss of function and organ failure.

PoM (27 decks)

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