Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How is inflammation initiated?

A

When cells in damaged tissue release DAMPS or PAMPS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What type of cells are recruited first in inflammation?

A

Innate immune cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Why do we have immune cell recruitment in inflammation?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What innate immune cell do we see especially in inflammation?

A

Neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How would you describe the first immune response?

A

Acute with a rapid onset.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the 4 cardinal features of inflammation?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the 3 phases of acute inflammation?

A
  1. Steady state
  2. Damage
  3. Immune cell recruitment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

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

A

Mast cells and macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

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

A

Leukocytes and neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What other soluble mediators are involved in acute inflammation?

A

Prostaglandins
Cytokines e.g. TNF
Chemokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are prostaglandins responsible for?

A

Pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are cytokines such as TNF responsible for?

A

Fever, pain and anorexia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is exudate?

A

Fluid that seeps out of blood vessels into tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions