Brainscape's Knowledge GenomeTM

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


See full index

Pom > Inflammation > Flashcards

Inflammation Flashcards

1
Q

What is inflammation

A

Inflammation is a non-specific response to cellular injury designed to remove the cause of the initial inflammatory signal (the injury) and repair inflamed tissue

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

What initiates inflammation

A

When cellular damage (non-apoptotic cell death) leads to release of damage associated molecular patterns (DAMPs) or body detects pathogen associated molecular patterns (PAMPs)

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

4 signs of inflammation

A

1) Redness (rubor)

2) Heat (calor)

3) Swelling (tumor)

4) Pain (dolor)
Vascular leakage increases blood flow into inflamed tissue leading to fluid build up and rbc build up. Heat results from increased presence of fluid as body temp at a site

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

Inflammation caused by

A
  • Pathogens
  • Allergens
  • Auto-antigens
  • Physical damage
  • Extreme temps
  • Non-apoptotic cell death
  • Infection
  • Autoimmunity
  • Hypersensitivity
  • Trauma
  • Fibrotic disease
  • cancer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Immune cell recruitment

A

At site of damage inflammation and chemokine signals are made which diffuse out to form a gradient. Leukocytes that have complementary chemokine receptors move to chemokine source

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

CXCL8/IL-8

A

Bind to CXCR1 and CXCR2 ( g coupled transmembrane proteins)
Expressed by neutrophils

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

Second stage of inflammation (damage)

A

1) inflammatory signals- non-apoptotic cell death occurs and detection of foreign material like bacteria

2) immune cells are activated by recognising DAMPs or PAMPs, especially mast cells, and release vasodilators like histamine and nitric oxide rapidly

3) rapid vasculature changes- increased permeability, dilation, reduced flow, plasma leakage into interstitium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the benefits of increased vascular permeability and leakage

A
  • Rapid movement of antibodies into site of inflammation specific to intruding pathogen
  • Recruiting proteins into tissue site which allows for increased activation of immune cells and source of protein for tissue repair
  • Recruitment of leukocytes
  • Formation of a physical barrier
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What other soluble mediators are released

A

Histamine-mast cells,basophils,platelets-vasodilation,increased vascular permeability,endothelial activation

Prostaglandins-mast cells,leukocytes-vasodilation,pain,fever

Cytokines-macrophages,endothelial cells,mast cells-endothelial activation,fever,malaise,pain,anorexia,shock

Complement-plasma-leukocytes,chemotaxis,opsonisation,vasodilation

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

Third stage immune recruitment

A
  • Recruitment and inflammation signals at the site of damage e.g. chemokines produced
  • These diffuse out to form a gradient
  • Leukocytes in vasculature expressing complementary chemokine receptors migrate towards the chemokine source
  • e.g. chemokine CXCL8 (IL-8) works on receptors CXCR1 and 2 (g-coupled 7-TM proteins) on neutrophils- neutrophils are often first cell type recruited to site of inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How does neutrophil extravasation work?

A

1) Chemo-attraction: cytokines (e.g. TNF-alpha) acts on endothelial layer to promote upregulation of adhesion molecules e.g. selectins

2) Rolling adhesion: carbohydrate ligands in a low affinity state on neutrophils bind selectins and migrate along blood vessel e.g. PSGL1 (selectin P ligand) binds P and E selectins

3) Tight adhesion: chemokines promote low to high affinity switch in integrins like LFA-1, Mac-1 → enhance binding to ligands e.g. ICAM-1

4) Transmigration: cytoskeletal rearrangement and extension of pseudopodia to move cell into interstitium. This is mediated by PECAM interactions on both cells

!https://s3-us-west-2.amazonaws.com/secure.notion-static.com/7a1cbe19-a6bd-4f09-adcd-29ee606a39d3/Untitled.png

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

3 functions of neutrophils

A

Pathogen recognition
Pathogen clearance
Cytokine secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Resolution of acute inflammation

A

1) Pathogen recognition: immune cells (e.g. neutrophils) and antimicrobials (e.g. antibodies) will recognise infections/particulates

2) Short half life: neutrophils (especially activated) have a rapid half-life. Inflammatory mediators like histamine are turned over rapidly

3) Macrophages: clear apoptotic cells + produce anti-inflammatory mediators to suppress inflammation

4) Repair/wound healing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is exudate and what is it’s purpose

A

Fluid, proteins and cells that have seeped out of a blood vessel

Forms a separation between healthy and inflamed tissue to prevent inflammatory stimuli and pathogens from migrating into healthy tissue and causing further damage

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

What is the antigen type which independently can be capable of driving an immune response in the absence of additional substances?

A

Immunogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are some examples of diseases are characterised by chronic inflammation?

A
  • Rheumatoid arthritis
  • Asthma
  • Inflammatory bowel disease
  • Glomerulonephritis
  • Hepatitis
  • Psoriasis
  • Multiple sclerosis
17
Q

What are some examples of diseases are associated with granulomatous inflammation?

A
  • TB
  • Leprosy
  • Foreign body granuloma
  • Tumour reactions
  • Sarcoidosis
  • Crohn’s disease (a specific type of IBS)
18
Q

Persistent inflammatory stimuli

A
  • Persistent/prolonged infection e.g. TB and hep B/C
  • Persistent toxic stimuli e.g. allergens, pollutants
  • Unclearable particulates e.g. silica
  • Autoimmunity e.g. self antigens
19
Q

A vicious cycle of damage and repair- what does this mean?

A

In some cases T cells and plasma cells can clear the pathogen that the standard neutrophil response couldn’t

However if there’s no clearance of the inflammatory agent then the cells will keep secreting inflammatory molecules to try and destroy the pathogen which can cause bystander tissue destruction

20
Q

Bad effects of macrophages

A
  • Cytotoxic- produce inflammatory molecules
  • Inflammatory- keep recruiting T cells, neutrophils etc if left unchecked
  • Pro-fibrotic- they normally promote collagen formation for wound repair but excessive promotion can lead to too much collagen produced
21
Q

What do T cells do in chronic inflammation

A
  • Pro-inflammatory e.g. TNF, IL-17, IFN-γ
  • Cytotoxic e.g. granzymes, perforin
  • Regulatory e.g. TGF-β
22
Q

What is granulomatous inflammation and what is it triggered by?

A
  • Chronic inflammation with distinct pattern of granuloma formation
  • Triggered by strong T cell responses
  • Form against resistant agents (e.g. mycobacterium, tumour)
23
Q

Granuloma

A

Aggregation of activated macrophages. A barrier designed for clearance of foreign material by macrophages

24
Q

Immediate vs chronic

A

Acute lasts a few days,vasodilation,neutrophils predominate,histamine release,prominent necrosis,completely resolves

Chronic has a delayed onset,monocytes predominate,ongoing cytokine release ,prominent scarring can cause loss of function

25
Q

Positive outcomes of inflammation

A
  • clear inflammatory agent
  • remove damaged cells
  • restore normal tissue function
26
Q

Negative outcomes of inflammation

A
  • Excessive tissue damage
  • Scarring- could reduce motility
  • Loss of organ function which could lead to organ failure
27
Q
  • What negative consequence could there be of wound healing?
A
  • Wound healing leads to extracellular matrix (e.g. collagen) deposition
  • When excess collagen can’t be removed, it forms a scar
  • Wound healing therefore in sensitive tissues could lead to loss of tissue function e.g. in heart
  • Broncho-pneumonia can be caused by collagen deposition as part of wound healing because thin epithelial walls that allow gas exchange in the lung are replaced with collagen filled scarred areas that don’t allow for gas exchange

Pom (44 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions