Inflammation Flashcards

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1
Q

What does Inflammation consist of?

A

Started at non-apoptotic cell death leading to DAMPS and PAMPS
Can be Acute, and involves recruitment of neutrophils to vascularised tissue.
Can become Chronic if response cannot remove the inflammatory stimuli.

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2
Q

What are the four main signs of acute inflammation?

A

Redness
Swelling
Heat
Pain

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3
Q

What Benefits does increased vascular permeability during inflammation bring?

A
Causes leakage:
Increases antibodies
Increases proteins ( tissue repair )
Increases barrier ( physical )
Increases leukocyte migration
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4
Q

Which 2 Vasodilators are released when inflammatory signals are released by non-apoptotic death/foreign material

A

Histamine

Nitric Oxide

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5
Q

Where are TNF, IL-1 cytokines released from and what do they do?

A

By Macrophages, endothelial cells and mast cells

causes : endothelial activation, fever, pain, anorexia, shock, malaise

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6
Q

Where are Chemokines released from and what do they do?

A

From Leukocytes and activated macrophages

Cause: chemotaxis and leukocyte activation

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7
Q

What Complement components are released and what do they do in response to injury?

A

Found in plasma, made in the liver

Cause: Leukocyte chemotaxis and activation
Vasodilation, Mast cell stimulation, Opsonisation.

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8
Q

Where are Prostaglandins released from and what do they do?

A

From Mast cells and Leukocytes

Cause : Vasodilation, pain, fever

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9
Q

Where is Histamine released from and what does it cause?

A

From Mast cells, Basophils and Platelets

Cause : Vasodilation, increased vascular permeability, endothelial activation

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10
Q

What is Exudate?

A

An exudate is any fluid, proteins and cells that filters from the circulatory system into lesions or areas of inflammation. Seeped out of blood vessel

Forms a barrier

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11
Q

How are cell recruited to site of damage?

A

Chemokines diffuse creating a gradient to which the leukocytes with the complementary receptors migrate towards.

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12
Q

How is Chemokine CXCR8 / IL-8 used for cell recruitment?

A

Gradients towards receptors:
CXCR1/CXCR2 g coupled receptors

Neutrophils recruited

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13
Q

Describe Neutrophil extravasation in 4 steps?

A
  • Chemo-attraction (endothelial creates adhesion molecules)
  • Rolling Adhesion (ligands on neutrophils bind to the selectins - adhesion molecule)
  • Tight Adhesion (low affinity binding in step 2 becomes high affinity due to chemokines)
  • Transmigration (pseudopedia extension from cytoskeleton- mediated by PECAM interactions)
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14
Q

How to neutrophils recognise pathogens?

A

TLR4 ( transmembrane protein )
CDI4 ( receptor )

These identify Lipopolysaccharides ( LPS ) present in gran negative bacteria

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15
Q

What three roles can Neutrophils play at the site of inflammation?

A

Pathogen clearance: Phagocytosis and Netosis

Cytokine secretion: Recruitment and activation of other immune cells

Phagocytosis: Engulfed into phagosomes. Fuse with lysosome to form phagolysosome. Reactive oxygen species phagocyte NADPH oxidase

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16
Q

How is Acute inflammation resolved?

A

Cells recruited have short half lives

Macriphages can clear apoptotic cells and produce anti-inflammatory mediators

Repair/wound healing

17
Q

What is an Antigen?

A

Molecule recognised by antibody

18
Q

What is an Immunogen?

A

Antigen independently capable of causing immune response without additional substances

19
Q

What is a Hapten?

A

Small molecule which when bound to a larger can create an antigen

20
Q

Examples of Chronic inflammation diseases?

A
Rheumatoid arthiritis
Asthma
IBS
Hepititis
Multiple sclerosis
21
Q

What diseases are associated with granulomatous inflammation?

A

TB
Leprosy
Crohns disease

22
Q

What are the distinct immune cell infiltrates for Chronic Inflammation?

A

Inflammatory macrophages
T cells
Plasma cells

  • it is a cycle with not clearance of inflammatory agent
    Bystander tissue is destroyed
    Concurrent repair process
23
Q

What Good macrophages are there?

A

Phagocytic
Cytotoxic
Anti-Inflammatory - TGF-beta, IL-10
Wound repair

24
Q

What bad macrophages are there?

A

IF these are not cleared away e.g. chronic inflammation, can cause damage

Cytotoxic
Inflammatory
Pro-fibrotic

25
Q

Which T cells can be found involved with inflammation?

A

Pro-inflammatory: TNI, IL-17, IFN-gamma

Cytotoxic: Granzymes, perforin

Regulatory: TGF-beta

26
Q

How are B cells involved with inflammation?

A

Create Plasma cells for antibodies

Clear infection

Could drive reaction against self

Can be local to site or operate remotely

27
Q

What are the characteristics of Granulomatous inflammation?

A

Triggered by strong T cell responses and resistent agents causing Chronic inflammation with granuloma formation

Aggregation of activated macrophages
A barrier is designed for clearance

28
Q

What are some differences between Chronic inflammation?

A

Acute vs Chronic

quick onset - delayed onset
neutrophils - macrophages
necrosis - scarring
resolution - scarring/loss of function

29
Q

How are wounds healed?

A

Fibrosis : ECM - Collagen deposition = scars
Angiogenesis

  • Scars can cause loss of function e.g. broncho pneumonia