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MBC > inflammation > Flashcards

inflammation Flashcards

1
Q

What is inflammation?

A

A complex and tightly regulated process which = Non specific response to cellular injury designed to remove the cause and consequence of that injury

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2
Q

What would happen without inflammation?

A

We would struggle to heal wounds, fail to fight infection and be susceptible to cellular injury

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3
Q

What are the canonical cardinal signs/features of inflammation? (Acute)

A

Redness (RUBOR)
Heat (CALOR)
Swelling (TUMOUR)
Pain (DOLOR)

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4
Q

What are the causes of inflammation?

A 
Pathogens, 
Allergens, 
Auto-antigens, 
physical damage, 
extreme temperatures 
Non-apoptotic cell death
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5
Q

What cells in our body undergo inflammation?

A

ALL

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6
Q

When can inflammation occur?

A 
some examples are
Infection
Autoimmunity 
Hypersensitivity 
Trauma
Fibrotic disease
Cancer
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7
Q

What is acute inflammation?

A

Short term rapid response non-specific to cellular injury
Instantaneous changes to blood flow
recruitment of immune cells

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8
Q

Why is there a change in blood flow in acute inflammation and what is the sign?

A

Bc of structural changes that occur in the microvasculature of tissue
Redness on skin

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9
Q

What does the structural change in microvasculature result in ?

A

(Change in blood flow) &

Accumulation of proteins and fluid and recruitment of immune cells to site of inflammation (swollen)

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10
Q

Where is the interstitium / interstitial layer located?

A

The intermediate layer between the epithelium and the vascular endothelium

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11
Q

What cells are resident in the interstitium?

A

Immune cells: Resident macrophages, mast cells

Dendritic cells?

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12
Q

What’s cells are present in the vasculature ?

A

White blood cells (prominently neutrophils)
Lymphocytes
Plasma and protein contents

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13
Q

What causes the release of signals activating the immune response after damage?

A

Non-apoptotic cell death ( in tissue and vasculature )

Detection of forgeign

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14
Q

What releases vasodilators ?

A

Immune cells esp Mast cells (but also basophils and platelets) release them rapidly upon activation/recognition of damage or recognition patterns

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15
Q

What are the 2 main vasodilators?

A

Histamine, nitric oxide

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16
Q

What vascular changes occur during inflammation?

A

Increased permeability
Dilation of bv (wider)
Reduced flow
Plasma leakage into interstitial membrane

17
Q

What are the benefits of increased vascular permeability and leakage?

A

Increases:
Antibodies
Protein

18
Q

What vascular changes are caused by vasodilators?

A

increased permeability
dilation of bv (wider)
reduced blood flow
plasma leakage into the interstitium

19
Q

In what order do the events occur when there is cellular damage?

A
  1. inflammatory signals produced
  2. vasodilators released
  3. vascular changes occur
20
Q

what benefits does increased vascular permeability and leakage bring?

A

increases:

  • amount of ab to site, if specific then may be able to kill patho etc.
  • protein in tissue site which allows increased activation of immune cells and source of protein for tissue repair to occur
  • physical barrier
  • leukocyte migration
21
Q

What are some soluble mediators released at an injury?

A 
histamine
prostaglandins
cytokines (TNF, IL-1)
chemokines
recruitment and production of complement (C5a, C3a, C4a)
22
Q

What is the primary sources of histamine and what are its actions?

A
  • Mast cells, basophils, platelets

- vasodilation, increased vascular permeability, endothelial activation

23
Q

What are prostaglandins produced by and what actions do they carry out?

A
  • Mast cells, leukocytes

- vasodilation, PAIN AND FEVER

24
Q

What are cytokines produced by and what are their functions?

A

(TNF, IL-1)

  • MACROPHAGES, endothelial cells, mast cells
  • endothelial activation (Adhesion molecules), fever, malaise, pain, anorexia - lethargy, shock
25
Q

What are chemokines released by and what are their functions?

A
  • Leukocytes, activated macrophages

- chemotaxis, leukocyte activation

26
Q

Where is complement produced and what is the function?

A

prod in the liver but the principle source is plasma

-Leukocyte chemotaxis and activation, vasodilation mast cell stimulation), opsonisation

27
Q

What is exudate?

A

fluid, proteins and cells that have seeped out of bv into inflamed tissue as a result of the endothelium becoming more permeable

28
Q

What does exudate form and why is this beneficial?

A

forms a separation between inflamed and healthy tissue:
acts as a physical barrier between site of inflammation and healthy tissue:
limits patho + inf stimuli from migrating into healthy tissue + causing further damage

29
Q

what causes immune cell recruitment?

A

happens as a result of the inflammatory signals produced by immune cells and stromal cells at the site of inflammation

chemokines produced

30
Q

what do chemokines do to recruit immune cells?

A

diffuse into the nearby vasculature and create a gradient

also act on endothelial cells themselves to promote this

31
Q

How do leukocytes in the vasculature migrate to chemokines source?

A

they have complimentary chemokine receptors which allow them to migrate towards the source

32
Q

What is an example of a chemokine?

A

IL-8
receptors of it most prominently expressed by neutrophils which are often the first cell type recruited to site of inflammation

33
Q

How do neutrophils migrate from bv to interstitium and site of inflammation?

A

neutrophil extravasation which is rapid

34
Q

First step of neutrophil extravasation

A
  1. chemo-attraction: cytokines and chemokines produced at site of inflammation which act on the endothelial layer to promote upregulation of adhesion molecules such as selectins
35
Q

Second step

A

2.rolling adhesion: carbohydrate ligands in a low-affinity state on neutrophils bind selectins - neutrophils recognise the selectins and they start to interact w the endothelium and undergo rolling adhesion (gently interact w endothelial layer whilst migrating along bv)

36
Q

Third

A
  1. tight adhesion - chemokines promote low to high-affinity switch in integrins which enhances binding of neutrophil binding to the endothelial wall
37
Q

Fourth

A

Transmigration of neutrophil through the endotheial wall
-involves cytoskeletal rearrangement of np & extension of membrane pseudopodia through the endothelial wall
mediated by PECAM molecules on both sides (endothelial and neutrophil)

38
Q

What are the functions of neutrophils at the site of inflammation?

A

Pathogen recognition
Pathogen clearance
cytokine secretion
phagocytosis

MBC (9 decks)

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