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Lily PoM MBC > Inflammation > Flashcards

Inflammation Flashcards

1
Q

What are the two types of inflammatory response?

A

Acute

Chronic

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2
Q

What is inflammation?

A

A non specific response to cellular injury

Designed to remove the cause and consequence of injury

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3
Q

What are the four main signs of inflammation?

A

Redness (Rubor)

Heat (calor)

Swelling (tumor)

Pain (dolor)

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4
Q

Why is it considered a universal process?

A

It is seen in all tissues

Obsorved in almost every disease

Caused by a huge range of different stimuli

Every cell in the body can be involved in the inflammatory process

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5
Q

What is the main feature af acute inflammation?

A

Quick

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6
Q

What happens in inflammation (simple), why does the area become red?

A

Change In local blood flow

Structural change in microcasvulature

Recruitment/accumulation of immune cells and proteins

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7
Q

What does a Tissue look like in the steady state?

A

Epithelium

Interstitial space - contains mast cells and macrophages

Vasculature - RBCs, leukocytes, neutrophils

This pretty much applies to all viable vascularised tissue

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8
Q

What happens to a tissue when it is damaged?

A
  1. A wound causes non apoptotic cell death and may introduce foreign (pathogens) material

This triggers the immune response

  1. Mast cells (and others) release vasodilators
    Namely histamine and nitric oxide
  2. Cause vascular changes. Increased permeability, dilation, reduces flow, plasma leakage
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9
Q

What benefits does increased vascular permeability and leakage bring?

A

More possibly specific antibodies that could killl the pathogen

More proteins for cell repair

Leukocyte migration

Provides a barrier

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10
Q

What are some of the main types of soluble mediators released at injury?

A

Histamine

Prostaglandins

Cytokines

Chemokines

Complement

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11
Q

What is the source of histamine and what does it do?

A

Comes from mast cells, basophils and platelets

Causes vasodilation, increased vascular permeability, endothelial activation and

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12
Q

What is the source of prostaglandins and what do they do?

A

Mast cells and leukocytes

Vasodilation, pain, fever

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13
Q

What is the source of cytokines and what do they do?

A

Eg TNF and IL-1

macrophages, endothelial cells, mast cells

Endothelial activation (adhesion molecules), fever, pain, anorexia, shock

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14
Q

What is the source of chemokines and what do they do?

A

Leukocytes, activated macrophages

Chemotaxis, leukocyte activation

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15
Q

What is the main source of complement and what do they do?

A

Eg C5a, C3a and C4a

Plasma

Leukocyte chemotaxis and activation, vasodilation (mast cell activation), opsonisation

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16
Q

What is the name of the fluid that seeps out of blood vessels?

A

Exudate

Contains proteins and cells (eg blood cells)

Provides a protective barrier against further spread of the cause of inflammation

17
Q

What happens in immune cell recruitment?

A

Recruitment and activation signals (chemokines) at the site of damage are produced

These diffuse out to form a gradient

Leukocytes express receptors for these chemokines, allowing them to migrate to the source of the chemokines

18
Q

What is one of the main chemokines involved in immune cell recruitment?

A

IL-8

Receptor: CXCR1 and 2 g coupled 7 transmembrane proteins

Secreted from : neutrophils, often the first cell type recruited to the site of inflammation

19
Q

What are the 4 steps involved in neutrophil extravisation?

A
  1. Chemo attraction. Cytokines released by macrophages (IL-1, TNF) causes up regulation of neutrophil adhesion molecules in the endothelium (eg selectins)
  2. Rolling adhesion. Carbohydrate Luganda in a low affinity state on neutrophils bind to selectins
  3. Tight adhesion. Chemokines promote change to high affinity binding to Ligands
  4. Transmigration. Cytoskeletal rearrangement and extension of pseudopodia. Leads to the movement of neutrophils into the interstitia
20
Q

What do neutrophils do at the site of inflammation?

A
  1. Pathogen recognition. Use of TLR4 and CD14 to identify lipopolysaccharides on gram negative bacteria
  2. Pathogen clearance. Phagocytosis
  3. Cytokines secretion. Recruitment and activation of other immune cells
21
Q

If the neutrophil response Is enough, what happens in the resolution of acute inflammation?

A
  1. Neutrophils and immune cells kill the pathogen
  2. Neutrophils have a short half life and turnover of inflammatory mediators (eg histamine) are turned over very quickly
  3. Macrophages. These clear apoptotic cells, and produce anti inflammatory mediators
  4. The wound is repaired
22
Q

What is the difference between acute inflammation and chronic and granulomatous inflammation with respect to antigens?

A

Acute doesn’t necessarily need an antigen

However chronic often results form prolonged presence of the antigen

23
Q

What are some examples of diseases involving chronic inflammation?

A

Rheumatoid arthritis, asthma,

Inflammatory bowel, hepatitis, psoriasis, MS

24
Q

What are some examples of diseases involving granulomatous inflammation?

A

TB, leprosy, some tumor reactions, sarcoidosis, crohns

25
Q

What is different in chronic inflammation that acute?

A

Same initial start

However, there is a persistent inflammatory stimuli (eg prolonged infection, unclearable particultes, autoimmunity)

There is a distinct immune cell infiltrate. In interstitial space, inflammatory macrophages, T cells, antibody secreting cells (plasma)

Leads to a vicious cycle as the inflammatory agent is not removed. This can lead to bystander tissue destruction

26
Q

What is the role of macrophages in chronic inflammation?

A

They are recruited as monocytes. But there are also tissue resident macrophages

GOOD:
Phagocytic, cytotoxic, anti inflammatory, wound repair

BAD:
Cytotoxic, inflammatory, profibrotic

27
Q

What is the role of lunphocytes in prolonged inflammation

A

Innate and adaptive work together, can be specific

T CELLS:
Pro inflammatory, cytotoxic, regulatory (reconstruction of tissue)

B CELLS:
Cenrste plasma cells that secrete antibody, clear infection, inflammatory (can cause a viscious cycle and poor more inflammation), can operate locally or remotely

28
Q

What is granulomatous inflammation?

A

Chronic inflammation with distinct pattern of granulomatous formation

Caused by the aggravation of activated macrophages, a barrier designed for clearance

Triggered by strong T cell responses. And resistant agents (mycobacterium, tumour)

29
Q

What are some differences between chronic and acute inflammation?

A

ACUTE:
Immediate, short lasting, vasodilation, increased vascular permeability, leukocyte response, neutrophils predominate, histamine release, prominent necrosis, leads to completer resolution or chronic inflammation

CHRONIC:
Delayed onset, can last years, persistent inflammation, ongoing tissue injury, attempts at healing, monocytes/macrophages predominate, ongoing cytokines release, prominent scarring, leads to scarring g or loss of function

30
Q

What are the outcomes (sequaele) of acute inflammation?

A

The inflammatory agent is cleared

Can lead to the formation of puss which may take longer to clear

Damaged cells are removed

Restoration of normal tissues function

31
Q

What are the outcomes of acute inflammation?

A

Excess tissue damage and scarring

Loss of organ function —> organ failure

32
Q

Wat are some consequences of inflammation and wound healing?

A

Can lead to collagen deposition forming a scar

In most cases this is fine, however in places such as the lungs it can cause broncho-pneumonia as the walls of the alveoli are no longer very thin

Can lead to loss of function (eg in the heart)

Lily PoM MBC (15 decks)

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