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POM > Inflammation > Flashcards

Inflammation Flashcards

1
Q

What are the key signs of inflammation

A 
Calor -heat - increased blood flow
Rubor - redness - increased blood flow
tumor -swelling 
Dolor - pain - white cells
functio laesa (loss of function)
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2
Q

What is meant by inflammation?

A

complex reaction in viable vascularised tissues to sublethal cellular injury

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3
Q

What is the general function of inflammation?

A

Protective response geared towards removing the cause and consequences of the injury
sets stage for potential healing

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4
Q

Outline the general key players in inflammation

A

Tightly regulated process consisting mainly of leukocyte and vascular responses
Triggered by various cell types and soluble mediators

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5
Q

Which cells are involved in inflammation?

A 
Neutrophils 
Macrophages 
Lymphocytes 
Eosinophils 
Mast cells
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6
Q

Which mediators are involved in inflammation?

A

Antibodies
Cytokines
Complement system
Coagulation system

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7
Q

What is acute inflammation?

A

Rapid non-specific response to cellular injury
Orchestrated by mediators released from injured cells
Leukocyte and vascular response

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8
Q

What is the key aim of acute inflammation and what are the three ways this is achieved?

A

Rapid delivery of leukocytes and plasma proteins to the site of injury

  • Achieved by alteration in the calibre of blood vessels to increase vasodilation
  • Structural changes to the microvasculature to allow proteins and leukocytes to leave the circulation (increased vascular permeability)
  • Emigration, accumulation and activation of leukocytes at the focus of injury
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9
Q

What are the three basic steps to acute inflammation.

A

Sublethal injury
Immune cell recruitment
Resolution of acute inflammation

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10
Q

Describe what happens when a sublethal injury occurs

A
  1. Inflammatory signals: non-apoptopic cell death
    detection of foriegn material
  2. Vasodilators released: histamine and NO
  3. Vascular changes: Increased permeability, dilation, reduced flow and plasma leakage
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11
Q

How is vascular permeability increased?

A

Endothelial cells contract: increased interendothelial spacing
Immediate transient response - natural
Histamine and nitric oxide causing cells to contract
Damage to endothelial cells

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12
Q

Why is increased vascular permeability useful?

A

Rapid movement of antibodies into the site due to slowed blood flow
Recruitment of proteins into tissue increasing activation of immune cells and a source of protein for tissue repair - increased bioavailabilty of substances
Leukocytes form a physical barrier
Leukocyte migration

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13
Q

What is exudate?

A

The fluid that leaks from the vasculature in acute inflammation (includes fluid, proteins and cells)

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14
Q

What is the purpose of exudate?

A

Dilute pathogens
Walls off pathogens by separating inflamed tissue from healthy tissue preventing the spread of pathogens
Permits spread of soluble inflammatory mediators to site of injury

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15
Q

Describe the structure of the steady state of skin

A

Thick epithelial layer, followed by an interstitial layer between epithelial cells and vasculature which is full of immune cells (mast cells and macrophages)
- vasculature contains white blood cells

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16
Q

How can increased permeability be dangerous?

A

Loss of fluid from blood, reduces volume of blood

particularly dangerous in severe burns where there is a large inflamed area

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17
Q

Which immune cells are important in the initial phase of immune cell recruitment?

A

Those capable of phagocytosis

predominantly neutrophils but also macrophages

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18
Q

Describe how the immune cells are recruited.

A

Chemokines produced by activated macrophages at the site of inflammation or help me signals from injured cells called DAMPS, these will diffuse out to form a gradient
Leukocytes ie neutrophils expressing complementary receptors will be attracted and thus migrate to the chemokine source.

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19
Q

What type of cells will an IL-8 chemokine attract?

A

Neutrophils expressing the CXCR1 and CXCR2 receptors

20
Q

Name the four basic steps to neutrophil extravasation.

A
  1. Chemo-attraction
  2. Neutrophil rolling
  3. Tight adhesion
  4. Transmigration (diapedesis)
21
Q

Explain chemo-attraction

A
  1. Chemo-attraction: cytokines at inflammation site will lead to upregulation of adhesion molecules (selectins P and E) on endothelial surface
22
Q

Explain neutrophil rolling

A 
Carbohydrate ligands (integrins ie PSGL1) in a low afinity state on neutrophils bind to selectins on the endothelial surface and undergo rolling adhesion
This is slowed by sialyl lewis X on neutrophils which bind to selectin
23
Q

Explain tight adhesion

A

Chemokines promote switching of integrins on neutrophil to a high affinity state (LFA1 to ICAM1)
This promotes a stronger binding to ligands (ICAM-1) on endothelium

24
Q

Explain transmigration

A

Transmigration of the neutrophil through the endothelium wall involves the cytoskeletal re-arrangement and extension of membrane pseudopodia
eventually movement directly into the interstitial mediated by PECAM molecules

25
Q

What is the function of neutrophils at the site of inflammation?

A
  1. Recognise pathogens and necrotic tissue - use of receptors to identify LPS present in bacteria
  2. Pathogen clearance by phagocytosis and netosis
  3. cytokine secretion for recruitment and activation of other immune cells
26
Q

Describe how neutrophils recognize pathogens and necrotic tissue

A

Toll-like receptors for certain microbial products such as endotoxin
G-protein coupled receptors for certain bacterial peptides (N-formylmethionyl residues)

27
Q

Describe how neutrophils clear the pathogen

A

By phagocytosis

  • Attachment of phagocyte which engulfs the pathogen (phagosome)
  • formation of phagocytic vacuole which joins to a lysosome forming a phagolysosome
  • degradation by reactive oxygen species, neutrophils (myleoperoxidase), lysosome, antimicrobial peptides
28
Q

What are the four ways to resolution of the acute inflammatory response?

A
  1. The cause of inflammation is removed
  2. Macrophages release anti-inflammatory mediators ie lipoxins and clear apoptotic cells
  3. Inflammatory mediates and neutrophils have a short half life
  4. Repair/wound healing
29
Q

Describe what is meant by chronic inflammation

A

Inflammation of prolonged duration in which inflammation, tissue injury and attempts at tissue repair coexist

30
Q

What is the time period for chronic inflammation

A

months to years

31
Q

What are the main ways chronic inflammation can arise?

A
  • Follows acute inflammation
  • low-grade smouldering inflammation (acute inflammation that never resolves)
  • Persistent infection
  • Prolonged exposure to toxins - either endogenous or exogenous
  • autoimmunity (rheumatoid arthritis)
  • Foreign body (silica)
31
Q

What are the main ways chronic inflammation can arise?

A
  • Follows acute inflammation
  • low-grade smouldering inflammation (acute inflammation that never resolves)
  • Persistent infection
  • Prolonged exposure to toxins - either endogenous or exogenous
32
Q

What are the key features of chronic inflammation?

A

Lots of T cells and other lymphocytes aswell as a lot of antibody producing B cells
Inflammatory macrophages
No clearance of inflammatory agent, nearby tissue is damaged
concurrent repair processes - fibrosis and angiogenesis

33
Q

Define what granulomatous inflammation is and give an example of where it is seen.

A

Distinct pattern of chronic inflammation showing granuloma formation
Seen in TB

34
Q

What is a granuloma and what is it triggered by?

A

Aggregate of activated macrophages, in an attempt to eliminate a resistant offending agent
Triggered by strong and specific T-lymphocyte reaction

35
Q

Describe the histological features of granulomatous inflammation

A

As the macrophages aggregate they form giant multi-nucleated cells with horse-shoe shaped nuclei
Swirl in centre and giant cells aggregate trying to clear something

36
Q

What can cause granulomatous inflammation?

A

infections like TB, Leprosy
Foreign body granuloma
Tumour reactions
Granulomatous diseases ie Sarcoidosis, Crohn’s disease
Suture material - suture granulomas common

37
Q

Compare acute inflammation to chronic inflammation

A

Time: acute immediate onset, chronic is delayed
Key lymphocyte: acute neutrophils, chronic monocytes/macrophages
Key mediator: acute histamine release, chronic ongoing cytokine release
acute=necrosis=complete resolution/progression to chronic
chronic=scarring=scarring and loss of function

38
Q

How do key cellular and molecular processes differ in acute and chronic inflammation?

A 
Acute = Vasodilation, increased vascular permeability, leukocyte response
Chronic = Persistent inflammation, ongoing tissue injury, attempts at healing
39
Q

What are the positive outcomes of inflammation?

A

Clears offending agents
Cessation of the inflammatory response
Healing of tissue damage with preservation of integrity and function (resolution)

40
Q

What are the undesireable outcomes of inflammation?

A

Excessive tissue damage and scarring - can have detrimental effects on adjacent tissue
systemic involvement with multi-organ failure due to septic shock (loss of fluid in a part of the body) or amyloid (binding of compounds to form abnormal proteins)

41
Q

What are the two ways in which wounds heal?

A

Resolution or scarring

42
Q

Describe healing by resolution

A

Resolution involves regeneration of parenchymal (functional cells) cells with restoration of function
Only occurs if tissue can regenerate and there is little structural damage
Skin and liver can regenerate

43
Q

Describe healing by scarring

A

Repair by scarring involves angiogenesis, migration and repair of fibroblasts, scar formation and connective tissue remodelling- molecules seal the piece of injured tissues from the external environment
Occurs when there is significant tissue loss and tissue is unable to regenerate; results in loss of function

44
Q

When may scars form in response to acute injury, and what are the consequences of these scars

A

Deep woundsor MI
Parenchymal cell death occurs
Fibrous scar tissue contracts as it matures
If scarring occurs across a joint it can cause poor joint mobility.
Impaired functione.g. fibrous scars in the myocardium after a hear attack, this will impair heart function and may lead to heart failure.

45
Q

What are the positives and negatives of macrophages in inflammation

A 
Positives:
phagocytic so clears apoptotic cell bodies 
Cytotoxic 
Can be Anti-inflammatory (IL-10)
Wound repair
Negative:
Cytotoxic 
Can be inflammatory 
Pro-fibrotic
46
Q

What do macrophages do?

A

Can be recruited as monocytes to the site of inflammation but also form tissue resident

POM (42 decks)

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