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Life Sciences - Sem 2 > 0.5 Chronic Inflammation > Flashcards

0.5 Chronic Inflammation Flashcards

1
Q

What is chronic inflammation?

A

A delayed, prolonged response to injury or infection

Continuous destruction and repair of normal tissue is ALWAYS seen

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2
Q

How can chronic inflammation be characterised?

A

Most common = presence of many macrophages + lymphocytes in affected tissues

Less common = presence of many neutrophils

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3
Q

What are the 3 causes of chronic inflamamtion?

A
  1. Persistent infections ie resistant pathogens or mycobacteria/viruses etc
  2. Hypersensitivity diseases ie autoimmune or allergic
  3. Prolonged exposure to exogenous/endogenous agents ie silica or cholesterol
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4
Q

How do persistent infections lead to granulomatous inflammation?

A
  1. Difficult to eradicate due to location/virulence fof agent eg periapical periodontitis
  2. Unresolved acute inflammation evolves into chronic inflammation
  3. Inflammatory response takes on a specific pattern called granulomatous inflammation
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5
Q

What are the 3 patterns of chronic inflammation?

A
  1. Granulomatous = macrophages predominate
  2. Suppuration = chronic pus formation
  3. Mixed / diffuse
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6
Q

What are the key characteristics of granulomatous inflammation?

A
  1. Characterised by accumulation of macrophages and T-cells into a ball (granuloma)
  2. Sometimes with central necorsis (eg TB cases)
  3. Cellular attempt to CONTAIN an offending agent that is difficult to eradicate
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7
Q

Macrophages may undergo changes in granulomatous inflammation. What are these changes?

A
  1. Differentiate = develop abundant cytoplasm and resemble epithelial cells (become epithelioid cells)
  2. Fuse = form multinucleated GIANT CELL (langhans cells)
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8
Q

What is the difference between granulation tissue and a granuloma?

A

Granulation tissue = newly formed tissue involved in healing damaged tissues via fibrosis, contains amcrophages, blood vessels, and fibroblasts

Granuloma = nodular inflammatory lesion predominantly containing macrophages, lymphocytes, and fibroblasts, which forms in response to persistent irritant

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9
Q

What are the three types of chronic granulomatous inflammation?

A
  1. Immune (eg TB)
  2. Foreign body (eg older surgical sutures)
  3. Unknown origin (eg sarcoidosis)
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10
Q

What is the cell progression in the formation of a granuloma?

A
  1. Monocyte (rolls, adheres, squeezes into ECM) and differntiate into macrophages
  2. Some macrophages differentiate into epithelioid cell
  3. Epitheloid cells combine into giant cells
  4. Sphere forms around giant cell with lymphocytes enclosed by fibroblasts
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11
Q

What are the two key roles of a granuloma?

A
  1. To contain a microorganism / irritant in order to prevent its dissemination
  2. To focus immune response against the initiating factor
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12
Q

What impacts do TNF and anti-TNF have on inflammation?

A

TNF = important in macrophage activatino + priamry signal for granuloma formation

Anti-TNF = neutralises TNF cytokine, interfering with granuloma formation and/or compromises its stability or structure

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13
Q

What are the 5 steps behind granuloma formation?

A
  1. Certain bacteria, fungi, and foreign particles are unable to be killed/digested by phagocytes = incites agents
  2. Chemokines regulate the recruitment of monocytes
  3. Cytokines + monocytes = differentiation of macrophages into epitheliod cells
  4. Cytokines + epithelioid cells = fusion into giant cells
  5. Growth factors + giant cells = recruitment of fibroblasts and formation of fibrous tissue
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14
Q

What are the two morphologies of giant cells?

A
  1. Foreign body giant cell
  2. Langhans giant cell
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15
Q

What are the 3 characteristics of a foreign body giant cell?

A
  1. Collection of fused macrophages
  2. Nuclei overlap and are disorganised
  3. Present in response to a large foreign body eg impants + amalgam tattoos
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16
Q

What are the 3 characteristics of Langhans giant cells?

A
  1. Formed by fusion of epithelioid cells
  2. Nuclei arranged in a horseshoe shape pattern in the cell periphery
  3. Found in nearly every form of granulomatous diseaseeg TB, sarcoidosis, syphilis
17
Q

What is tuberculosis?

A

Granulomas with necrosis

Caseous necrosis = TB always

18
Q

What are examples of hypersensitivity diseases, and how do they cause chronic inflammation?

A
  1. Autoimmune diseases (rheumatoid arthritis, MS, rheumatic heart disease)

Auto-antigens evoke a perpetuating immune response that causes chronic inflamamtion + tissue damage

  1. Allergic diseases

Common environmental substances trigger an excessive immune response causing chronic inflammation

19
Q

Prolonged exposure to exogenous and endogenous agents can cause chronic inflammation, depending on concentration and duration of exposure. What are examples of such exogenous and endogenous agents?

A

Exogenous agents = silica (inhaled for long periods = inflamamtory lung disease aka silicosis

Endogenous agents = cholesterol (excessive production and tissue deposition in arterial wall aka atherosclerosis)

20
Q

What are examples of non-conventional inflammatory diseases?

A
  1. Alzheimer’s disease
  2. Metabolic syndrome
  3. Tyep II diabetes
  4. Tumour development
21
Q

What are the two key mediators of chronic inflammation?

A
  1. Macrophages
  2. Lymphocytes
22
Q

Macrophages are the dominant cell type during chronic inflammation and persistent infections. What roles do they play?

A
  1. Destroy invaders directly via phagocytosis
  2. Secret cytokines and growth factors to activate T-lymphocytes
23
Q

What are the characteristics of classically activated macrophages (M1)?

A

Strongly pro-inflammatory = secretes cytokines that stimulate inflammation

Induced by microbial products (endotoxins) which engage TLRs and by IFN-y

Produce NO and ROS species to enhance killing of ingested organisms

24
Q

What are the characteristics of alternatively activated macrophages (M2)?

A

Induced by cytokines produced from T-cells etc

Not microbial, but aid tissue repair

Secrete growth factors to promote angiogenesis, activate fibroblasts, and stimulate fibrosis

25
Q

What are the key differences between classically activated macrophages (M1) and alternatively activated macrophages (M2)?

A

M1 = microbicidal actions + phagocytosis works to kill bacteria and fungi

M2 = Anti-inflammatory effects + wound repair via fibrosis

26
Q

In most circumstances, macrophages disappear when the irritant and subequent inflammatory response is eliminated. What is the pathophysiology when macrophage accumulation persists?

A

Result of continuous recruitment and proliferation at site of inflammation

Excessive tissue damage occurs via ROS species + increased fibrosis

27
Q

Lymphocytes are the predominant population in chronic inflammation caused from autoimmune and other hypersensitive diseases. What role do they play?

A

Microbes + other environmental antigens activate T and B lymphocytes, which amplify and propagate chronic inflammation

Once activated, inflammation tends to be persistent and severe

Granulomatous inflammation is dependent upon lymphocyte responses

28
Q

T-cells amplify reactions included by the early acute inflammatory response. What are some of the crucial subsets of T-cells and what do they do?

A

Th1 = (IFN-y) activates amcrophages by the classical pathway

Th2 = recruit and activate eosinophils and are responsible for the alternative pathway of macrophage activation

Th17 = (IL-17 + cytokines) induce secretion of chemokines responsible for recruiting neutrophils locally

28
Q

What are the key differences between Th1 + Th17 cells compared to Th2 cells?

A

Th1 + Th17 = defence against bacteria, viruses, and autoimmune diseases

Th2 = defence against helminth parasites and allergic inflammation

29
Q

What is the role of eosinophils in chronic inflammation?

A

Abundant during parasitic infections and mediate IgE effects

Contain major basic protein, toxic to parasites but also to host epithelial cells

30
Q

What is the role of mast cells in chronic inflammation?

A

Express IgE receptors and degranulate to release histamine prostaglandins

Typically respond during allergic reactions

Promote inflammation via the plethora of cytokines they produce

31
Q

What is a typical emigration pattern during inflammation?

A
  1. PMNs are the predominate cell
  2. Monocytes emigrate to become macrophages (new predominate cell)
  3. As the amount of macrophages start to decrease, the amount of lymphocytes increase
  4. Lymphocytes emigrate to contribute to immune response and fades out shortly after macrophages fully disappear from site
32
Q

What is osteomyelitis?

A

Inflammation or swelling that occurs in the bone

33
Q

What is the progression of osteomyelitis?

A
  1. Bacteria enter bone canaliculi
  2. Necrosis of osteocytes/bone
  3. PMN + other antimicrobials unable to penetrate into osteocytic canaliculi or lacunae
  4. Ensuing inflammation leads to bone destruction
  5. Constant re-infection of tissue from infected necrotic bone
  6. Hard to treat / recover from
34
Q

What is protective against osteomyelitis?

A

Bone resorption with formation of granulation tissue

35
Q

What are the key characteristics of mixed/difuse chronic inflammation patterns?

A

Mixed inflammatory infiltrate of PMN, macrophages, lyphocytes, plasma cells

Usually specific immune responses

Often has chronic inflammatory granulation tissue with fibrosis

May undergo acute flare ups

36
Q

What is an example of mixed type chronic inflammation?

A

Rheumatoid arthritis
- Neutrophils in synovial fluid
- Lymphocytes and macrophages in pannus

Life Sciences - Sem 2 (27 decks)

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