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Pathology Yr1 > Chronic inflammation > Flashcards

Chronic inflammation Flashcards

1
Q

What does the stimulus do, that causes chronic inflammation to begin?

A

Prolonged inflammation (weeks-months) due to persistence of the stimulus

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2
Q

What are the 3 main cell types involved in chronic inflammation?

A

Macrophages

Lymphocytes

Plasma cells

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3
Q

Why is chronic inflammation more specific than acute inflammation?

A

Involves adaptive immune system

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4
Q

What are the 5 most common causes of chronic inflammation?

A

Excessive allergic reaction

Autoimmune disease

Persistent infection that is hard to eradicate

Foreign material eg. blocks hair follicle and causes hair to grow in foreign compartment

Carcinoma

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5
Q

Why can carcinoma cause chronic inflammation?

A

Immune response due to abnormal proteins in tumour cells

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6
Q

What is the main and most dominant cell type, that regulates chronic inflammation?

A

Macrophage

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7
Q

Give 6 body areas where macrophages reside?

A

Connective tissue

Kupffer cells: liver resident macrophages

Spleen

Sinus histiocytes: lymph nodes resident macrophages

Microglia: CNS resident macrophages

Alveolar macrophages: lung resident macrophages

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8
Q

What are the 3 characteristic microscopic findings of macrophages?

A

Lots of cytoplasm

Foreign material granules

Phagocytic vacuoles

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9
Q

In chronic inflammation, which macrophage subtype stimulates inflammation?

A

M1

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10
Q

In chronic inflammation, which macrophage subtype stimulates repair/healing?

A

M2

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11
Q

What 2 substances stimulate M1 macrophages to cause chronic inflammation?

A

Bacteria

Interferon gamma produced by T cells

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12
Q

When M1 macrophages have be recruited in chronic inflammation, what is their primary and initial role?

A

To present antigens

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13
Q

What 2 substances stimulate M2 macrophages to cause repair after chronic inflammation?

A

IL-13

IL-14

Both are produced by T cells

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14
Q

When M2 macrophages have be recruited in chronic inflammation, what is their primary and initial role?

A

To build ECM

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15
Q

Apart from chronic inflammation, lymphocytes are the dominant population in which 2 types of conditions?

A

Autoimmune diseases

Hypersensitivity diseases

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16
Q

What is the difference between T and B lymphocytes, in terms of where they mature?

A

T-cells mature in thymus, B-cells mature in bone marrow

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17
Q

In the thymus, what 2 cell subtypes do progenitor T lymphocytes mature into?

A

CD4+ helper T-cells

CD8+ cytotoxic T-cells

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18
Q

How is the T-receptor complex formed, what is its main role and how is it activated?

A

Combination of CD3 antigen and T-receptor

Used by T cells to recognises antigen-bound MHC molecules (the first signal)

Needs second signal to be activated

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19
Q

What is the first signal to activate CD4+ T helper cells, in chronic inflammation?

A

Foreign materials processed, fragments bound to MHC II, complex is presented on outside of APC cell membrane

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20
Q

What is the second and final signal to activate CD4+ T helper cells?

A

T-cell receptor complex binds to presented antigen on MHC II, CD28 from T-cell binds to B7 from APC

This provides second signal

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21
Q

When CD4+ TH-1 cells are activated, what is their main role?

A

Secrete interferon gamma to stimulate M1 macrophages

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22
Q

When CD4+ TH-2 cells are activated, what is their main role?

A

Recruit eosinophils so that B-cells are stimulated to produce IgE (eg. in allergy)

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23
Q

What is the first signal to activate CD8+ T cytotoxic cells, in chronic inflammation?

A

Intracellular antigens processed, fragments bound to MHC I, complex is presented on APC cell membrane

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24
Q

What cell types express MHC I?

A

All nucleated cells and platelets

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25
Q

How does the CD8+ cytotoxic T cell bind to the APC?

A

Cytotoxic T-cell receptor with CD8 co-receptor binds to antigen-MHC I complex

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26
Q

What is the second and final signal to activate CD8+ T cytotoxic cells?

A

TH-1 CD4+ cells produce IL-2, which provides second activation signal

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27
Q

What are the 2 killing methods of CD8+ cytotoxic T cells?

A

Perforin and granzyme secretion: Perforin creates pores for granzymes to enter target cell

Binding of FAS ligand to FAS on target cell: Apoptosis of target cell

28
Q

How do B lymphocytes become naive B cells in chronic inflammation?

A

Undergo immunoglobulin gene arrangement to become naive B-cells which express IgD and IgM

29
Q

What triggers the conversion of naive B cells into mature plasma cells, in chronic inflammation?

A

Antigen binds to IgD or IgM (which are both expressed by naive B cells)

Triggers maturation of naive B-cell into IgD or IgM-secreting plasma cell

30
Q

How is the plasma cell activated by T helper cells in chronic inflammation, to start secreting antibodies?

A

CD40 receptor on B-cell binds to CD40 ligand on helper T-cell

31
Q

What determines whether a mature plasma cell will secrete IgM or IgD antibodies, in chronic inflammation?

A

Cytokines which are present determine the class of immunoglobulin which the B-cell will produce

32
Q

What form of chronic inflammation is used for pathogens that are hard to eradicate?

A

Granulomatous inflammation

33
Q

What cell type makes up a granuloma?

A

Epithelioid histiocytes (resembles epithelial cells but there are actually no epithelial cells, just plump macrophages)

34
Q

Are granulomas caseating or noncaseating?

A

Can be either

35
Q

Give 5 examples of conditions that can activate granulomatous inflammation?

A

Sarcoidosis,

Crohn’s disease,

Cat scratch disease,

mycobacterial infection,

fungal infection

36
Q

If the granulomatous inflammation occurs due to a foreign material, is the granuloma more likely to be caseous or noncaseous?

A

Noncaseous

37
Q

What is the role of interferon gamma in formation of caseating granulomas, and where does the interferon gamma come from?

A

TH-1 CD4+ cells secrete interferon gamma

interferon gamma converts macrophages into epithelioid histiocytes and giant cells

38
Q

Do all types of tissue have the same ability to repair and heal wounds?

A

No, each tissue has different regenerative capacity

Ability of tissue to repair depends on type of tissue that is damaged

39
Q

What is the regenerative capacity of labile tissue, and give 3 examples of labile tissue?

A

Contains stem cells so can heal

eg. Skin, bowel lining, bone marrow

40
Q

What is the regenerative capacity of stable tissue, and give an example of stable tissue?

A

Normally quiescent but can regenerate if the need arises

eg. Liver

41
Q

What is the regenerative capacity of permanent tissue, and give 3 examples of permanent tissue?

A

Lack significant regenerative potential so needs to be repaired if damaged

eg. myocardium, skeletal muscle and neurons

42
Q

What are the 4 phases of wound healing?

A

Coagulation phase

Inflammatory phase

Proliferative phase

Remodeling phase

43
Q

What is the main regulatory system that initiates the coagulation phase of wound healing, and what is it activated by?

A

Clotting system activated by hageman factor

44
Q

In the inflammatory phase of wound healing, what do platelets do?

A

Platelets congregate and degranulate, release platelet derived growth factor

45
Q

In the inflammatory phase of wound healing, what 2 cell types regulate inflammation?

A

Neutrophils: Acute

Macrophages: Chronic

46
Q

In the proliferative phase of wound healing, which 3 cell types produce growth factors and what is their purpose?

A

Damaged epithelial cells, platelets, macrophages

Growth factors cause new vessels to grow into wound

47
Q

In the proliferative phase of wound healing, what 2 new tissues form?

A

Granulation tissue

Scar tissue

48
Q

In granulation tissue during the proliferative phase of wound healing, what cells does it contain apart from new blood vessels and what are their roles?

A

Fibroblasts: deposits type III collagen (stretchy, pliable)

Myofibroblasts: causes wound contraction as they have actin in cytoplasm

49
Q

In scar tissue during the proliferative phase of wound healing, what 2 layers does it have?

A

Top: Granulation tissue layer

Bottom: Predominantly fibroblast layer with type I collagen

50
Q

In scar tissue during the proliferative phase of wound healing, what type of collagen is in the fibroblast layer and how is it formed?

A

Type I collagen

Breakdown of type III collagen by collagenase with zinc cofactor produces type I collagen

51
Q

In the remodeling phase of wound healing, what 2 steps lead to the formation of an acellular scar?

A
  1. myofibroblasts begin to remodel the extracellular matrix
  2. myofibroblasts undergo apoptosis leading to the formation of an acellular scar
52
Q

What is the importance of platelet derived growth factor in wound healing?

A

Causes new vessels to grow and help scars to form

53
Q

What is the importance of TGF-beta in wound healing, and what cell type secretes it?

A

Secreted by macrophages

Stops inflammation and causes fibroblasts to proliferate

54
Q

Why can lack of vitamin C cause delayed wound healing?

A

Vitamin C is needed for collagen cross-linking

55
Q

Why can lack of copper cause delayed wound healing?

A

Copper is needed for collagen cross-linking

56
Q

Why can lack of zinc cause delayed wound healing?

A

Zinc is a cofactor for the enzyme collagenase, which replaces the type III collagen of granulation tissue with stronger type I collagen

57
Q

Why can diabetes delay wound healing?

A

Diabetes can impair growth factor production

58
Q

What are the 2 types of scars that can form as a result of excess scar tissue?

A

Hypertrophic: confined to area of the wound

Keloid: overgrown wound, not confined to area

59
Q

Where are keloid scars most likely to form, after wound healing?

A

Head and neck, ear lobes, shoulder and chest

60
Q

Which 2 growth factors specifically promote scar formation and vessel growth, in wound healing and repair?

A

Fibroblast growth factor

Vascular endothelial growth factor

61
Q

What is meant by surgical wound healing by primary intention, and what kind of scar does this leave?

A

Wound edges are brought together (suturing)

Minimum scarring

62
Q

What is meant by surgical wound healing by secondary intention, and what kind of scar does this leave?

A

Edges not brought together, so granulation tissue forms in between

Forms scar

63
Q

What is meant by surgical wound healing by tertiary intention?

A

Wound closing is delayed

64
Q

Why is surgical wound healing by tertiary intention used to close infected tissue?

A

Infected tissue needs to be treated with antibiotics first

Once infection has resolved, wound is closed

65
Q

What type of collagen is present in excess in keloid scars?

A

Type III collagen

Pathology Yr1 (20 decks)

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