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Pathoma > Chapter 2.2 Chronic Inflammation > Flashcards

Chapter 2.2 Chronic Inflammation Flashcards

1
Q

How is chronic inflammation characterized?

Are cells mononuclear or multilobar nucleated? Describe.

A

lymphocytes and plasma cells (nuclei off to edge of cell, glossy clearing) in tissue

-mononuclear

(delayed response, but more specific; adapative immunity)

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2
Q

List some stimuli for chronic inflammation.

A

persistent infection (most common)

infection with viruses, mycobacteria, parasites, fungi

autoimmune disease

foreign material

some cancers

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3
Q

Where are T lymphocytes produced?

A

prod. in bone marrow as progenitor T cells

further develop thymus (TCR undergoes rearrangement and progenitor cells become CD4+ helper T cells or CD8+ cytotoxic T cells)

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4
Q

How do T cells detect antigen?

A

T cells use TCR complex for antigen surveillance (CD3 is a part of this TCR)

TCR complex only recognizes antigens presented on MHC

CD4 T cells- MHC II
CD8 T cells- MHC I

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5
Q

How are T cells activated?

A

1) binding of antigen and MHC complex

2) additional 2nd signal (B7 on APC binds CD28 on CD4+ T cell)

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6
Q

How are CD4+ T cells activated?

A

extracellular antigen is phagocytosed, processed, and presented via MHC class II (APC - DC or macrophages)

B7 on APC binds CD28 on CD4+ T cells providing 2nd activation signal

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7
Q

What do activated CD4 do?

A

secrete cytokines that “help” inflammation (can help B cells, or CD8+ T cells)

divided into two subsets (Th1 or Th2)

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8
Q

Describe Th1 subset of CD4+ T cells.

A

helps CD8+ T cells by generating IL-2 (T cell growth factor and CD+ T cell activator)

IFN-gamma (macrophage activator)

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9
Q

Describe Th2 subset of CD4+ T cells.

A

helps B cells

IL-4 (class switching from IgG to IgE)

IL-5 (eosinophil chemotaxis and activation, maturation of B cells to plasma cells, and class switching to IgA

IL-10 (inhibits Th1 phenotype) … (macrophages can prod IL-10 to shut down inflammatory response too)

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10
Q

How are CD8+ T cell activated?

A

Intracellular antigen is processed and presented on MHC I (sampling of protein being prod in cell is loaded on MHC I and allows CD8+ T cell to determine if foreign protein prod. in a cell)

(second signal:)
IL-2 from CD4+ Th1 cell provides 2nd activation signal

cytotoxic T cells are activated for killing

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11
Q

Describe the mechanism of cytotoxic killing.

A

secretion of perforins and granzyme; induce apoptosis of the target cell (granzyme will activate CASPASE)

expression of FasL, binds Fas on target cell activating apoptosis

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12
Q

What are the three pathways by which apoptosis is activated?

A

1) intrinsic mitochondrial pathway (driven by cytochrome c leaking out of mitochondria and activating caspaces
2) extrinsic receptor pathway (TNF binding cells, FasL)
3) CD8+ T cell dumping granzyme which activates caspases which activate apoptosis

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13
Q

Where are B lymphocytes produced? Distinguish between immature B cells and naive B cells.

A
  • produced in bone marrow

- undergo Ig rearrangement to become naive B cells that express IgM and IgD

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14
Q

How are B cells activated? 2 ways

A

antigen binding by surface IgM or IgD

B cell antigen presentation to CD4+ helper T cell via MHC II

CD40 receptor on B cell binds CD40L on helper T cell providing 2nd activation signal

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15
Q

What does activation of Helper T cell result in?

A

Helper T cell then secretes IL-4 and IL-5 (mediate B cell isotype switching, hypermutation, and maturation to plasma cells)

plasma cells now can secrete IgG, IgE, IgA (starts with IgM or IgD… to go beyond that it must undergo this reaction from Helper T cell)

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16
Q

What is granulomatous inflammation?

A

subtype of chronic inflammation

characterized by granuloma

17
Q

What is the key characteristic that defines a granuloma?

A 
epitheloid histiocytes (macrophages with abundant pink cytoplasm)
...aggregate of these histiocytes= granuloma

(macrophages usually have clear cytoplasm)

18
Q

What is the defining feature of a granuloma?

What other things CAN be seen?

A

defining feature: epitheloid histiocytes (macrophages with abundant pink cytoplasm)

can be surrounded by giant cells and rim of lymphocytes

19
Q

How can you distinguish noncaseating vs caseating granulomas?

A

noncaseating granulomas lack central necrosis

20
Q

Patient has history of breast cancer and breast is removed, she gets implants, she feels lymph nodes in axilla. What is the differential diagnosis?

A

reaction of foreign material: implants leak and release foreign material in lymphatics and go into axillary lymph node and produce enlarged lymph nodes within axilla (which then is creating granulomas)

or recurrence of breast cancer or spread and now involves axilla

so biopsy could show noncaseating granuloma or cancer

21
Q

What is the defining feature of sarcoidosis?

A

production of noncaseating granulomas in multiple tissues throughout body in particular the lung

22
Q

What can Beryllium exposure lead to?

A

can cause formation of noncaseating granulomas

23
Q

What is histological mark of Crohn’s disease?

Ulcerative colitis?

A

noncaseating granulomas

crypt abscesses (at bottom of crypt you get neutrophils..)

24
Q

What does Cat scratch disease give you?

A

a stellate formed granuloma (noncaseating)

25
Q

What is key differential diagnosis for caseating granuloma?

A

TB and fungal infections

can do AFB stain to look for TB

can do GMS (silver) stain to look for fungus

26
Q

What are the steps involved in granuloma formation?

A

macrophages find antigen and present antigen via MHC II to CD4 Th1 helper T cells

(when that interaction occurs macrophages then secrete IL-12 and induce CD4+ T cells to Th1 subtype)

Th1 helper cells then secrete IFN-gamma which converts macrophages to epithelioid histiocytes and giant cells

27
Q

What step occurs in both caseating and non caseating granulomas?

A

IL-12 step

macrophages find antigen and present antigen via MHC II to CD4 Th1 helper T cells

(when that interaction occurs macrophages then secrete IL-12 and induce CD4+ T cells to Th1 subtype

Pathoma (23 decks)

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