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PCM1 Exam 1 > GP 09 - Chronic Inflammation > Flashcards

GP 09 - Chronic Inflammation Flashcards

1
Q

What are the key features of chronic inflammation?

A
  1. Infiltration with mononuclear cells
  2. Tissue destruction
  3. Attempted healing with new vessel formation and fibrosis
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2
Q

What are the cells of chronic inflammation?

A
  • Macrophages
  • Lymphocytes
  • Others
    • eosinophils
    • mast cells
    • some neutrophils
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3
Q

What are the different forms of macrophages found during chronic inflammation? What term is used to describe all of these forms?

A
  • Monocytes
  • Resident tissue macrophages
  • Free macrophages
  • Epithelioid cells
  • Gian cells

All together, these compromise the mononuclear phagocytic system.

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4
Q

Briefly describe the formation and differentiation of macrophages.

A
  1. Myeloid progenitor in the bone marrow becomes a monoblast
  2. Monoblast becomes monocyte as it enters the blood
  3. Once in the tissues, a monocyte becomes a macrophage
    • Microglia (CNS)
    • Kupffer Cell (liver)
    • Alveolar Macrophage (lung)
    • Osteoclast (bone)
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5
Q

What is this? Where is this?

A

Monocyte in the blood

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6
Q

What is an epithelioid cell? How do you spot it on a micrograph? What is its function?

A
  • It is a form of activated macrophage
  • They have abundant cytoplasm and resemble epithelial cells
  • They have some phagocytic activity but function primarily as secretory cells
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7
Q
A

Epithelioid cells

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8
Q

What are giant cells?

A

Activated macrophages that have fused together. They are multinculeated cells and are named based on the arrangement of their nuclei:

  • Langhans Giant Cells have a U-shaped nucleus
  • Foreign Body Giant Cells have randomly arranged nuclei
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9
Q
A

Langhans Giant Cells

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10
Q
A

Foreign Body Giant Cells

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11
Q

What are the basic roles of macrophages in chronic inflammation?

A

Contribute in inflammatory reactions by secreting cytokines and growth factors which:

  • Destroy foreign invaders with collateral tissue damage
  • Activate other inflammatory cells
  • Promote angiogenesis by activating fibroblasts and stimulating collagen synthesis
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12
Q

Describe the classically activated macrophage pathway.

A
  • Macrophage becomes activated by microbe products or interferon gamma (IFN-γ). This is called M1 activation
  • Macrophage phagosytoses and destroys microbes/dead tissues utilizing ROS, NO, and lysosomal enzymes
  • Macrophage releases IL-1, IL-12, IL-23, and chemokines to promote inflammation
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13
Q

Describe the alternatively activated macrophage pathway.

A
  • Macrophage is activated by IL-13 and IL-4. This is called M2 activation
  • Macrophage releases growth factors, most notably transforming growth factor beta, TGF-ß, to promote tissue repair and fibrosis
  • Macrophage releases IL-10 and TGF-ß which will have anti-inflammatory effects
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14
Q

What is happening in this tissue? What is each arrow pointing to?

A

Chronic Inflammation

Red Arrow - Foreign Body Giant Cell

Blue Arrow - Lymphocytes

Green Arrow - Neutrophil

Orange Arrow - Epithelioid Cells

Yellow Arrow - Plasma Cells

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15
Q

List the lymphocytes important to chronic inflammation. What are their key roles in chronic inflammation?

A
  • Helper T Cells
    • THI1 cells produce IFN-γ which cause M1 activation
    • TH2 cells produce IL-4, IL-5, and IL-13 which recruit eosinophils and cause M2 activation
    • TH17 cells produce IL-17 which recruits neutrophils
  • Cytotoxic T cells, when activated, release perforins and granzymes that will initiate cell death in microbes
  • Plasma Cells - antibody secretion
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16
Q

Why do eosinophils stain red? For what types of infections are these cells most important?

A

They contain major basic protein in their granules which bind eosin strongly

They play an important role in parasitic infections and allergic reaction.

17
Q
A

Eosinophil

18
Q

Describe why mast cells can be important to chronic inflammation.

A

They have IgE surface receptors that, when bound, can cause the cell to release hitamine and prostaglandins

They play a role in allergic reactions to food, insect venom, and drugs

19
Q

What is granulomatous inflammation?

A

A form of chronic inflammation where the cells are attempting to contain an offending agent that is difficult to eradicate. The cell types presents are:

  • Activated Macrophages
    • Epithelioid cells
    • Giant Cells
  • T-lymphocytes

Sometimes central necrosis is present

20
Q

What is this?

A

A granuloma

21
Q

What is this?

A

A Granuloma

22
Q

What are the most common causes of granulomatous inflammation that we need to know?

A
  • Tuberculosis (mycobacterium tuberculosis)
  • Leprosy (mycobacterium leprae)
  • Syphilis (treponema pallidum)
  • Cat scratch disease (bartonella sp.)
  • Indigestible Material (talcosis and berylliosis)
  • Idiopathic (sarcoidosis, Crohn’s disease)
23
Q

What is this?

A

A Caseous Granuloma

24
Q

What are the most common morphological features of chronic inflammation?

A
  • Fistula Formation (connection between two epithelial sufaces)
  • Sinus Formation (connection between a granulomatous cavity and an epithelial surface)
  • Chronic Ulcer (abnormal discontinuity or break in a biological membrane)
  • Chronic Abscess
  • Thickening of a hollow viscus
  • Stricture formation (wall thickening that narrows a lumen)
25
Q

What are the systemic effects of inflammation and what causes them?

A
  • Fever - increased body temp by 1-4 C. Caused by pyrogens but mechanism is unknown
  • Leukocytosis - increased WBC count up to 15000-20000 cells/mL. Sometimes a leukemoid reaction (40000-100000 cells/mL) can occur. Caused by increased [cytokine]
  • Acute phase response - decerase in liver synthesis of albumin and an increase in synthesis of acute phase proteins - CRP, serum amyloid A (SAA), fibrinogen. Caused by increased release of IL-1, IL-8, and TNF
  • Other Manifestation - increasted HR & BP, chills, rigor, decreased or increased sweating, lethargy, sepsis, and/or septic shock
26
Q

What are the primary outcomes of chronic inflammation?

A
  • Healing by fibrosis
    • Fibroblast proliferation and activation leads to increased ECM production which occupies the space where parenchyma once was
  • Lack of resolution with persistence of inflammatory process
    • Metaplasia to Dysplasia to Neoplasm
    • Amyloidosis from prolonged production of SAAs
  • Loss of function
    • ECM changes normal mix of ECF proteins
    • Fibrosis alters the function of the area
27
Q

List the cardinal signs of inflammation and give their pathogeneses.

A
  • Redness & Hotness - vasodilation
  • Swelling - edema nd cell infiltrates
  • Pain - direct stimulation of nociceptors by K+, bradykinin, PGs, and Substance P
  • Tenderness - decreased nociceptor threshold caused by IL-1, IL-6, IL-8, & TNFα, and increased tension (from swelling, abscess, etc.)
  • Loss of function - lack of resolution in chronic inflammation

PCM1 Exam 1 (40 decks)

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