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Benjamin's Pathology > Chronic Inflammation and Healing > Flashcards

Chronic Inflammation and Healing Flashcards

1
Q

Define Chronic Inflammation

A

Inflammation of prolonged duration (weeks or months) in which active inflammation, tissue destruction and attempts at repair are proceeding simultaneously.

Develop from prolonged exposure to agent e.g. silica, wear particles from prothetic implants

Autoimmune disease states e.g. Rheumatoid arthritis, Crohns, Lupus

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2
Q

What are the causes of chronic inflammation?

A

Can develop from unresolved acture inflammation due to infection, injury e.g. gastritis, osteomyelitis

Develop from prolonged exposure to agent e.g. silica, wear particles from prosthetic implants

Autoimmune disease states e.g. SLE, RA

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3
Q

How long does chronic inflammation last?

A

Will persist until the damagin stimulus is eradicated

If damaging stimulus is eradicated —-> organisation and repair

Ongoing inflammation and tissue damage proceed at the same time as attempts at healing

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4
Q

List 4 (of 7) cells involved in chronic inflammation

A

Macrophages

Lymphocytes

Plasma cells

Mast cells

Fibroblasts

Endothelial cells

Eosinophils

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5
Q

Discuss the Maturation of macrophages.

A

Lifespan of blood monocyte - 1 day

Lifespan of tissue macrophages can be several months or years

Several growth factors, cytokines, adhesion molecules and cellular interactions regulate the conversion from bone marrow stem cell to tissue macrophage.

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6
Q

What is the role of macrophages?

A

Produce chemokines, cytokines and growth factors. These cause:

Cell influx

Fibroblast proliferation

Stimulate growth of blood vessels

Activation and recruitment of lymphocytes

Participate in bacterial and cell killing

Clear extracellular debris, fibrin and other foreign material

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7
Q

What are some advantages to the pagocytotic nature of Macrophages?

A

Increased lysosomal enzymes and ROS which is toxic to microbes

Production of cytokines, growth factors etc.

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8
Q

What are some disadvantages to the pagocytotic nature of Macrophages?

A

Cause dissolution of extracellular material or cells by producing some toxic products (e.g. NO metabolites or proteases)

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9
Q

T and B lymphocytes: Give time length, how they are activated?

A

Many long lived

Some present normally in certain tissues

Antigen activation

Release macrophage activating cytokines (+ve feedback until inflammatory stimulus removed)

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10
Q

What type of immunity are T cells primarily found?

A

Cell mediated immunity

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11
Q

What type of immunity are B cells primarily found?

A

In humoral mediated immunity

Differentiate into plasma cells which produce antibody

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12
Q

What do fibroblasts do?

A

Synthesises collagen (fibrosis) which leads to scar tissue

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13
Q

The process of forming new vessels via endothelial cells is called?

A

Angiogenesis

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14
Q

Eosinophils are primarily involved in what type of infection?

A

Parasitic

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15
Q

What is osteomyelitis?

A

Infection in the bone and marrow

Aetiology
Systemic or local infection
Mycobacteria and pyrogenic bacter common

Complications
Lose regions of bone,
Children - epiphyseal growth disturbance
Epidermoid carcinoma (longer term), septic arthritis

Treatment - antibiotic, surgical debridement

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16
Q

Granulomatous Inflammation: Persistent agent. Define.

A

E.g. peri-implant loosening

Clusters of T cell activated macrophages having engulfed foreign bodies

“Epithelioid” granulomas: resemble squamous cells

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17
Q

Picture before and after Foreign body granuloma
Osteoclast

A
18
Q

Rheumatoid Arthritis: What is it? Where is it? What happens?

A

Local and systemic inflammation

Occurs in the joint

Due to chronic synovitis

Synovial cells hyperplasia and proliferation

Increased vascularity (angiogenesis)

Cell infiltrate: T cells, macrophages, plasma cells

Increased osteoclast number

Pannus invasion

Fibrosis and calcification

19
Q

Crohns disease, name the type of inflammation circled and the cell.

A
20
Q

What is regenerative healing?

A

Tissue replaced with parenchymal tissue. e.g. fracture healing, primary intension

21
Q

What is non-regenerative healing?

A

Healing occurs by replacement with CT scar e.g. MI. Connective scar tissue - replaces dead tissue but not functioning parenchymal cells.

22
Q

What is repair/healing?

A

If severe or chronic tissue injury resulting in both damage to parenchyma and the stromal framework.

Healing cannot be accomplished by regeneration (resolution)

Healing process is repair by deposition of collagen and other ECM components resulting in a scar.

Scar is formed by an intermediary tissue: granulation tissue.

23
Q

What happens if a cell can’t regenerate and is injured? e.g. heart and muscle.

A

Extensive tissue and frameowkr destruction

Tissues cannot regenerate even if they can divide

In this case: Healing is not through resolution of the inflammatory exudate

Insead it is through organization and repair

24
Q

What are the components of Granulation Tissue?

A

New blood vessels (angiogenesis)

Fibroblasts —> Collagen —-> scar

Macrophages and other mononuclear cells clear away dead tissue

25
Q

What is vascular grannulation tissue?

A

Network of newly formed capillaries, macrophages and support cells which replace the area of tissue damage.

1st step

26
Q

What is fibrovascular granulation tissue?

A

Proliferating fibroblasts, capillaries and macrophages.

Second step

27
Q

What is fibrous granulation tissue?

A

Fibroblasts synthesize collagen and align themselves so collagen is deposited in a uniform patter

Contraction frequently occurs, size of damaged area is reduced

28
Q

Which of these is vascular and fibrous

A

Vascular Left

Fibrous R

29
Q

What are the aims of wound healing?

A

To remove damaged tissue

To fill gap caused by tissue destruction

To restore structural continuity of injured part

30
Q

What is secondary intention healing?

A

When there has been more extensive loss of cells and tissue

The reparative process is more complicated

31
Q

Why does a large wound take alot longer to heal?

A

Inflammatory reaction is more intense to carry away the large amounts of necrotic debris and exudate

Much larger amounts of granulation tissue are formed

Greater amount of collagen synthesis to “fill in” damaged area

Wound contraction is more frequent

Scar tissue formation replacing normal tissue

32
Q

What are local factors that influence wound healing?

A

Infection

Mechanical factors

Foreign bodies

Size, location, and type of wound

Vascular supply

Radiation

33
Q

What are systemic factors that influence wound healing?

A

Nutrition - e.g. vitamin C and A, and protein deficiency inhibits collagen synthesis

Metabolic status: diabetes mellitus

Circulatory status : inadequate blood supply

Hormones: glucocorticoids have anti inflammatory effects
Immunosuppression

Age

34
Q

What are the three phases of fracture healing?

A

Reactive

Repair

Remodeling

35
Q

Discuss Haematoma/inflammation

A

Rupture of vessels

Haematoma formation

Inflammatory cell infiltrate

e.g macrophages, leukocytes, platelets

Bone cells die, mesenchymal cells differentiate into osteoblasts

36
Q

Discuss the inflammatory phase and the time within this phase.

A

Granulation tissue/ soft callus

Connective tissue + cartilage = callus

Days - 2 weeks

37
Q

What is the reparative phase and how long does it last?

A

Fourth Phase

Osteoclasts resorb dead bone

Soft callus —> bony callus

OB deposit woven bone

Bone deposited on ends of cortical bone (endochondral ossification)

Callus mineraltion: 4-16 weeks.

38
Q

What is the remodelling phase and how long does it last?

A

Callus replaced with lamellar bone

Osteoclasts and osteoblasts active and in concert

Remodelling 1-4 years

May elminate any evidence of fracture

39
Q

Give the overview of steps in a bone fracture

A

Fracture

Clot formation

Soft callus formation

Bony callus formation

Remodelling

Union

40
Q

Myocardial infarction. Time taken to occur, what happens?

A

Myocardial infarction (12-24 hours) The nuclei fade (karyolysis) >disappear from the cells
- Neutrophils (black arrows- infiltrate the dead myocardium as an acute inflammatory
response. - Most of the myocytes in this field are dead (increased eosinophilia and lack of
nuclei (compare with the few viable cells still present).
- Contraction bands can be seen (green arrows) in the dead myocytes.

Myocardial infarction (48-72 hours)
 neutrophils infiltrating the dead myocardium

Myocardial infarction (one - several weeks).
Fibroblasts and endothelial cells start to migrate into the area of injury about 3 days after
the injury but it will take some days for granulation tissue to be readily seen.
Granulation tissue predominantly comprises macrophages, fibroblasts, newly formed
capillaries and lymphocytes.

Scar tissue (high power) in healed MI
- fibroblasts lay down more connective tissue
- inflammatory cells drain via lymphatics and capillaries degenerate leaving mature scar
that takes 6-8 weeks to form.
- collagen rich extracellular matrix with a few residual fibroblasts (e.g. green arrows) and
capillaries (green star). A few myocytes (black star) are present at the edge of the
scar.

41
Q
A

Benjamin's Pathology (10 decks)

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