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PATHOLOGY > Week 2 (2) Chronic Inflammation and Healing > Flashcards

Week 2 (2) Chronic Inflammation and Healing Flashcards

1
Q

Define CHRONIC INFLAMMATION

A

“Inflammation of prolonged duration (weeks or months) in which atice inflammation, tissue destriction and attempts of repair are proceeding simultaneously”

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2
Q

What CAUSES Chronic Inflammation?

A
  • Can develop from UNRESOLVED ACUTE INFLAMMATION due to infection (e.g. gastritis, osteomyelitis)
  • Can develop from _exposed exposur_e to agent (e.g. silica, prosthetic implants)

- autoimmune diseases (RA)

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3
Q

List the main cell types involved in Chronic Inflammtion

A

*Mast Cells

*Macrophages

*Fibroblasts

*Endothelial Cells

*Lymphocytes

* Plasma Cells

*Eosinophils

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4
Q

Explain the maturation of macrophages

A

Stem cell changes to a monoblast ( in the bone marrow)

Monocyte (in the blood)

Macrophage ( in tissue) -> **then DIFFERENTIATION ** into microglia (CNS), Kupffer cells (liver), Alveolar macrophages (lungs) and osteoclasts (bones) OR ACTIVATION –> giant cells, epithelioid cells, macrophages

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5
Q

Role of MACROPHAGES in Chronic Inflammation

A

They are active compounds that produce chemokines, cytokines and growth factors (which causes fibroblast proliferation, blood vessel growth, activation and recruitment of lymphocytes)

Participate in bacterial and cell killing

Clear debris, fibrin and other foreign material

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6
Q

Macrophages and Phagocytosis - Pros and Cons

A

Pros:

increased lysosomal enzymes and ROS (toxic to mocrobes)

production of cytokines, growth factors

Cons

cause dissolution of extracellular material or cells by producing toxic products (nitric oxide metabolites of proteases)

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7
Q

Lymphocytes in Chronic Inflammation

A

TWO TYPES:

T and B lymphocytes

  • long lived, some present normally in certain tissues
  • Antigen activated
  • release macrophage activating cytokines
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8
Q

Difference between T Cells and B Cells

A

T Cells - in cell mediated immunity

B Cells - in humoral mediated immunity, differentiate into plasma cells which produce antibody

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9
Q

Chronic Inflammation - HISTOPATHOLOGY

A

Plasma Cells: Terminally differentiated B cells, produces antibodies

Fibroblasts: synthesises collagen (fibrosis) scar tissue

Endothelial cells: forms new vessels

Eosinophils: paracitic infection

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10
Q

Osteomyelitis

(An infection that can arise from acute UNRESOLVED inflammation)

A

Infection in the bone and marrow

Complications - loss of bone, growth disturbance in children, epidermoid carcinoma

Treatment - antibiotic or surgical debeidement

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11
Q

Granulomatous Inflammation:

(Persistent agent causing chronic inflammation)

A

Clusters of T cells activated macrophages having engulfed foreign bodies

  • epitheloioid granulomas: resemble squamous cells
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12
Q

Rheumatoid Arthritis

(Example of Autoimmune disease causing Chronic Inflammation)

A

Local and systemic inflammation:

Joint - chronic synovitis, synovial cells hyperplasia and proliferation

Increased Vascularity

Cells come along - t cells, macrophages, plasma cells

Increased osteoclasts

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13
Q

Crohn’s Disease

(Example of autoimmune disease causing chronic inflamamtion)

A

Understand the diagrams (red surfaces and giant multinucleated cell)

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14
Q

What are the NORMAL phases of healing?

A
  1. REACTIVE - inflammation (days)
  2. REPAIR - granulation tissue (months)
  3. Maturation/Remodellign - collagen (weeks)
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15
Q

SCARS

What are they and when do they form?

A

Severe or chronic tissue injury may mean that healing cannot be accomplished.

Healing process is now repairing the area using COLLAGEN.

A scar is formed by an intermediary tissue called…. GRANULATION TISSUE

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16
Q

What is GRANULATION TISSUE?

A

made of:

  • new blood vessels (growth factors)
  • fibroblasts –> collagen –. scars
  • macrophages clear away dead tissue.

WHY: some cells are uable to regenerate, or there may be extensive tissue destriction. Healing is NOT through the inflammatory exudate response but by ORGANISATION AND REPAIR

17
Q

Granulation tissue will undergo THREE sequential changes

A

1. Vascular Granulation Tissue

  • newly formed capillaries, macrophages and support cells.

2. Fibrovascular granulation tissue

  • proliferatine fibroblasts, capilliaries and macrophages

3. Fibrous Granulation Tissue

  • fibroblasts synthesize collagen adn align themselves so that collagen is deposited in a uniform manner.
18
Q

Aims of Wound Healing:

A

- remove damamged tissue

- fill gap caused by destruction

19
Q

Why would a bigger woud take longer to heal?

A
  • needs to carry away more necrotic debris and excudate
  • much larger amounts of granulation tissue are formed
  • greater amount of collagen synthesis needed to fill damaged areas
  • scar tissue formation replaces normal tissue
20
Q

List both LOCAL and SYSTEMIC factors that influence wound healing

A

LOCAL

  • infection
  • mechanical factors
  • foreign bodies
  • size, location and type of wound
  • vascular supply

SYSTEMIC

NUTRITION: --vitamin C and A, protein deficiency inhibits collagen synthesis.

METABOLIC STATUS - diabetes

CIRCULATORY STATUS - no blood

HORMONES - glucocotricoids have anti-inflammatory response

IMMUNOSUPPRESSION

AGE

21
Q

Regenerative HEALING

EG - A BROKEN BONE

LIST THE STAGES, will need to refer to diagrams in lecture slides

A

1. Early Fracture:

Haematoma/Inflammation: rupture of cessels, inflammatory cell infiltrate (macrophages, leukocytes, platelets), bone cells die

Inflammation Stage - granulation tissue/soft callus (callus is CT and cartilage)

2. Reparative Phase

Osteoclasts resorb dead bone, bone deposited on the end of cortical bone, soft callus develops

3. Remodelling Phase

  • callus replaced with lamellar bone, osteoclasts and blasts still active
22
Q

NON REGENERATIVE REPAIR E.G Myocardial Infacrtion

Please list the stage of _non-regenative repai_r in a myocardial infarction from 6 hours to several weeks

A
  1. 6-12 Hours
    - no macroscopi changes, increased eosinophilia of dead cells
  2. 12-24 Hours
    - Nuclei fade (karyolysis)
    - neutrophils infiltrate the dead myocardium as acute inflammatory response.
    - Most monocytes are dead
  3. 48-72 Hours
    - many neutriphils infiltrate the dead myocardium.
  4. Several Weeks
    - fibroblasts and endothelial cells migrate into the area of injury.
    - granulation tissue develops - comprises of macrophages, fibroblasts, capilliaries and lymphocytes.

5. Scar Tissue

  • fibroblasts lay down more CT
  • scar takes 6-8 weeks to form
23
Q
A

PATHOLOGY (17 decks)

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