Week 7 Healing & cell injury & neoplasia Flashcards

1
Q

Tissue response to injury

A
  1. Acute inflammation
  2. Demolition
    3, Healing and repair (stimulus removed)
  3. Resolution
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2
Q

Events in repairing

A
  1. Replacement of lost tissue by granulation tissue

2. Granulation tissue matures and forms fibrous tissue (scar)

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3
Q

3 types of cells according to regenerative capacities

A
  1. Labile cells - continually dividing
  2. Stable cells - normal proliferative activity, capable of dividing during injury
  3. Permanent cells - terminally differentiated, non-proliferative
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4
Q

Mechanisms of wound healing

A
  1. Migration and regeneration of parenchymal cells
  2. Migration and proliferation of connective tissue cells
  3. Synthesis of extracellular matrix proteins
  4. Remodelling of connective tissue and parenchyma
  5. Collagenization and acquisition of wound strength
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5
Q

4 stages of healing for skin wounds

A
  1. Formation of scab and acute inflammation
  2. Regeneration of epithelial covering and formation of granulation tissue in underlying connective tissue stroma
  3. Deposition of collagen and resorption of capillaries
  4. Formation of scar
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6
Q

Healing of bone fractures

A
  1. Haematoma formation and inflammation
  2. Demolition
  3. Callus formation (new bone)
  4. Formation of lamellar bone (stronger, replace callus)
  5. Remodelling
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7
Q

Differences between primary intention and secondary intention healing

A

Healing by primary intention:
clean incision wound, minimal scarring

Healing by secondary intention:

  1. open wound
  2. greater tissue loss
  3. more granulation tissue needed -> larger scar
  4. more liable to infection
  5. more inflammatory exudate and necrotic tissue to be removed
  6. wound contraction needed
  7. slower process
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8
Q

Components of granulation tissue

A
  1. Proliferating capillaries - supplies nutrients and oxygen
  2. Fibroblasts and myofibroblasts - produce connective tissue stroma
  3. Macrophages
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9
Q

Factors influencing wound healing

A

Local factors: type of wound, blood supply, presence of foreign body in wound, infection, etc

General adverse factors:

  1. poor nutrition
  2. steroid administration
  3. systemic diseases

General enhancing factor:
UV light

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10
Q

Are cartilage and tendons capable of regenerating?

A

Cartilage: poor
Tendon: good but slow

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11
Q

How can peripheral nerves be repaired?

A
  1. Wallerian degeneration - total degeneration of axon and secondary demyelination in the distal area of transection
  2. Regeneration by Schwann cell proliferation and sprouting of axons from surviving neurons
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12
Q

2 important properties of stem cells

A
  1. Self-renewal

2. Asymmetric division

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13
Q

3 Sources of stem cells

A
  1. Adult (e.g. marrow, blood, skin)
  2. Embryonic
  3. Induced pluripotent
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14
Q

3 Important processes underlying wound healing

A
  1. Growth factor
  2. Cell-cell and cell-matrix interaction
  3. Extracellular matrix synthesis and collagenization
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15
Q

3 Main determinants of final outcome of wound

A
  1. Regenerative capacity of constituent cells
  2. Type and extent of injury
  3. Extent of damage to extracellular matrix
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16
Q

Pathogenesis of cell injury

A
  1. Biochemical alterations
  2. Ultrastructural changes
  3. Light microscopic changes
  4. Gross morphologic changes
17
Q

Causes of cell injury

A
  1. Hypoxia
  2. Physical agent
  3. Chemical agent
  4. Biological agent
  5. Immunological reaction
  6. Others: genetic defects, nutritional imbalance
18
Q

Determinants of result of cell injury

A
  1. Injury: type, duration, severity

2. Cell: type, state, adaptability

19
Q

4 Types of Reversible cell injury

A
  1. Intracellular oedema
  2. Fatty change - abnormal accumulation of fat inside cell (large fat vacuole displaces nucleus to periphery)
  3. Hyaline degeneration
  4. Intracellular accumulation
20
Q

What are the alternative names for reversible and irreversible cell injuries?

A

Reversible injury: cell degeneration

Irreversible injury: cell death

21
Q

Mechanism of apoptosis

A
  1. DNA fragmentation by endonuclease
  2. Condensation and shrinkage of nucleus and cytoplasm -> form apoptotic bodies
  3. Phagocytosed by adjacent cells
22
Q

Causes of apoptosis

A

Physiological causes:

  1. programmed cell death during embryonic devleopment
  2. normal cell turnover

Pathological causes:

  1. UV / ionizing radiation
  2. drugs
  3. tumour cell death
  4. cell-mediated immunity
23
Q

2 Ways for cells to die in necrosis?

A
  1. Autolysis - release of lysosomal hydrolases from necrotic cells -> self digestion
  2. Heterolysis - digested by immigrant leukocytes
24
Q

Nuclear changes during necrosis

A
  1. Pyknosis - dark nucleus due to condensation of DNA
  2. Karyorrhexis - fragmented nucleus
  3. Karyolysis - complete dissolution of nucleus
25
Q

2 main behavioural characteristics of malignant tumour

A
  1. Invasion into surrounding tissues

2. Distant metastases

26
Q

6 Types of necrosis according to morphology

A
  1. Coagulative Necrosis
  2. Liquefaction Necrosis
  3. Caseous Necrosis (TB)
  4. Enzymatic Fat Necrosis
  5. Traumatic Fat Necrosis
  6. Fibrinoid Necrosis