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Regeneration and repair Flashcards

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1
Q

What processes are involved in wound healing?

A
  1. Injury
  2. Haemostasis – limitation of blood loss
    • Formation of blood clot to limit loss of blood
  3. Inflammation
  4. Regeneration or repair
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2
Q

Where do new cells come from

A

Stem cells

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3
Q

Stem cells

A

can become specialised cells e.g. neuron, cardiac myocyte, macrophage

Can self-renew

Replace dead/damaged cells

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4
Q

types of stem cell

A

totipotent

multipotent

unipotent

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5
Q

Totipotent

A

– produce all cell type e.g. embryonic stem cells

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6
Q

Multipotent-

A

become several cell types e.g. haematopoietic stem cells

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7
Q

Unipotent

A
  • produce one cell type

E.g. all the epithelial stem cells will only ever become epithelial cells

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8
Q

Regernation is: (2)

A
  1. The regrowth of cells
  2. Can be physiological
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9
Q

Regeneration: regrwoth of cells

A

Minimal evidence of injury (no scar)

  • Only possible with minor injuries e.g. superficial skin incision/abrasion
  • The regrowth of cells
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10
Q

regernation: can be physiologal

A

e.g. production of white cells in bone marrow (leucocytosis)

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11
Q

where are stem cells found

A
  1. In the skin
    • Epidermis- basal level
    • Unipotent stem cells which divide and differentiae into squamous cell
  2. Intestinal mucosa
    • Bottom of crypts
    • Unipotent stem cells producing simple columnar cells
  3. Liver
    • Between hepatocytes
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12
Q

Cells can be organised into 3 different groups depending on their proliferative activity. These are:

A

Labile

Stable

Permanent

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13
Q

labile tissue

A
  • These cells are short lived, and can easily be replaced by replication and maturation of stem cells.
  • This means these tissues have a high reproductive capacity.
  • For example, epithelial cells (such as those in the gastrointestinal tract) and haematopoietic tissue
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14
Q

stable tissue

A
  • These cells normally have a slow rate of cell replication.
  • However, they can divide rapidly when required.
  • Hepatocytes, renal tubular cells and pancreas are examples of stable cells.
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15
Q

Permanent

A
  • These cells are unable to undergo effective replication.
  • left cell cycle and cannot re-enter
  • Only a few stem cells are present.
  • Neurones, skeletal muscle and cardiac muscle are an example of permanent cells.
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16
Q

which tissue types can regenerate

A

within labile and stable tissues when tissue damage isn’t extensive.

The presence of stem cells makes this possible, as they can divide and differentiate to replace the lost cells.

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17
Q

control of regeneration

A

Cell to cell communication occurs via local mediators such as growth factors, hormones or by direct cell-cell or cell-stroma contact. This communication allows control of regeneration.

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18
Q

Contact inhibition

A

Isolated cells replicate until they encounter other cells or ECM

  • Cadherins bind between cells
  • Inhibiting further proliferation
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19
Q

growth factors

A

Growth factors are polypeptides which are coded for by proto-oncogenes. The act in an autocrine (acting on the cell itself that secretes the growth hormone) or paracrine (acting on cells a short distance away) manner. They stimulate or inhibit cell proliferation through binding to specific receptors to stimulate gene transcription.

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20
Q

examples of growth factors

A
  • Epidermal growth factor
  • Vascular endothelial growth fact
  • Platelet derived growth factor
  • Tumour necrosis factor
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21
Q

Epidermal growth factor

A

induces mitosis in epitheilial cells, hepatocytes and fibroblasts

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22
Q

Vascular endothelial growth factor

A

induces developemnt of blood vessels in tumours, chronic inflammation and wound healing

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23
Q

platelet derived growth factor

A

causes migration and proliferation of fibroblasts, smooth muscle cells and monocytes

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24
Q

tumour necrosis factor

A

causes migration and proliferation of fibroblasts and secretion of collagenase

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25
fibrous repair is the opposite of
regeneration
26
when does fibrous repair take place instead of regeneration
1. necrosis of permanent tissue 2. Labile or stable tissue * collagen framwork destroyed * on-going chronic inflammation
27
define fibrosis
replacemnt of functioning tissue with a scar
28
outline fibrous repair (formation of a scar)
1. **Bleeding**- blood clot formation 2. **Inflammation** * Acute then chronic digestion of the blood clot, damaged tissue and foreign body * Minutes- days 3. **Proliferation** * Of capillaries (angiogenesis) * Fibroblast * Myofibroblasts * Extracellular matrix * Collectively turns to granulation tissue 4. **Remodelling** * Maturation of scar * Reduced cell population * Increased collagen * Myofibroblasts contract * Fibrous scar (weeks- years)
29
function of granulation tissue
fills the gap; capillaries supply oxygen and nutrient; contracts and closes the defect
30
cells invovled in fibrous repair
Neutrophils macrophages lymphocytes endothelial cells fibroblasts myofibroblassts
31
neutrophils and macrophages
phagocytosis and release of mediators
32
lymphocytes
eliminates pathogens and coordinates other cells
33
endothelial cells
proliferation and angiogenesis
34
35
fibroblast structure
* Spindle shaped nucleus * Cytoplasmic extensions- interdigitate with each other
36
fibroblasts function
* Secrete collagen and elastin * Form ECM
37
myofibroblasts
* Secrete collagen and elastin * Form ECM
38
39
how are myofibroblasts like smooth muscle
can contract like smooth muscle due to expression of **intracellular actin**
40
collagen is the most common
protein in the body 29 different types
41
type 1 collagen
bones, ligaments, tendons, skin, sclera, cornea, vessels
42
type II
cartiliginous tissue
43
type III
skin, ligaments, blood vessels and internal organs
44
type IV
basement membrane, lens, glomerular filtration
45
type 5
skeletal muscle, blood vessels, lung, bone, tendon
46
collagen function
Provides extracellular framework
47
synthesis of collagen
1. Pre-procollagen – polypeptide alpha chain produced in the ER of fibroblasts 2. Undergoes V**itamin C dependent hydroxylation** 3. Pro-collagen alpha chains are then cross-lined to form triple helix in the cytoplasm of the (myo)fibroblast 4. Procollagen secreted outside the cell and C and N terminals of procollagen cleaved à tropocollagen in ECM 5. Tropocollagen become crosslinked to form microfibrils, fibrils and collagen fibres
48
49
acquired defective collagen disease
Scurvy * Vitamin C deficiency * Inadequate hydroxylation of pre-procollagen * Defective triple helix= defective collagen * Unable to heal wounds * Tendency to bleed * Tooth loss
50
inherited defective collagen disease
ehlers-danlos syndrome and osteogenesis imperfecta
51
the skin can heal in two ways
by .... 1. primary intention 2. secondary intention
52
primary intention
* **Incised wound** * **Apposed edges (sutured)** * Minimal blood clot and granulation tissue * Epidermis regenerates * Dermis undergoes fibrous repair
53
Secondary intention
* Significant tissue loss * Unopposed edges * Infection * Ulcers * Abscess * Abundant clot, inflammation and granulation tissue * Considerable wound contraction required (myofibroblasts) * Dermis requires significant repair * Epidermis regenerates from edges
54
Outline fracture healing
1) **Haematoma** surrounds the injury- granulation tissue forms, angiogenesis 2) **Soft callus** forms (1 week) * Fibrous tissue and cartilage * Woven bone begins to form 3) **Hard callus** (several weeks) * Woven bone gradually organised into lamellar bone- osteoclasts 4) **Remodelling** (months- years) * Lamellar bone remodelled to original outline of bone
55
Factors influencing wound healing can be
local or systemic
56
Factors influencing wound healing: local
Size Location Mechanical stress Blood supply Local infection Foreign bodies
57
Factors influencing wound healing: systemic
* Age- older people take longer to heal * Anaemia, hypoxia, hypovolaemia * Obesity * Diabetes- bacteria love sugary blood * Drugs * Vitamin deficiency * Malnutrition
58
complications of fibrous repair
* Wound dehiscence * excessive fibrosis * adhesions * loss of functions * disruption of architecture * excessive scar contraction
59
wound dehiscence
* Not enough collagen being laid down * Occurs in: * Obesity * **Increased pressure from inside by subcutaneous fat** * Elderly * Malnutrition * Steroid use
60
excessive fibrosis
Keloid scar Too much collagen and elastin exceeding the edges of the wound
61
excessive scar contraction
Constriction of tubes Fixed flexion deformities (contractures)
62
Adhesions
* Fibrous bands of collagen and elastin (typically seen in abdominal cavity after operation) * Post-operative adhesions * Can cause obstruction of tubes
63
loss of function
* Replacement of specialised tissue by fibrous tissue * E.g. in the heart after MI * Develop arrythmia due to fibrosis tissue not being able to carry electrical conduction
64
Disruption of architecture
E.g. long term alcohol abuse and the liver

Pathological processes (19 decks)

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