Regeneration and repair Flashcards

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Where do new cells come from

A

Stem cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Stem cells

A

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

Can self-renew

Replace dead/damaged cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

types of stem cell

A

totipotent

multipotent

unipotent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Totipotent

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Multipotent-

A

become several cell types e.g. haematopoietic stem cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Unipotent

A
  • produce one cell type

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Regernation is: (2)

A
  1. The regrowth of cells
  2. Can be physiological
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

regernation: can be physiologal

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

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

A

Labile

Stable

Permanent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Contact inhibition

A

Isolated cells replicate until they encounter other cells or ECM

  • Cadherins bind between cells
  • Inhibiting further proliferation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

examples of growth factors

A
  • Epidermal growth factor
  • Vascular endothelial growth fact
  • Platelet derived growth factor
  • Tumour necrosis factor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Epidermal growth factor

A

induces mitosis in epitheilial cells, hepatocytes and fibroblasts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Vascular endothelial growth factor

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

platelet derived growth factor

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

tumour necrosis factor

A

causes migration and proliferation of fibroblasts and secretion of collagenase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

fibrous repair is the opposite of

A

regeneration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

when does fibrous repair take place instead of regeneration

A
  1. necrosis of permanent tissue
  2. Labile or stable tissue
    • collagen framwork destroyed
    • on-going chronic inflammation
27
Q

define fibrosis

A

replacemnt of functioning tissue with a scar

28
Q

outline fibrous repair (formation of a scar)

A
  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
Q

function of granulation tissue

A

fills the gap; capillaries supply oxygen and nutrient; contracts and closes the defect

30
Q

cells invovled in fibrous repair

A

Neutrophils

macrophages

lymphocytes

endothelial cells

fibroblasts

myofibroblassts

31
Q

neutrophils and macrophages

A

phagocytosis and release of mediators

32
Q

lymphocytes

A

eliminates pathogens and coordinates other cells

33
Q

endothelial cells

A

proliferation and angiogenesis

34
Q
A
35
Q

fibroblast structure

A
  • Spindle shaped nucleus
  • Cytoplasmic extensions- interdigitate with each other
36
Q

fibroblasts function

A
  • Secrete collagen and elastin
  • Form ECM
37
Q

myofibroblasts

A
  • Secrete collagen and elastin
  • Form ECM
38
Q
A
39
Q

how are myofibroblasts like smooth muscle

A

can contract like smooth muscle due to expression of intracellular actin

40
Q

collagen is the most common

A

protein in the body

29 different types

41
Q

type 1 collagen

A

bones, ligaments, tendons, skin, sclera, cornea, vessels

42
Q

type II

A

cartiliginous tissue

43
Q

type III

A

skin, ligaments, blood vessels and internal organs

44
Q

type IV

A

basement membrane, lens, glomerular filtration

45
Q

type 5

A

skeletal muscle, blood vessels, lung, bone, tendon

46
Q

collagen function

A

Provides extracellular framework

47
Q

synthesis of collagen

A
  1. Pre-procollagen – polypeptide alpha chain produced in the ER of fibroblasts
  2. Undergoes Vitamin 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
Q
A
49
Q

acquired defective collagen disease

A

Scurvy

  • Vitamin C deficiency
    • Inadequate hydroxylation of pre-procollagen
    • Defective triple helix= defective collagen
  • Unable to heal wounds
  • Tendency to bleed
  • Tooth loss
50
Q

inherited defective collagen disease

A

ehlers-danlos syndrome and osteogenesis imperfecta

51
Q

the skin can heal in two ways

A

by ….

  1. primary intention
  2. secondary intention
52
Q

primary intention

A
  • Incised wound
  • Apposed edges (sutured)
  • Minimal blood clot and granulation tissue
  • Epidermis regenerates
  • Dermis undergoes fibrous repair
53
Q

Secondary intention

A
  • 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
Q

Outline fracture healing

A

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
Q

Factors influencing wound healing can be

A

local or systemic

56
Q

Factors influencing wound healing: local

A

Size

Location

Mechanical stress

Blood supply

Local infection

Foreign bodies

57
Q

Factors influencing wound healing: systemic

A
  • Age- older people take longer to heal
  • Anaemia, hypoxia, hypovolaemia
  • Obesity
  • Diabetes- bacteria love sugary blood
  • Drugs
  • Vitamin deficiency
  • Malnutrition
58
Q

complications of fibrous repair

A
  • Wound dehiscence
  • excessive fibrosis
  • adhesions
  • loss of functions
  • disruption of architecture
  • excessive scar contraction
59
Q

wound dehiscence

A
  • Not enough collagen being laid down
  • Occurs in:
    • Obesity
      • Increased pressure from inside by subcutaneous fat
    • Elderly
    • Malnutrition
    • Steroid use
60
Q

excessive fibrosis

A

Keloid scar

Too much collagen and elastin exceeding the edges of the wound

61
Q

excessive scar contraction

A

Constriction of tubes

Fixed flexion deformities (contractures)

62
Q

Adhesions

A
  • Fibrous bands of collagen and elastin (typically seen in abdominal cavity after operation)
  • Post-operative adhesions
  • Can cause obstruction of tubes
63
Q

loss of function

A
  • 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
Q

Disruption of architecture

A

E.g. long term alcohol abuse and the liver