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Semester 2 - PathPro > 7. Regeneration and repair > Flashcards

7. Regeneration and repair Flashcards

1
Q

What 2 things happen after acute inflammation?

A

1 - Complete resolution

2 – Repair with connective tissue (fibrosis) - If there has been substantial tissue destruction

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2
Q

What is chronic inflammation?

A

Prolonged inflammation with associated repair

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3
Q

List the 4 processes involved in wound healing

A
  1. Injury
  2. Haemostasis – as vessels are open
  3. Inflammation – as there has been tissue injury
  4. Regeneration (also called resolution or restitution) and repair – asstructures have been injured or destroyed.
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4
Q

What is regeneration?

A

•Regeneration is the regrowth of cells and tissues to replace lost structures.
• It can be a normal process, e.g., the replacement of red and white blood cells by the bone marrow, or it can occur after injury if the harmful agent is removed and if there is limited tissue damage
• Only possible with minor injuries
Eg superficial skin incision/abrasion

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5
Q

Where do new cells come from?

A

Stem cells

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6
Q

What are stem cells?

A

Stem cells are cells that can differentiate into it other cell types and self renew.

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7
Q

Function of stem cells?

A

They’re used to produce new cells, it can allow growth and repair.
Replace dead/damaged cells

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8
Q

What types of stem cell are there?

A
  • totipotent: Produce all cell types (embryonic)
  • multipotent: Produce several cell types (haematopoietic)
  • unipotent: Produce one cell type (epithelial stem cells)
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9
Q

Where can stem cells be found in the body ?

A
  • Epidermis - basal layer
  • intestinal mucosa - bottom of crypts
  • liver - between hepatocytes
  • embryo
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10
Q

Which of the 3 tissue types can regenerate?

A
  1. Labile tissue
  2. Stable tissues
  • when the collagen framework has stayed intact, regeneration can occur
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11
Q

What are labile tissues? give examples.

A

Continuously dividing tissues

  • proliferate throughout life replacing cells that are destroyed
  • cells are usually short lived

e. g.
- surface epithelia
- lining mucosa of secretory ducts of the glands of the body
- columnar epithelia of GI tract and uterus
- transitional epithelium of urinary tract
- cells of bone marrow and haematopoietic tissues

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12
Q

What are stable tissues? give examples.

A

Quiescent tissues

  • normally have a low level of replication but cells in these tissues can undergo rapid division in response to stimuli and can reconstruct the tissue of origin.
  • These have left the cell cycle but are able to re-enter.

e. g.
- parenchymal cells of the liver
- kidneys and pancreas
- mesenchymal cells such as fibroblasts
- bone osteoclasts and smooth muscle cells
- vascular endothelial cells
- resting lymphocytes and other white blood cells.

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13
Q

Which of the 3 tissue types cannot regenerate?

A

Permanent tissues

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14
Q

What are permanent tissues? give examples.

A

Non-dividing tissues
- these tissues contain cells that have left the cell cycle and can’t undergo mitotic division in postnatal life

e. g.
- neurones
- skeletal and
- cardiac muscle cells.

They have no or only a few stem cells that can be
recruited to replace cells.

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15
Q

Explain the importance of maintaining an intact tissue architecture for regeneration

A

In order for regeneration to take place damage to the tissue cannot be extensive as regeneration requires an intact connective tissue scaffold.

However, if the harmful agent persists, if there is extensive tissue damage or if the damage occurs to a permanent tissue then regeneration is not possible and instead the tissue will heal with a scar.

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16
Q

What determines whether an injury results in regeneration or repair?

A

LABILE/stable: if collagen framework intact then immediate regeneration, if collagen framework destroyed or there is ongoing chronic inflammation then fibrous repair via scar
Permanent: straight to fibrous repair with a scar

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17
Q

What is fibrous repair?

A

This is the replacement of functioning tissue with a scar.

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18
Q

What are the 4 steps in scar formation

A

1) bleeding and haemostasis —> preventing blood loss; seconds - minutes
2) inflammation - acute then chronic; digestion of blood clot, and you get phagocytosis of any necrotic tissue debris. -> minutes - days

3) proliferation of:
- capillaries (angiogenesis)
- fibroblasts, myofibroblasts (synthesise collagen and cause wound contraction),
- extracellular matrix
(all to form granulation tissue; days - weeks)

4) remodelling (maturation of scar) - The granulation tissue will become less vascular and matures into a fibrous scar. reduced cell population, increased collagen production from myofibroblasts/ fibroblasts, myofibroblasts contract —> forms fibrous scar; weeks-years

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19
Q

What does granulation tissue do in scar formation?

A
  • fills the gap
  • capillaries supply oxygen and nutrients
  • contracts and closes the defect
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20
Q

What does granulation tissue contain?

A
  • Fibroblasts
  • Myofibroblasts
  • capillaries
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21
Q

Give the 4 cells involved in fibrous repair and provide their respective functions

A
  1. Neutrophils
    Involved in the phagocytosis and release of mediators
  2. Macrophages
    Involved in the phagocytosis and release of mediators
  3. Lymphocyte
    This eliminates pathogens and co-ordinates other cells
  4. Endothelial cells
    This is involved in proliferation and the development of new blood vessels.
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22
Q

Structure of fibroblasts

A

It has a spindle shaped nucleus meaning that it’s elongated.

It also has cytoplasmic extensions.

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23
Q

Function of fibroblasts

A

It’s function is to secrete collagen and elastin.

It produces the extracellular matrix.

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24
Q

Structure of myofibroblasts

A

It has a spindle shaped nucleus and long cytoplasmisc extensions
It also contains intercellular actin
has characteristics of fibroblasts and SM cells

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25
Q

Function of myofibroblasts

A

Due to the presence of intracellular actin myofibroblasts can contract which allows them to take part in wound contraction.

26
Q

What is collagen?

A

Collagen is the main structural protein in the extracellular matrix. It’s used to provide extracellular framework. There are lots of different types but the main are type 1 and type 4.

27
Q

Where is type 1 collagen found?

A

bone, skin, tendon, ligaments, sclera, cornea, vessels

28
Q

Where is type 4 collagen located?

A

Basement membrane, lens, glomerular filtration

29
Q

Describe the process of collagen synthesis

A
  • pre-pro collagen: polypeptide alpha chain in ER of (myo)fibroblasts
  • undergoes vit C dependent hydroxylation
  • pro collagen: alpha chains cross link to form triple helix in cytoplasm of (myo)fibroblasts
  • C and N terminals of pro collagen cleaved to form tropocollagen in extracellular space
  • tropocollagen cross linked to form microfibrils, fibrils and collagen fibres
30
Q

Differentiate between acquired and inherited diseases of defective collagen and give examples of both

A

Inherited collagen diseases are defects an individual is born with.
Examples include Ehlers-danlos syndrome, osteogenesis imperfecta and alport syndrome.

An example of an acquired collagen disease would be scurvy, this is due to a vitamin C deficiency.
People with scurvy are unable to heal wounds adequately and have a tendency to bleed as capillaries are fragile.

31
Q

What causes scurvy and what are some symptoms?

A
  • inadequate hydroxylation of pre-pro collagen - as vitamin c is needed
  • defective triple helix = defective collagen

Symptoms:

  • poor wound healing
  • bleeding
  • bruising
  • gum disease/tooth loss
  • old scars break down, open up as fresh wounds
32
Q

Ehlers-Danlos syndrome

A
  • a heterogeneous group of six inherited disorders where the collagen fibres lack adequate tensile strength.
  • Skin is hyperextensible, fragile and susceptible to injury and joints are hypermobile.
  • Wound healing is poor and patients have a predisposition to joint dislocation.
  • Because the collagen in internal organs is also affected patients can suffer from rupture of the colon and, in some forms, large arteries.
  • Corneal rupture and retinal detachment can also be seen
33
Q

Osteogenesis imperfecta

A
  • also called brittle bone disease.
  • Patients have too little bone tissue and hence extreme skeletal fragility.
  • They also have blue sclerae as there is too little collagen in the sclerae making them translucent.
  • They can also have hearing impairment and dental abnormalities
34
Q

Alport syndrome

A

• usually an X-linked disease.
• Type IV collagen is abnormal and this results in dysfunction of the glomerular
basement membrane, the cochlea of the ear and the lens of the eye.
• Patients, usually male, present with haematuria as children or adolescents.
• This progresses to chronic renal failure.
• They also have neural deafness and eye disorders

35
Q

How are Regeneration and Repair Controlled?

A

Regeneration and repair is heavily based on the communication between cells in order to produce a fibroproliferative response.
Cell to cell communication can be via 3 modes:
1. Direct cell-cell contact
2. Local mediators such as growth factors
3. Hormones

36
Q

What do GFs do?

A
  • Growth factors are polypeptide proteins that act on the cell surface.
  • They bind to specific receptors and stimulate transcription of genes that causes cell to enter cell cycle and proliferate
  • However mutations in a cell can cause it to believe that it’s being stimulated which causes unauthorised proliferation.
  • They stimulate cell proliferation or inhibition but may also affect cell locomotion, contractility, differentiation, viability, activation and angiogenesis
37
Q

What are examples of GFs?

A

• Epidermal Growth Factor - – mitogenic for epithelial cells, hepatocytes and fibroblasts; produced by keratinocytes,
macrophages and inflammatory cells; binds to epidermal growth factor receptor (EGFR)
• Vascular Endothelial Growth Factor - potent inducer of blood vessel development (vasculogenesis) and role in growth of new blood vessels (angiogenesis) in tumours, chronic inflammation
and wound healing
• Platelet Derived Growth Factor - stored in platelet alpha granules and released on platelet activation; also produced by macrophages, endothelial cells, smooth muscle cells and tumour cells; causes migration and proliferation of fibroblasts, smooth muscle cells and monocytes
• Tumour Necrosis Factor - induces fibroblast migration, fibroblast proliferation and collagenase secretion.

38
Q

How does cell-cell contact inhibit replication?

A

Cell-cell contact is used for a process called contact inhibition. Isolated cells will replicate until they encounter other cells. They have proteins on their surface known as cadherins which bind between cells and inhibit further proliferation.
However in cancer the mutation of cadherin proteins means that proliferation won’t stop and the cell will continue to divide and multiply.

39
Q

How does the skin heal by primary intention?

A

• Healing by primary intention occurs when the wound is non-infected and is an incised wound with apposed edges, there’s minimal clotting and granulation tissue.
• In such wounds there is disruption of epithelial basement membrane continuity but death of only a limited number of epithelial and connective tissue cells.
• The epidermis will regenerate whilst the dermis will undergo fibrous repair.
• The process involves; haemostasis, inflammation, migration of cells, regeneration, early scarring, scar maturation.
check workbook 1 page 71

40
Q

How does the skin heal by secondary intention?

A
  • Secondary intention healing is found inexcisional wounds or wounds where there’s significant tissue loss, separated/unapposed edges and/ or infected wounds.
  • There’s also an abundance of blood clots, inflammation and granulation tissue.
  • Considerable wound contraction takes place to close the large wound.
  • You’d get substantial scar formation, the dermis require significant repair whilst the epidermis regenerates from the edges but it’s usually thinner than normal.
  • Healing will be delayed if infection is present.
41
Q

Describe the process of fracture healing

A
  1. A fracture results in a haematoma which fills the gap and surrounds the bone injury.
    It provides a foundation for the subsequent cell growth.
  2. A fibrin mesh and then granulation tissue is formed. Platelets and inflammatory cells release cytokines. These activate osteoprogenitor cells to osteoclastic and osteoblastic activity.
  3. Soft callus (also called procallus or fibrocartilaginous callus) It consists of fibrous tissue and cartilage within which woven bone begins to form.
    It usually extends beyond the volume occupied by the uninjured bone and forms a bulge around the fracture site.
  4. Hard callus (or bony callus) appears after several weeks. It is laid down by osteoblasts. The bone formed initially is woven bone. It is weaker as it is less organised than lamellar bone but it can form
    quickly.
  5. Woven bone gradually organized into lamellar bone which is more organised and stronger than woven bone.
  6. Remodelling of the bone occurs in response to mechanical stresses placed on it. Bone not physically stressed is resorbed
    and the outline of the bone is re established.
42
Q

Give the local factors that influence wound healing

A
  • Size, location and type of wound - indicates if healing is by primary or secondary intention and if regeneration or scarring will occur
  • Blood supply - e.g., arteriosclerosis impedes healing, areas with high vascularity (e.g., face) heal well
  • Denervation – impairs healing (and increases the risk of injury)
  • Local infection – produces persistent tissue injury and inflammation
  • Foreign bodies – produce persistent inflammation and favour infection
  • Haematoma – if large and persistent can slow healing
  • Necrotic tissue – needs clearing during the process of repair, therefore if a large amount is present healing can take longer
  • Mechanical stress – can pull apart delicate tissue in the early stages of healing
  • Protection (dressings) – help to keep the wound clean and free from infection
  • Surgical techniques – good techniques promote rapid healing and minimise scarring
43
Q

Give the systemic factors that influence wound healing

A
  • Age – children heal quickly, elderly people more slowly
  • Anaemia, hypoxia and hypovolaemia (e.g., following trauma) – poorer oxygen delivery to healing tissue
  • Obesity – can cause increased tension on wounds and wound dehiscence
  • Diabetes – microangiopathy impairs blood supply to damaged area. There is also a decreased resistance to infection
  • Malignancy – due to the cachexia (wasting of the body) seen with malignant tumours
  • Genetic disorders - e.g., Ehlers-Danlos syndrome
  • Drugs - steroids (immunosuppressive and inhibit collagen synthesis), cytotoxics (anti-mitogenic and impair cell proliferation and healing), antibiotics (treat bacterial infections, reduce inflammation and can speed up healing)
  • Vitamin deficiency - vitamin C deficiency inhibits collagen synthesis
  • Malnutrition or protein loss – lack of essential substances such as amino acids for protein synthesis
44
Q

What does it mean for stem cells to show asymmetric replication?

A

one of the daughter cells remains as a stem cell while the other differentiates into a mature, non-dividing cell.

45
Q

What replaces damaged tissue in the CNS?

A

The space where the neurones were is filled with glial cells

46
Q

Which cells replace terminally differentiated cells in labile tissue?

A

Labile tissues contain cells that are short-lived and are continually being replaced by cells derived from stem cells.

47
Q

Which cells replace terminally differentiated cells in stable tissue?

A

mature cells as well as stem cells are involved in
proliferation.

The mature cells are usually non-replicating but can be induced to enter the cell cycle and replicate if necessary, i.e., these cells are in G0 but can enter G1. Stem cells are present in these tissues and are normally quiescent or proliferate very

48
Q

In what situations would fibrous repair occur?

A
  • collagen framework of a tissue is destroyed
  • if there is on-going chronic inflammation
  • or if there is necrosis of specialised parenchymal cells that cannot be replaced
49
Q

What cells are involved in fibrous repair and what are their functions?

A

• Inflammatory cells

  • Phagocytosis of debris - neutrophils, macrophages
  • Production of chemical mediators - lymphocytes, macrophages

Endothelial Cells
- Proliferation results in angiogenesis

Fibroblasts and myofibroblasts

  • Produce extracellular matrix proteins, e.g. collagen
  • Responsible for wound contraction - contraction of fibrils within myofibroblasts
50
Q

What is wound dehiscence?

A

surgical complication in which a wound ruptures along a surgical incision

51
Q

What are the complications of fibrous repair?

A
  • Formation of fibrous adhesions (e.g., pleural adhesions) compromising organ function or blocking tubes
  • Loss of function due to replacement of specialised functional parenchymal cells by non functioning collagenous scar tissue (e.g., healed myocardial infarction)
  • Disruption of complex tissue relationships within an organ, i.e., distortion of architecture interfering with normal function (e.g., as seen in liver cirrhosis)
  • Overproduction of fibrous scar tissue, i.e., keloid scar
  • Excessive scar contraction causing obstruction of tubes, disfiguring scars following burns or joint contractures (fixed flexures). If very severe it can even impair blood circulation.
52
Q

What are keloid scars?

A

A keloid scar is an overgrowth of fibrous tissue, due to an overproduction of collagen that exceeds the borders of the scar. They don’t regress and excision just creates another one. They are commoner in Afro-Caribbeans.

53
Q

What is proud flesh?

A

Excessive granulation tissue

54
Q

Describe the healing ability of the following bodily components:

  1. Cardiac muscle
  2. Liver
A
  1. Cardiac muscle
    This muscle has very limited (baskcally none) regeneration properties.
    Damage to the muscle (MI) usually results in scar formation which affects cardiac function.
  2. Liver
    The liver has ana amazing regeneration property.
    If a section of the liver has to be taken out the liver can regenerate by increasing the mass of the lobes tha5 remain.
    You first get the production of hepatocytes then other non-parenchymal cells. However issue occurs if the architecture of the liver Is seriously damaged, if so regeneration cannot occur and fibrosis occurs.
55
Q

Describe the healing ability of the following bodily components:

  1. Peripheral nerve
  2. Cartilage
  3. Central nervous system
A
  1. Peripheral nerve
    The severing if a nerve causes the axons to degenerate, the degenerated axons will then sprout and elongate.
    They’ll use the Schwann cells vacated by the distal degenerated axons to guide them back to the tissue that the nerve innervates
  2. Cartilage
    Cartilage doesn’t heal well as it lacks blood supply, lymphatic drainage and innervation.
  3. Central nervous system
    Neural tissue is a permanent, non-proliferative tissue, this means that wen damage occurs in the CNS the neural tissue will be replaced by the proliferation of CBS supportive elements in a process known as gliosis.
56
Q

Describe haemostasis stage of primary intention.

A
  • Seconds to minutes
  • Severed arteries contract.
  • narrow space fills with clotted blood
  • dehydration of the surface clot and a scab is formed.
57
Q

What is the importance on scab formation?

A

The scab seals off the wound from the environment and prevents bacteria entering - it is a natural wound dressing.

58
Q

Describe inflammation stage of primary intention.

A
  • minutes to hours
  • neutrophils appear at the margins of the incision - wards off bacteria
  • inflammation is triggered automatically without waiting for bacteria to do so
  • In a sterile wound the number of leukocytes is not enough for the fluid to be classified as pus
59
Q

Describe migration of cells stage of primary intention.

A
  • up to 48 hrs
  • macrophages start to appear and begin to scavenge dead neutrophils.
  • they become activated and secrete cytokines that attract other cells such as fibroblasts, and endothelial cells (capillary sprouts start to appear). - spurs of basal epidermal cells at the edge of the cut creep over the denuded cells travelling at approximately 0.5mm/day
  • they deposit basement membrane components as they go
  • they fuse in the midline beneath the scab.
60
Q

Describe regeneration stage of primary intention.

A

3 days

  • macrophages replace neutrophils.
  • granulation tissue invades the space
  • epithelial cell proliferation thickens the epidermal layer and epidermal cells undermine the scab which then falls off.
  • activated fibroblasts produce collagen
  • angiogenesis progresses.
61
Q

Describe early scarring stage of primary intention.

A
  • 7 to 10 days
  • the wound is filled with granulation tissue
  • the fibroblasts proliferate and deposit collagen fibres which form a fibrous mass, i.e., a scar
  • the epidermis normalises and keratinises but skin appendages, e.g., hair and sweat glands, don’t form
  • white cell infiltrate, oedema and increased vascularity disappear.
  • regression of vascular channels
62
Q

Describe scar maturation stage of primary intention.

A
  • one month to two years
  • the scar is a mass of fibrous tissue with many collagen fibres, few cells and few vessels
  • it also has few elastic fibres and therefore little recoil (this is why scars tend to stretch)
  • as capillaries disappear old scars appear white (new scars are pink).

Semester 2 - PathPro (16 decks)

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