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ESA2 Callum's Cards - Complete > MoD S5 - Healing and Repair > Flashcards

MoD S5 - Healing and Repair Flashcards

1
Q

What is the definition of regeneration?

A

The replacement of dead or damaged cells by functional, differentiated cells derived from stem cells

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2
Q

What are stem cells?

What happens to a stem cell when it divides?

A

Undifferentiated cells with limitless proliferation potential

Daughter cells either:

  • Remain as stem cells
  • Differentiate into specialised cells
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3
Q

What are stem cells used for?

A

Internal repair system that replaces lost or damaged cells

Can possibly be used to treat degenerative disease

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4
Q

What are the three major types of stem cell?

A

Unipotent
Multipotent
Totipotent

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5
Q

Where can stem cells be found in the gut?

What is their function there?

A

At the base of crypts in the mucosa

Replace cells lost from the mucosa

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6
Q

Blood cells are derived from what type of stem cell?

A

Multipotent haemopoietic stem cells

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7
Q

What is the function of stem cells in the embryo?

A

Differentiate into the different tissues of the body

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8
Q

How are cells classified by propensity to regeneration?

Give a breif description and example of each type

A

Labile cells:

  • Normally in active cell division
  • Rapid proliferation
  • E.g. Epithelial cells

Stable cells:

  • Resting state - G0, but can divide in the right conditions
  • Speed of regeneration variable
  • E.g. Hepatocytes

Permanent cells:

  • Unable to divide - G0
  • Unable to regenerate
  • E.g. Neurones, Cardiomyocytes
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9
Q

Give two examples of stable cell proliferation

A

Renal tubular epithelium, when damaged can proliferate and replace lost and damaged cells

Hepatocytes can regenerate when they are damaged during cirrhosis of the liver (nodules)

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10
Q

What factors control regeneration?

A

Growth factors

Contact between cell and basement membrane and adjacent cells

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11
Q

What do growth factors do?

A

Promote proliferation in the stem cell population via extracellular signals that are transduced into the cell hence promoting expression of genes controlling the cell cycle

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12
Q

Give some examples of growth factors

A

Proteins:

  • Epidermal GF
  • Platelet derived GF
  • Fibroblast GF
  • Some Cytokines

Hormones:

  • Oestrogen & Testosterone
  • Growth hormone
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13
Q

What types of cell signalling do growth factors use?

A

Autocrine
Paracrine
Endocrine

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14
Q

Give an example mechanism by which a growth factor might induce cell proliferation

A

Binds to extracellular receptor

Receptor has intrinsic enzyme activity and will autophosphorylate (tyrosine kinase)

This sets of a phosphorylation cascade which results in increased transcription of genes which regulate the cell cycle

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15
Q

How is contact between cell and basement membrane and adjacent cells involved in regulating regeneration?

A

Signalling is done through adhesion molecules

Signals inhibit proliferation when the cell being signalled is in contact with other cells (Contact inhibition)

Loss of contact will promote proliferation

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16
Q

In what group of pathologies do the mechanisms controlling cellular proliferation become deranged?

A

Cancer

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17
Q

Give an example of a mechanism by which contact inhibition is achieved

A

E-cadherin is a protein spanning the cell membrane that will dimerise with other E-cadherin molecules on adjacent cells

The end result of this dimerisation is contact inhibition

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18
Q

What is ‘fibrous repair’?

A

The replacement of functional tissue by scar tissue

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19
Q

What are the 2 main outcomes of inflammation or injury and how do they come about?

Hint: relate this back to proliferation potential of the cells that were damaged

A

When injury leads to necrosis of permanent cells:
- Fibrous repair and scarring occurs

When injury leads to necrosis of stable or labile cells:

  • If collagen framework preserved, insult is resolved
  • If collagen framework destroyed, Fibrous repair and scarring
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20
Q

What are the 3 main components of fibrous repair and all together, what do they form?

A

Cells that migrate in
Blood vessels - Angiogenesis
Extracellular matrix protein production and remodelling

Granulation tissue

21
Q

What are the important cell types in fibrous repair?

How is each type involved?

A

Inflammatory cells:

  • Phagocytosis of debris - neutrophils and macrophages
  • Chemical mediators - lymphocytes and macrophages

Endotheial cells:
- Angiogenesis

Fibroblasts/Myofibroblasts

  • Produce extracellular matrix proteins E.g. Collagen
  • Myofibroblasts can contract the wound
22
Q

Why is angiogenesis vital to wound healing?

A

Provides access to the wound for inflammatory cells and fibroblasts as well as oxygen and nutrients

23
Q

How does angiogenesis begin?

A

Endothelial proliferation induced by proangiogenic growth factors such as VEGF

Pre-existing blood vessels will sprout off new blood vessels (they don’t arise de novo)

24
Q

Describe the process of angiogenesis

A

Growth factors such as VEGF produced at sites of chronic inflam, tissue injury or hypoxia

Endothelial proteolysis of basement membrane

Migration of endothelial cells into surrounding interstitium via chemotaxis

Endothelial proliferation into primitive tubular structures

Maturation and tubular remodelling

Linkage with venous system

Recruitment of periendocardial cells

25
How is angiogenesis involved in malignancy?
Tumours require rich blood supply Tumours require angiogenesis to supply metabolic demand once tumour has grown to a larger size Potential therapeutic target
26
What are the functions of the extracellular matrix?
Supports and anchors cells Separates tissue components (E.g. basement membrane) Sequesters growth factors Facilitates cell communication and migration
27
Describe collagen Structure? Types?
``` Provides extracellular framework Composed of triple helices of various polypeptide alpha chains Fibrillar collagens (I - III) Amorphous collagen (IV - VI) Remodelled by specific collagenases ```
28
Describe the synthesis of collagen fibres Hint: FIBRES
Polypeptide alpha chains synthesised in ER Enzymatic modification steps including Vit C dependent hydroxylation Alpha chains align and cross link to form procollagen triple helix Soluble procollagen secreted from cell After secretion cleaved to form tropocollagen Tropocollagen will polymerise to form fibrils Bundles of fibrils form fibres
29
List 4 major defects of collagen synthesis
Vit C Deficiency - Scurvy! Ehlers-Danos syndrome Oseogenesis imperfecta Alport syndrome
30
Describe some of the features of scurvy
Inadequate Vit C dependent hydroxylation of alpha chains leads to defective helix formation Lacks strength, vunerable to enzymatic degradation Causes heamorrhage due to affecting collagen supporting blood vessels
31
What is the major defect in Ehlers-Danos syndrome?
Defective conversion of procollagen to tropocollagen
32
Apart from collagen what are some of the other constituents of the ECM in fibrous repair?
Matrix glycoproteins: - Organise and orientate cells - Support cell migration - E.g. Fbronectin, laminin Proteoglycans: - Matrix organisation, cell support, regulate availability of growth factors Elastin: - Provides elasticity
33
What are the 3 main stages of fibrous repair?
Inflammatory cells infiltrate Clot replaced by granulation tissue Maturation
34
Describe the process of Fibrous repair
Inflammation: - Blood clot forms - Acute inflammation occurs, neutrophils digest clot - Chronic inflammation begins and macrophages and lymphocytes are recruited Granulation tissue replaces clot: - Capillaries begin to sprout and infiltrate in response to pro-angiogenic growth factors - Myo/fibroblasts migrate and differentiate and begin producing ECM (Collagen and friends) Maturation: - Cell population falls - Collagen increases, matures and remodels - Myofibroblasts contract, reducing volume of defect - Vessels differentiate and are reduced - Left with fibrous scar
35
How is fibrous repair controlled?
Complex and poorly understood: - Inflammatory cells recruited via chemotaxis - Pro-angiogenic factors release by platelets and ECM in response to hypoxia E.g. VEGF - Macrophages produce pro-fibrotic cytokines (E.g. IL-1, TNF-alpha) leading to fibroblast proliferation and ECM production
36
What is healing by primary intention?
Occurs following an incised wound in the skin with apposed edges Minimal clot and granulation tissue Epidermis regenerates Dermis undergoes fibrous repair (granulation tissue transitions to scar tissue) Sutures out at 10 days (when tissue has approx 10% strength) Maturation of scar continues for up to 2yrs resulting in minimal scarring with good strength Risk of trapping infection
37
What is healing by secondary intention?
Occurs after infarct, ulcer or any large wound Unapposed wound edges Large clot dries to form as scar or eschar Epidermis regenerates from base up Produces far more granulation tissue than primary intention healing and produces a larger scar (takes longer) Myofibroblasts must produce much more contraction to reduce defect volume
38
What are the 4 stages of bones repair?
Haemotoma formation Procallus formation Bony callus formation Remodelling
39
Describe healing of bone after a fracture
Haemotoma: - Forms from ruptured periosteal and marrow cavity vessels - Provides framework for ingress of macrophages, endothelial cells, fibroblasts and osteoblasts - Necrotic tissue removed by macrophages - Capillaries develop Procallus: - Normal granulation tissue forms + osteoblasts and osteoblast matrix - Bones is laid down in irregular woven pattern sometimes with islands of cartilage - Mineralisation begins - External Hyaline cartilage callus provides support Bony callus and remodelling: - Woven bones gradually replaced by lamellar bones - Lamellar bone remodelled to direction of mechanical stress
40
What local factors affect wound healing?
Type, size, location of wound Apposition (important in skin, bone, nerves) Lack of movement Blood supply Infection (gangrene, systemic) Foreign material (dirt, glass, sutures, necrotic tissue) Radiation damage
41
What are the general or systemic factors affecting healing?
Age Drugs (steroids, hormones) Dietary deficiency (general e.g. proteins, Vit.C, essential amino acids) General health (Diabetes, rheumatoid arthritis) Cardiovascular health
42
What are the common complication of wound healing?
Insufficient fibrosis: - Wound dehiscence (rupture of sutures) - Hernia, ulceration - Risk factors: Obesity, malnutrition, steroids Excessive fibrosis: - Cosmetic scarring, keloids - Cirrhosis, lung fibrosis Excessive contraction: - Obstruction of tubes or channels (strictures) - Limitation of joint movement (contractures)
43
Describe regeneration of the liver following acute and chronic damage
Acute: - Only organ capable of regeneration of lost tissue - Can completely regerate lost hepatocytes and structural damage Chronic: - Liver cirrhosis - Fibrous tissue replaces damaged liver tissue - Normal hepatic structure lost, hepatocytes form 'nodules' of regenerating tissue between fibrous tissues
44
Describe the healing response to acute tubular necrosis
Death of kidney tubule cells Due to toxins or hypoxia Some epithelial cells remain due to patchy necrosis of tissue, structural framework also remains intact Epithelial regeneration via mitosis occurs and epithelia is regrown on the basement membrane This leads to complete regeneration
45
Describe healing of the heart post MI
Myocardium is completely incapable of regeneration of damaged tissue Healing will always occur via fibrous repair This leads to a loss of contractile force the heart can generate, may lead to heart failure or cardiogenic shock
46
Describe the healing of cartilage
Cannot normally regenerate Chondrocytes cant migrate to damaged areas due to being trapped in lacunae Avascular, so deposition of new matrix is slow Hyaline cartilage damage may result in fibrocartilagenous scar tissue repair
47
What is Wallerian degeneration? What follows?
Degeneration of a nerve fibre distal to a cut or crushing injury Neurolemma doesn't degenerate leaving a hollow tube Axonal regrowth (sprouting) can occur in the CNS and PNS If neurolemma is held in good apposition then the proximal nerve axon can sprout into the distal neurolemma and regenerate and reinnervate the target If neurolemma is lost or not held in apposition, this is not possible
48
What is the response to CNS damage?
Gliosis Macrophages and microglia invade site of damage and begin clearing cell debris (E.g. Degenerating axons) Oligodendrocytes precursor cells then invade and begin the process of remyelination of demyelinated neurones Surrounding astrocytes will proliferate and form a glial scar This process will inhibit axonal regrowth, but can have other positive effects

ESA2 Callum's Cards - Complete (36 decks)

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