Session 4 - Healing And Repair Flashcards

1
Q

What does regeneration require for complete resolution?

A

An intact connective tissue scaffold

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2
Q

What are labile tissues?

A

Tissues which proliferate throughout life, replacing cells that are destroyed

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3
Q

Give some examples of labile tissues

A

Surface epethelia, lining mucosa of secretory ducts of glands, columnar epethelia of GI tract and uterus, cells of bone marrow and haemopoietic tissues

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4
Q

What are stabile tissues?

A

Tissues that normally have a low level of replication but cells in these tissues can undergo rapid division in response to stimuli

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5
Q

Give some examples of stable tissues

A

Parenchymal cells of liver, kidneys and pancreas, mesenchymal cells such as fibroblasts and smooth muscle cells, vascular endothelial cell, resting lymphocytes and other wbc’s

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6
Q

What are permanent tissues?

A

Tissues that contain cells that have left thee cell cycle and can’t undergo mitotic division in postnatal life

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7
Q

Give some examples of permanent tissues

A

Neurones, skeletal and cardiac muscle cells

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8
Q

What are stem cells?

A

Cells with prolonged proliferative activity

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9
Q

What are totipotent stem cells?

A

Stem cells that can give rise to any of the tissues in the human body (embryonic)

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10
Q

What are pluripotent stem cells?

A

Stem cells that can give rise to many types of cell

Eg haemetopoietic stem cells

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11
Q

What are unipotent stem cells?

A

Stem cells that can only give rise to one type of adult cell

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12
Q

What is fibrous repair?

A

When fibrovascular connective tissue grows into an area of damage

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13
Q

When may fibrous repair occur?

A
  • If collagen framework is damaged
  • If on-going chronic inflammation occurs
  • If there is necrosis of specialised parenchymal cells that cannot be replaced
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14
Q

What are the processes that occur in fibrous repair?

A
  • Phagocytosis of necrotic tissue debris
  • Angiogenesis
  • Proliferation of fibroblasts and Myofibroblasts
  • Granulation tissue becomes vascularised -> fibrous scar
  • Scar matures and shrinks due to contraction of Myofibroblasts
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15
Q

What happens in scurvy?

A
  • Vit C deficiency
  • Vit C required for hydroxyl action of ProCollagen
  • makes sufferers unable to heal wounds properly
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16
Q

What happens in Ehlers-Danlos syndrome?

A
  • collagen lacks tensile strength
  • skin is hyper extensible, fragile and susceptible to injury
  • joints are hyper mobile
  • poor wound healing and predisposition to joint dislocation
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17
Q

What happens in Osteogenesis Imperfecta?

A
  • brittle bone disease
  • too little bone tissue
  • blue sclera as not enough collagen to make them clear
18
Q

What happens in Alport Syndrome?

A
  • Type IV collagen abnormal
  • dysfunction of glomerular basement membrane, cochlear of ear and lens of eye
  • presents in boys with haematuria
  • progresses to chronic renal failure
19
Q

What is Autocrine signalling?

A

Cells respond to the signalling molecule that they produce

20
Q

What is paracrine signalling?

A

Cells produce signalling molecule that acts on adjacent cells. The responding cells are close to secreting cells and are often a different cell type

21
Q

What is endocrine signalling?

A

Hormones are synthesised in an endocrine organ, and are then conveyed in the bloodstream to target cells

22
Q

What are growth factors?

A
  • Polypeptides that act on specific cell surface receptors
  • coded for by proco-oncogenes
  • stimulate or inhibit cell proliferation
  • Effect transcription of genes that regulate whether or not cells enter the cell cycle
23
Q

What does epidermal growth factor do?

A
  • Binds to epidermal growth factor receptor

- is mitogenic for epithelial cells, hepatocytes and fibroblasts

24
Q

What does Vascular endothelial growth factor do?

A
  • Causes both vasculogenesis and angiogenesis

- in tumours, chronic inflammation and wound healing

25
Q

What does platelet derived growth factor do?

A
  • stored in platelet alpha granules
  • 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
26
Q

What do tumour necrosis factors do?

A

Induces fibroblast migration, proliferation and collagenase secretion

27
Q

What is contact inhibiton?

A

When normal cells become isolated they will replicate until they touch other cells

28
Q

What are adhesion molecules and give two examples of them and what they adhere to what?

A

Cells adhere to each other and the ECM by means of adhesion molecules.
Caherins - Binds cells to cells
Integrins - Binds cells to the ECM

29
Q

When may healing my primary intention occur?

A

When there is an incisional, closed, non-infected and sutured wound.
There is damage to the basement membrane but number of CT and epithelial cells is limited

30
Q

What are the stages of healing by primary intention?

A
  • Haemostasis (severed arteries contract)
  • Inflammation (Neutrophils appear)
  • Migration of cells (macrophages appear, scavenge neutrophils)
  • Regeneration (granulation tissue forms)
  • Early scarring (wound is filled with granulation tissue)
  • Scar maturation (mass of fibrous tissue lots of collagen)
31
Q

When will healing by secondary intention occur?

A

When there is an excisional wound with tissue loss and unopposed edges

32
Q

Define regeneration

A

Growth of cells and tissues to replace lost structures

33
Q

What is the process of healing by secondary intention?

A
  • wound is filled by abundant granulation tissue
  • Large clot and necrotic debris
  • considerable wound contraction must occur (after a week this occurs)
  • Substantial scar formation
  • healing will be delayed if infection occurs
34
Q

Describe the process of healing bone fractures

A
  • Haemotoma forms and fills and surrounds fracture site
  • Fibrin mesh and granulation tissue forms
  • Soft callus -fibrous tissue+cartilage, woven bone begins to form
  • Hard callus -laid down by osteoblasts - initially woven bone
  • Formation of lamellar bone
  • Remodelling to match original contours of bone
35
Q

Give some examples of local factors that influence healing and repair
(Long List)

A
  • Size, Location and Type of wound
  • Blood supply
  • Denervation
  • Local Infection
  • Foreign Bodies
  • Haematoma
  • Necrotic tissue
  • Mechanical Stress
  • Protection (dressings)
  • Surgical techniques (better techniques = better healing)
36
Q

Name some systemic factors influencing healing and repair

Long List

A
  • Age
  • Anaemia, hypoxia + hypovolmia (lower total blood volume)
  • Obesity
  • Diabetes
  • Malignancy
  • Genetic disorders (Eg Ehlers-danlos syndrome)
  • Drugs (Eg steroids inhibit collagen synthesis)
  • Vit deficiency (less Vit C = weaker collagen)
  • Malnutrition
37
Q

Give some examples of harmful complications of fibrous repair

A
  • formation of fibrous adhesions (may block tubes or stop function of organ)
  • Loss of function due to replacement of parenchymal cells with collage nous scar tissue
  • overproduction of fibrous scar tissue (keloid scar)
  • excessive scar contraction causing obstruction of tubes, disfiguring (scars following burns) or joint contractures
38
Q

What aspects of healing are present in Cardiac muscle?

A
  • very limited, if any regenerative capacity

- MI is followed by scar formation

39
Q

What aspects of healing are present in the Liver?

A
  • remarkable capacity to regenerate
  • remaining lobes enlarge to restore size
  • almost all hepatocytes replicate in regeneration
40
Q

What aspects of healing are present in Peripheral nerves?

A
  • if a nerve is severed the axon degenerates
  • proximal stumps of axons sprout and elongate
  • use Schwann cell to guide them back to tissue
  • grow around 1-3mm a day
41
Q

What aspects of healing are present in cartilage?

A
  • doesn’t heal well

- this is due to lack of blood supply, innervation or lymphatic drainage

42
Q

What aspects of healing are present in the CNS?

A
  • neural tissue is a permanent tissue

- if damage occurs to neural tissue it is replaced by the proliferation of glial cells