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2 - PP > Healing and Repair > Flashcards

Healing and Repair Flashcards

1
Q

Define regeneration

A

Restitution with no, or minimal, evidence that there was previous injury
Healing by primary intention
Superficial abrasion

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2
Q

What type of tissue can regeneration take place

A

Labile or stable

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3
Q

What is abrasion and ulceration

A

Abrasion - lose top few layers of cells

Ulceration is severe form of abrasion - injury into submucosa

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4
Q

What are labile tissues

A

Contain short live cells that are replaced from cells derived from stem cells
Constantly regenerating
Eg. Surface epithelia, haematopoietic tissue

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5
Q

What are stable tissues

A

Normally low level of replication but if necessary can undergo rapid proliferation
Both stem cells and mature cells proliferate
Eg. Liver parenchyma, bone fibrous tissue, endothelium

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6
Q

What are permanent tissues

A

Mature cells can’t undergo mitosis and no or only a few stem cells present
Eg. Neural tissue, skeletal muscle, cardiac muscle

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7
Q

Where are cells involved in regeneration derived from

A

Stem cells

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8
Q

What does asymmetric replication of stem cells mean

A

One stays as stem cells while other becomes a mature cell in differentiation

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9
Q

How do stem cells differentiate

A

Stem cells become transit amplifier progenitor and then different cells
Most are TA progenitor - involved in proliferation and give rise to differentiated cells
Stem cells need to be protected from mutation, so occasionally are in cell cycle

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10
Q

Describe the three types of stem cells

A

Unipotent - only give rise to one type of differentiated cell
Most adult stem cells
Eg. Epithelia
Multipotent - produce several types of differentiated cell
Eg. haematopoietic stem cells in bone marrow produce blood cells
Totipotent - can produce any type of cell and therefore any tissue in the body
Embryonic stem cells

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11
Q

What is fibrous repair and when does it occur

A

Healing with formation of fibrous connective tissue - scarring
Healing by secondary intention
Specialised tissue is lost
Occurs when collagen framework is damaged, on-going chronic inflammation or necrosis of permanent tissue

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12
Q

What is granulation tissue and its functions

A

Consists of developing capillaries, fibroblasts and myofibroblasts, chronic inflammatory cells
Functions - fills the gap, capillaries supply oxygen nutrients and cells, contracts and closes the hole

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13
Q

Explain the process of fibrous repair

A
  1. Haemostasis - blood clots
  2. Acute inflammation - neutrophils infiltrate and digest clot
  3. Chronic inflammation - macrophages and lymphocytes are recruited
  4. Granulation tissue forms - vessels sprout, fibroblasts and myofibroblasts make glycoproteins
  5. Early scar - vascular network, collagen synthesised, macrophages reduced
  6. Scar maturation - cells much reduced, collagen matures, contracts and remodels
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14
Q

What is the difference between regeneration and fibrous repair

A

Regeneration replaces dead cells with the same type of cells

Fibrous repair replaces dead cells with scar tissues and causes loss of function

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15
Q

Distinguish between primary and secondary healing intention

A

Primary intention occurs when the tissue surfaces have been closed
eg. surgical excision
Secondary intention occurs when there is significant tissue loss and the edges cannot be brought together
Lasts longer, more scarring, more susceptible to infection

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16
Q

What cells are involved in fibrous repair

A

Inflammatory cells
Phagocytosis debris - neutrophils + macrophages
Production of chemical mediators - lymphocytes, macrophages
Endothelial cells
Proliferation results in angiogenesis (formation of new blood vessels)
Fibroblasts and myofibroblasts
Produce extracellular matrix proteins - collagen
Responsible for wound contraction - contraction of fibrils within myofibroblasts

17
Q

What are scars white and stretch

A

Scars become white as no regeneration of melanocytes
Scars may stretch as fibroblasts cannot lay down elastin
Epidermis cannot regenerate complex structures such as hair follicles and sweat glands

18
Q

Describe collagen

A

Provides extracellular framework for all multicellluar organisms
Responsible for holding body together, including skeleton
Composed of triple helices of polypeptide alpha chains
Type I most common, found in hard and soft tissue
Type IV makes up basement membranes - secreted by epithelial cells

19
Q

How is collagen made

A
  1. Polypeptide alpha chains (preprocollagen) synthesised in ER of fibroblasts and myofibroblasts
  2. Enzymatic modification steps including vitamin C dependent hydroxylation
  3. Alpha chains align and cross link to form procollagen triple helix
  4. Soluble procollagen is secreted
  5. Procollagen ends cleaved to give tropocollagen
  6. Tropocollagen polymerises to form microfibrils and then fibrils
  7. Bundles of fibrils form fibres
  8. Cross-linking between molecules produces tensile strength
  9. Slow remodelling by specific collagenases
20
Q

Explain the role of growth factors

A

Local mediators important in would healing
Coded by proto-oncogene
Bind to specific receptors, stimulate transcription of genes that regulate entry of cell into cell cycle and the cell’s passage through it
Cyclin dependent kinase activated by cyclin and phosphorylates pRb to enter cell cycle
Restriction point on cell cycle - when beyond restriction point, cell no longer depends on growth factors
Produced by cells such as platelets, macrophages, endothelial cells
Growth factors include epidermal growth factor, vascular endothelial growth factor, platelet derived growth factor and tumour necrosis factor
Growth factors also involved in inhibition of division, locomotion, contractility, differentiation, viability, activation, angiogenesis

21
Q

Explain contact inhibition

A

Signalling through adhesion molecules - cadherins bind cells to each other, integrins bind cells to the ECM
Inhibits proliferation in intact tissue, promotes proliferation in damaged tissue
Cells will grow and differentiate until it is touching another cell
Malignant cells do not stop growing and overlap over each other

22
Q

Describe primary intention healing

A

Incised, closed, non-infected and sutured (stitched) wounds
Disruption of basement membrane continuity but death of only small number of epithelial and connective tissue cells
Epidermis regenerates until they join, then grow up to push scab off
Dermis undergoes fibrous repair
Minimal contraction and scarring of wounds
Eg. Surgical excision

23
Q

Explain secondary intention healing

A

Excisional wound, wounds with tissue loss, inflected wounds
Eg. Infarct, ulcer, abscess
Open wound filed by abundant granulation tissue - grows in from wound margins
Considerable wound contraction to close wound
Substantial scar formation, new epidermis often thinner than usual
Takes longer than healing by primary intention
Contracture - scar over joint that will contract and cause deformity - physiotherapy needed

24
Q

Explain the process of bone healing

A
  1. Haematoma - fills gap and surrounds injury
  2. Granulation tissue forms - cytokines activate osteoprogenitor cells
  3. Soft callus - at 1 week, fibrous tissue and cartilage within which woven bond forms
  4. Hard callus - after several weeks, initially woven bone - weaker and less organised than lamellar bone but can form quickly
  5. Lamellar bone - replaces woven bone, remodelled to direction of mechanical stress
    Bone not stressed is resorbed and outlines is re-established
25
Q

What are local wound healing factors

A 
Type, size, location of wound 
Mechanical stress - movement around wound 
Blood supply
Local infection 
Foreign bodies
26
Q

What are general/systemic wound healing factors

A 
Age
Anaemia, hypoxia, hypovolaemia
Obesity
Diabetes
Genetic disorders
Drugs - steroids disrupt collagen synthesis 
Vitamin deficiency
Malnutrition
27
Q

Describe some complications of fibrous repair

A

Insufficient fibrosis - wound dehiscence, hernia, ulceration
Eg. Obesity, elderly, malnutrition, steroids
Formation of adhesions - block tubes and compromise organ function
Eg. Intestinal obstruction following abdominal surgery
Loss of function - due to replacement of specialised functional parenchymal cells by scar tissue
Eg. Healed myocardial infarction with non-contracting area of myocardium
Disruption of complex tissue relationships within an organ
Distortion of architecture interfering with normal function
Eg. Liver cirrhosis
Overproduction of fibrous scar tissue
Keloid scar
Excessive scar contraction
Can cause obstruction of tubes, disfiguring scars following burns or joint contractures

28
Q

What is special about healing in heart

A

Cardiac muscle has limited regenerative capacity and MI is followed by scar formation
Compromise cardiac function

29
Q

What is special about healing in liver

A

Remarkable capacity to regenerative even when part is removed
Replication of hepatocytes and non-parenchymal cells

30
Q

What is special about healing in peripheral nerve

A

When nerve is severed, axons degenerate
Proximal stumps of degenerated axons sprout and elongate
Use Schwann cells vacated by the distal degenerated axons to guide them back to the tissue that the nerve innervates

31
Q

What is special about healing in cartilage

A

Does not heal well as it lacks blood supply, lymphatic drainage or innervation

32
Q

What is special about healing in CNS

A

Neural tissue is permanent and when tissue damage occurs in the CNS, neural tissue is replaced by proliferation of CNS supportive elements (glial cells)

33
Q

Outline the time frame of fibrous repair

A 
Haemostasis: seconds - minutes
Acute inflammation: minutes - hours
Chronic inflammation: 1-2 days
Granulation tissue formation: 3 days
Early scar: 7-10 days - when stitches taken out
Scar maturation: weeks - years
34
Q

Scurvy cause, pathophysiology, presentation

A

Vitamin C deficiency
Inadequate vitamin C dependent hydroxylation of procollagen alpha chains leads to reduced cross linking and defective helix formation
Unable to heal wounds, tend to bleed
Tooth loss - collagen holding teeth have short half life, normal collagen replaced by defective collagen
Old scars breakdown and open up as fresh wounds - continuous replacement of collagen

35
Q

Ethers-Danlos syndrome description, clinical manifestation

A

Defective conversion of procollagen to tropocollagen
Collagen fibres lack adequate tensile strength
Would healing poor
Skin hyperextensible, thin, fragile and susceptible to injury
Joints - hypermobile, predisposition to joint dislocation

36
Q

Osteogenesis imperfecta description, clinical manifestation

A

Brittle bones
Little bone tissue and therefore extreme skeletal fragility
Blue sclerae - too little collagen within them and become translucent
Hearing impairment and dental abnormalities

37
Q

Alport syndrome description, clinical manisfestation

A

Usually X-linked disease - patients mostly male
Abnormal type IV collagen
Dysfunction of glomerular basement membrane, cochlea of ear and lens of eye
Haematuria (RBC in urine) progressing to renal failure

38
Q

Keloid scar microscopic and macroscopic appearance

A

Microscopic - thick collagen bundles surrounded by paler staining fibroblasts, collagen arranged irregularly
Macroscopic - red and itchy. exceed boundaries of injury

2 - PP (15 decks)

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