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MoD > Lesson 4 > Flashcards

Lesson 4 Flashcards

1
Q

What is the underlying principle of wound healing?

A
  • Close the gap
  • Repair it with a scar
  • The smaller the scar the better
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2
Q

What process are involved in wound healing?

A
  1. Haemostasis – as vessels are open
  2. Inflammation – as there has been tissue injury
  3. Regeneration (resolution, restitution) and/or repair (organisation) – as structures have been injured or destroyed
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3
Q

What is the difference between an abrasion and an ulcer?

A

Abrasion superficial scrapes

Ulcers - deeper ‘gouges’/more superficial injury by bacteria or other pathogen

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4
Q

Which cells replicate in regeneration?

A

New differentiated cells are mainly derived from stem cells (many terminally differentiated cells can’t divide)

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5
Q

What are stem cells?

A
  • Prolonged proliferative activity
  • Show asymmetric replication
  • ‘Internal repair system’ to replace lost or damaged cells in tissues
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6
Q

Whereabouts in the tissues are the stem cells?

A
  • Epidermis – basal layer adjacent to the basement membrane
  • Intestinal mucosa – bottom of crypts
  • Liver – between hepatocytes and bile ducts
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7
Q

What are the three types of stem cells?

A

Unipotent
Multipotent
Totipotent

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8
Q

Explain unipotent cells

A

Most adult stem cells

Only produce one type of differentiated cell, e.g. epithelia

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9
Q

Describe multipotent cells

A

Produce several types of differentiated cell

e.g. haematopoietic stem cells

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10
Q

Describe totipotent cells

A
  • Embryonic stem cells

* Can produce any type of cell and therefore any tissues of the body

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11
Q

Can all tissues regenerate?

A

No depends where the tissues are:
Labile tissues - surface epithelia, haematopoietic tissues
Stable tissues - liver parenchyma, bone, fibrous tissue
Permanent tissues - neural tissue, skeletal/cardiac muscle

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12
Q

What are examples of Labile tissues?

A

Surface epithelia, haematopoietic tissues

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13
Q

What are examples of Stable tissue?

A

Liver parenchyma, bone, fibrous tissue, endothelium

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14
Q

What are examples of Permanent tissues?

A

neural tissue, skeletal muscle, cardiac muscle

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15
Q

In what circumstances can regeneration take place?

A
  • If the damage occurs in a labile or stable tissue
  • If the tissue damage is not extensive
    • Regeneration requires an intact connective tissue scaffold
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16
Q

What is fibrous repair (organisation) and when does it occur?

A
  • Healing with formation of fibrous connective tissue = scar
    • Specialised tissue is lost
    • Healing by secondary intention
  • Occurs with:
    • Significant tissue loss
    • If permanent or complex tissue is injured
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17
Q

How does a scar form?

A
  • Seconds - minutes: haemostasis
  • Minutes - hours: acute inflammation
  • 1-2 days: chronic inflammation
  • 3 days: granulation tissue forms
  • 7-10 days: early scar
  • Weeks – 2 years: scar maturation
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18
Q

What is granulation tissue?

A
  • Has a granular appearance and texture
  • 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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19
Q

State the steps of fibrous repair?

A
  1. Blood clots
  2. Neutrophils infiltrate/digest clot
  3. Macrophages/lymphocytes are recruited
  4. Vessels sprout, myo/fibroblasts make glycoproteins
  5. Vascular network, collagen synthesised, macrophages reduced
  6. Maturity, cells reduced, collagen matures, contracts/remodels
20
Q

Which cells are involved fibrous repair?

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 myofibroblast

21
Q

What is collagen?

A
  • Most abundant protein in animals, 28 different types known numbered in order of discovery
  • Accounts for almost a third of mammalian body’s proteins
  • Provides extracellular framework for all multicellular organisms
  • Composed of triple helices of various polypeptide alpha chains, rope-like appearance
  • Fibrillar collagens: I – III, responsible for tissue strength
  • Amorphous collagens: IV-VI, e.g. basement membrane
22
Q

Where is type 1 collagen found?

A
  • Type I most common, found in hard and soft tissues:

* Bones, tendons, ligaments, skin, sclera, cornea, blood vessels, hollow organs

23
Q

Where is Type IV collagen found?

A

•Type IV makes up basement membranes • Secreted by epithelial cell

24
Q

How are fibrillar collagens made?

A
  • Whole process takes 1-2 hours
  • Polypeptide alpha chains synthesised in ER of fibroblasts and myofibroblasts
  • Enzymatic modification steps including vitamin C dependent hydroxylation
  • Alpha chains align and cross-link to form procollagen triple helix
  • Soluble procollagen is secreted
  • After secretion procollagen cleaved to give tropocollagen
  • Tropocollagen polymerises to form microfibrils and then fibrils
  • Bundles of fibrils form fibres
  • Cross-linking between molecules produces tensile strength
  • Slow remodelling by specific
25
Q

What diseases are the result of defective collagen synthesis?

A 
Acquired 
	• Scurvy
Inherited
	• Ehlers-Danlos syndrome
	• Osteogenesis imperfecta 
	• Alport syndrome
26
Q

Describe scurvy

A
  • Vitamin C Deficiency
  • Inadequate vitamin C dependent hydroxylation of procollagen alpha chains leads to reduced cross-linking and defective helix formation
  • Lacks strength, vulnerable to enzymatic degradation
  • Particularly affects collagens supporting blood vessels
27
Q

What is the impact of scurvy on the body?

A
  • Unable to heal wounds, tendency to bleed
  • Tooth loss
    • Collagen in periodontal ligament has short half life and normal collagen is replaced by defective collagen
  • Old scars break down and open up as fresh wounds
    • Collagen turnover in scars remains high long after healing process appears clinically complete
28
Q

Describe Ehlers-Danlos syndrome

A
  • Heterogeneous group of 13 subtypes of inherited disorders
  • Defective conversion of procollagen to tropocollagen
  • Collagen fibres lack adequate tensile strength
  • Wound healing poor
  • Skin - hyperextensible, thin, fragile and susceptible to injury

NB. Skin can recoil because elastic fibres are normal, it is just missing the tethering effect of normal collagen fibres

29
Q

Where does Ehlers-Danlos syndrome effect the body?

A
  • Joints – hypermobile, predisposition to joint dislocation
  • In some forms:
    • Rupture of colon, large arteries or cornea
    • Retinal detachment
  • ‘Rubber people’
30
Q

Describe osteogenesis imperfecta

A
  • = brittle bone disease, Lobstein’s disease
  • Too little bone tissue -> extreme skeletal fragility
  • Affected people - avoid mechanical stress
  • Some develop severe, progressive deformation of long bones
  • Blue sclerae – too little collagen within them, translucent
  • Hearing impairment/dental abnormalities
31
Q

Describe Alpert syndrome

A
  • Usually X-linked disease -> patients usually male
  • Type IV collagen abnormal
  • Dysfunction of glomerular basement membrane, cochlea of ear and lens of eye
  • Presents with haematuria in children/adolescents progressing to renal failure
  • Also neural deafness and eye disorders
32
Q

How are regeneration and repair triggered and controlled?

A
  • Complex/poorly understood processes
  • Cells communicate with each other to produce a proliferative response
  • Cell to cell signalling can be via:
    • Hormones
    • Local mediators (e.g., growth factors)
    • Direct cell-cell or cell-stroma contact
33
Q

What are growth factors?

A
  • Particularly important in wound healing
  • Polypeptides that act on cell surface receptors
  • Coded by proto-oncogenes
  • ‘Local hormones’
  • Bind to specific receptors, stimulate transcription of genes that regulate entry of cell into cell cycle and the cell’s passage through it
34
Q

Apart from cell proliferation, what other effects can growth factors have?

A
  • Inhibition of division
  • Locomotion
  • Contractility
  • Differentiation
  • Viability
  • Activation
  • Angiogenesis
35
Q

What are examples of growth factors?

A
  • Epidermal growth factor
  • Vascular endothelial growth factor
  • Platelet derived growth factor
  • Tumour necrosis factor
  • Produced by cells such as platelets, macrophages, endothelial cells
  • NB: Names can be obsolete or misleading!
36
Q

What is the role of cell-cell and cell-stroma contact?

A

Contact inhibition
– Signalling through adhesion molecules
– Cadherins bind cells to each other
– Integrins bind cells to the extracellular matrix
Inhibits proliferation in intact tissue, promotes proliferation in damaged tissues
Altered in malignant cells

37
Q

What is meant by healing by primary intention and healing by secondary intention?

A
  • Descriptions of wound healing related to the size of the wound and the amount of lost tissue
  • Most often used for skin wounds
38
Q

What is healing by primary intention?

A
  • Incised, closed, non-infected and sutured wounds
  • Disruption of basement membrane continuity but death of only small number of epithelial and connective tissue cells
  • Minimal clot and granulation tissue
39
Q

What occurs in healing by primary intention?

A
  • Epidermis regenerates
  • Dermis undergoes fibrous repair
  • Sutures out at about 10 days - approximately 10% normal strength
  • Minimal contraction & scarring, good strength
40
Q

What is healing by secondary intention?

A
  • Excisional wound, wounds with tissue loss and separated edges, infected wounds, e.g., infarct, ulcer, abscess
  • Open wound filled by abundant granulation tissue – grows in from wound margins
41
Q

How does bone heal?

A
  • Haematoma: fills gap and surrounds injury
  • Granulation tissue forms: cytokines activate osteoprogenitor cells
  • Soft callus: at 1 week, fibrous tissue and cartilage within which woven bone forms
  • Hard callus: after several weeks, initially woven bone – weaker and less organised than lamellar bone but can form quickly
  • Lamellar bone: replaces woven bone, remodelled to direction of mechanical stress, bone not stressed is resorbed and outline is re-established
42
Q

What are the four stages of bone healing?

A

Haematoma -> soft callus -> hard callus -> remodelling

43
Q

What things can influence wound healing?

A

Local factors:

  1. Type, size, location of wound
  2. Mechanical stress
  3. Blood supply
  4. Local infection
  5. Foreign bodies
44
Q

What things can influence wound healing?

A

General Factors:

  1. Age
  2. Anaemia, hypoxia and hypovolaemia
  3. Obesity
  4. Diabetes
  5. Genetic disorders
  6. Drugs
  7. Vitamin deficiency
  8. Malnutrition
45
Q

What are the complications of fibrous repair?

A

•Insufficient fibrosis
• Wound dehiscence, hernia, ulceration
• For example obesity, elderly, malnutrition, steroids
•Formation of adhesions
• Compromising organ function or blocking tubes
e.g., intestinal obstruction following abdominal surgery
•Loss of function
• Due to replacement of specialised functional parenchymal cells by scar tissue
e.g., healed myocardial infarction with non-contracting area of myocardium
• Disruption of complex tissue relationships within an organ
• Distortion of architecture interfering with normal function
e.g., liver cirrhosis
• Overproduction of fibrous scar tissue
• Keloid scar
• Excessive scar contraction
• Can cause obstruction of tubes, disfiguring scars following burns or joint contractures (fixed flexures)

MoD (11 decks)

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