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Pathological Processes > PP 4 Regeneration + Repair > Flashcards

PP 4 Regeneration + Repair Flashcards

1
Q

What happens after acute inflammation?

A

Complete resolution
Repair with connective tissue

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2
Q

Chronic inflammation meaning

A

Prolonged inflammation with associated repair

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3
Q

Process of wound healing

A

1- injury
2- haemostasis
3- inflammation
4- regeneration + repair

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4
Q

Haemostasis meaning

A

Stop blood flow out due to formation of blood clot

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5
Q

Regeneration meaning

A

Regrowth of cell
Minimal evidence of injury

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6
Q

What is regeneration only possible with?

A
  • Minor injuries e.g. superficial skin incision/abrasion
  • Connective tissue architecture must be intact
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7
Q

Types of stem cells

A

Totipotent
Multipotent
Unipotent

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8
Q

Totipotent meaning
Examples

A

Produce all cell types
e.g. Embryonic SC

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9
Q

Multi potent meaning
Example

A

Produce several cell types in one category
e.g. Haematopoietic SC

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10
Q

Unipotent meaning
Example

A

Produce one cell type
e.g. Epithelial SC

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11
Q

Stem cell locations

A
  • Epidermis - basal layer
  • Intestinal mucosa - bottom of crypts
  • Liver - between hepatocytes
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12
Q

Which tissue types can regenerate?

A

Labile tissue
Stable tissue

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13
Q

What tissue cant regenerate?

A

Permanent tissue

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14
Q

Describe labile tissue
Examples

A
  • Continuous replication of cells
  • Continuously cycling cell cycle
    e.g. epithelium, haematopoetic tissue
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15
Q

Describe stable tissue
Examples

A
  • Normally low levels of replication
  • Can undergo rapid replication if needed
  • Have left cell cycle - in G0, but can re-enter
    e.g. kidneys, liver, pancreas, bone, smooth muscle
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16
Q

Describe permanent tissue
Examples

A
  • Cells do not replicate
  • Heal by repair
  • Left cell cycle, cannot reenter
    e.g. neurones, skeletal + cardiac msucle
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17
Q

Repair meaning

A

Replacement of functioning tissue with a scar

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18
Q

Process of scar formation

A

1- bleeding + haemostasis - prevents blood loss
2- inflammation - digestion of blood clot
3- proliferation - ^ capillaries, fibroblasts, myofibroblasts
4- remodelling - maturation of scar

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19
Q

Describe proliferation in scar formation

A
  • days to weeks
  • Angiogenesis
  • Increased fibroblast and myofibroblasts > granulation tissue
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20
Q

Function of granulation tissue

A

Fills the gap
Contracts and closes the hole
Capillaries supply oxygen, nutrients + cells

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21
Q

Angiogenesis meaning

A

Development of new blood vessels

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22
Q

Function of angiogenesis in scar formation

A

New capillaries provide O2 + nutrients
Contract and close the gap

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23
Q

Describe remodelling in scar formation

A
  • Decreased cell population
  • Increased collagen from fibroblast
  • Myofibroblasts contract
  • Fibrous scar is formed
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24
Q

Cells involved in fibrous repair

A

Neutrophils
Macrophages
Lymphocyte
Endothelial cell
Fibroblast
Myofibroblasts

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25
Q

What do fibroblasts and myofibroblasts look like?

A

Spindle shaped nucleus
Cytoplasmic extensions

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26
Q

Fibroblast function

A

Secret collagen and elastin
Forms the extracellular matrix

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27
Q

What do myofibroblasts have that fibroblasts don’t?
What function does this give them?

A

Myofibroblasts contain actin
Wound contraction

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28
Q

Examples of where type 1 collagen is found

A

Bones
Tendons
Ligaments
Skin
Vessels
Sclera

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29
Q

Examples of where type 4 collagen is found

A

Basement membrane
Lens
Glomerular filtration

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30
Q

Outline the synthesis of collagen

A

1- preprocollagen undergoes vit C dependent hydroxylation of proline + lysine
2- precollagen formed - 3 PPC cross linked to form triple helix
3- C and N terminals of PC cleaved
4- tropocollagen formed
5- TP cross link formation
6- microfibrils, fibrils + collagen fibres made

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31
Q

Examples of diseases of defective collagen

A

ACQURIED
- Scurvy

INHERITED
- Osteogenesis imperfecta
- Alport syndrome
- Ehlers-Danilo’s syndrome

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32
Q

Describe scurvy

A
  • vit C deficiency
  • inadequate hydroxylation of PPC > defective triple helix > defective collagen
  • unable to heal wounds
  • tooth loss
  • tendency to bleed
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33
Q

Cause of scurvy

A

Vit C deficiency

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34
Q

Scurvy symptoms

A

Tooth loss
Insufficient wound healing
Tendency to bleed
Red gums

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35
Q

Inherited diseased of defective collagen examples and symptoms

A

Osteogenesis imperfecta
Alpert syndrome
Ehlers-Danlos syndrome

Hyper flexibility
Stretchy/fragile skin
Blue sclera (OI)
Weak bones
Poor wound healing

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36
Q

Ways of cell communication

A

Direct cell-cell contact
Local mediators - growth factors
Hormones

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37
Q

Explain cell to cell contact

A
  • Isolated cells replicate until they encounter other cells
  • Cadherins bind between cells
  • further proliferation inhibited
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38
Q

What method of communication do growth factors use?

A

Autocrine
Paracine

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39
Q

Autocrine meaning

A

Messengers acts on the cell itself

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40
Q

Paracrine meaning

A

Communication in a short distance to adjacent cells

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41
Q

What do growth factors cause?

A

The cell to leave G0 + enter cell cycle + proliferate

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42
Q

Growth factor examples

A

Epidermal GF
Vascular endothelial GF
Platelet derived GF
Tumor necrosis factor

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43
Q

What do epidermal GF induce?

A

mitosis in epithelial cells, hepatocytes and fibroblasts

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44
Q

What do vascular endothelial GF induce?

A

Angiogenesis in tumours
Chronic inflammation
Wound healing

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45
Q

What do platelet derived GF cause?

A

Migration + proliferation of fibroblasts, smooth muscle + monocytes

46
Q

What does tumour necrosis factor cause?

A

Migration + proliferation of fibroblasts
Collagenase secretion

47
Q

Fracture healing process

A

1- haematoma formation
2- soft callus formation
3- hard callus formation
4- remodelling

48
Q

Haematoma meaning

A

Solid swelling of blood

49
Q

When do soft calluses form in fracture healing?

A

After 1 week

50
Q

What forms woven bone?

A

Fibrous tissue and cartilage

51
Q

Describe soft callus formation

A

After 1 week
Fibrosis tissue + cartilage laid down > woven bone
Woven bones lacks tensile strength

52
Q

When do hard calluses form in fracture healing?

A

After several weeks

53
Q

Describe hard callus formation

A

After several weeks
Woven bone gradually organised into lamellar bone (hard, strength, structure)

54
Q

When does remodelling occur in fracture healing?

A

Month to years

55
Q

Describe remodelling in fracture healing

A

Months to years
Lamellar bone remodelled to original outline of bone

56
Q

Local factors influencing would healing

A

Size
Location
Blood supply
Denervatin
Protection
Mechanical stress
Necrotic tissue
Local infection
Foreign bodies

57
Q

Systemic factors influencing wound healing

A

Age
Anaemia, hypoxia, hypovolaemia- poor O2
Diabetes
Drugs
Vitamin deficiencies
Malnutrition

58
Q

How does diabetes influence wound healing?

A

Blood supply to damaged areas affected
Decreased infection resistance

59
Q

Complications in fibrous repair

A

Loss of function
Excessive fibrosis
Adhesions
Disruption of architecture
Excessive scar contraction

60
Q

Explain loss of function complications in fibrous repair

A

Specialised tissues replaced by fibrous tissue

61
Q

What does excessive fibrosis form?
Who is at higher risk of this?

A

Keloid scar
Afro-Caribbean population

62
Q

What can adhesions in fibrosis repair causes?

A

Obstruction of tubes due to fibrous bands from inappropriate fibrosis

63
Q

What can excessive scar contraction cause?

A

Constriction of tubes
Fixed flexion deformities

64
Q

Types of skin healing

A

Primary intention
Secondary intention

65
Q

When does primary intention occcur?

A

Small, non infected apposed edged injury

66
Q

What happens to the epidermis and dermis in primary intention?

A

Epidermis regenerate
Dermis undergoes fibrous repair > scar

67
Q

Primary intention process

A

1- haemostasis
2- inflammation
3- migration of cells
4- regeneration
5- early scarring
6- scar maturation

68
Q

Describe haemostasis in primary intention

A

Seconds to minutes
Arteries contract > space fills with blood
Scab forms > bacterial entry prevention

69
Q

Describe inflammation in primary intention

A

Minutes to hours
Neutrophils appear at edges

70
Q

Describe migration of cells in primary intention

A

Up to 48 hours
- Macrophages phagocytose dead neutrophils +
secrete cytokines e.g. fibroblast, endothelial
cells

71
Q

Describe regeneration in primary intention

A

3 days
- Macrophages replace neutrophils
- Granulation tissue invades space
- Epithelial call proliferation > epidermis thickens > scab falls off
- angiogenesis continues

72
Q

Describe early scarring in primary intention

A

7-10 days
Fibroblasts deposit collagen fibres > scar

73
Q

Describe scar maturation in primary intention

A

1 month - 2 years
Capillaries disappear over time > white scar left

74
Q

When does secondary intention occur?

A

Significant tissue loss
Infected, unopposed edged injury

75
Q

What is needed in secondary intention but not in primary?

A

Large injury
Myofibroblast contraction needed

76
Q

What happens to the epidermis and dermis in secondary intention?

A

Epidermis regenerates from edge
Dermis undergoes significant repair

77
Q

Cardiac muscle healing

A
  • Permanent cells
  • Very limited regenerative capacity
  • Myocardial infarction > scar formation >
    compromises cardiac function
78
Q

Liver healing

A

Stable cells
Can regenerate well if needed
Hepatocytes regenerate first then non-parenchyma cells

79
Q

Peripheral nerve healing

A
  • Axons degenerate in damage
  • Axon regrowth occurs at 1-3mm/day
  • Schwann cells guide axons back to nerve
    innervation
80
Q

How fast does axon regrowth occur?

A

1-3mm/day

81
Q

Cartilage healing

A

Doesn’t heal well
Lacks blood supply, innervation + lymphatic drainage

82
Q

Why does cartilage not heal well?

A

Lacs blood supply, innervation + lymphatic drainage

83
Q

CNS healing

A

Neural tissue is permanent
When damaged, CNS supportive elements (glial cells) replace them

84
Q

What replaced damaged neural tissue?

A

Glial cells

85
Q

What is would dehiscence?

A

When an unstable wound splits open

86
Q

What is proud fresh?

A

When granulation tissue grows out and protrudes from wound

87
Q

Treatment of proud flesh

A

Surgical removal by scraping or cutting

88
Q

Common complication from wound healing

A

Infection

89
Q

Four types of ulcers

A

Venous
Arterial
Diabetic
Pressure

90
Q

What causes diabetic ulcers?

A

Diabetic peripheral neuropathy

91
Q

What causes arterial ulcers?

A

Peripheral vascular disease

92
Q

What causes pressure ulcers?

A

Pressure on bony prominence

93
Q

What causes venous ulcers?

A

Stasis dermatitis

94
Q

Common locations for pressure ulcers

A

Elbows
Sacrum
Heels

95
Q

Why are headed wounds hairless?

A

Hair follicles don’t regenerate in areas of damaged skin as they are a complex structure

96
Q

Why don’t hair follicles regenerate after being damaged?

A

They are a complex structure

97
Q

Why are headed wounds lighter/whiter?

A
  • melanocytes don’t regenerate
  • fibrous scar with less small blood vessels
98
Q

Why are headed wounds stretched?

A

Elastic fibres don’t regenerate in areas of damaged skin
This meaning scars stretch as they mature

99
Q

Why are scars stretch as they mature?

A

Elastic fibres don’t regenerate in areas of damaged skin

100
Q

What are abdominal adhesions?

A

Bands of fibrous tissue that form between abdominal tissues + organs

101
Q

What is Alpert syndrome?

A

Condition with abnormal type IV collagen

102
Q

What is abnormal is Alport syndrome and what does this result in?

A

Type IV collagen
Dysfunction of the glomerular basement membrane, cochlea of ear + lens of eye

103
Q

Presentation of Alport syndrome?

A

Haematuria as children
Neural deafness
Eye disorders:
- Keratoconus - thinning of cornea
- Lenticonus - protrusion of lens capsule
- Cataracts

104
Q

How do skeletal muscle fibres undergo repair after damage?

A

Contain satellite cells that retain their mitotic ability + act as muscle stem cells

105
Q

How do corticosteroids inhibit wound healing?

A

Immunosuppressive
Inhibit collagen synthesis

106
Q

What is Ehlers-Danlos syndrome?

A
  • Inherited disorder due to defective conversion of procollagen to troprocollagen due to no lysyl oxidase
  • Collagen fibres lack adequate tensile strength&raquo_space; skin is hyperextensible ‘stretchy skin’ + susceptible to injury + joints are hypermobile
107
Q

What are the associated risks of Ehlers-Danlos syndrome?

A

Poor wound healing
Predisposition to joint dislocation
Rupture of colon, large arteries + cornea
Retrial detachment

108
Q

What is osteogenesis imperfecta?
Presentations

A

Brittle bone disease

Patients have too little bone tissue > extreme skeletal fragility

Blue sclera - little collagen
Hearing impairment
Dental abnormalities

109
Q

What type of drugs inhibit wound healing?

A

Corticosteroid - immunosuppressive + inhibit collagen synthesis

110
Q

How long do each of the processes last in scar formation?

A
  • bleeding + haemostasis: second to minutes
  • inflammation: minutes to days
  • proliferation: days to weeks
  • remodelling: weeks to years

Pathological Processes (14 decks)

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