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Semester 2 > MoD Session 4 > Flashcards

MoD Session 4 Flashcards

0
Q

Where do the differentiated cells used in regeneration derive from?

A

Stem cells

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1
Q

What is regeneration?

A

Replacement of dad or damaged cells by functional differentiated cells

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2
Q

Describe the proliferation of stem cells.

A

Potentially limitless

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3
Q

What are multipotent stem cells?

A

Cells that can produce several types of differentiated cell e.g. Haemopoietic

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4
Q

What are totipotent stem cells?

A

Cells that can produce any type of cell e.g. Embryonic stem cells

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5
Q

What are uni potent stem cells?

A

Cells that can only produce one type of differentiated cell e.g. Epithelilal

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6
Q

How do stem cells differentiate?

A

Asymmetrically - one remains stem cell to maintain pool and one differentiates

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7
Q

In what type of disease can stem cells have therapeutic utility?

A

Degenerative

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8
Q

Where area totipotent stem cells found?

A

Blastocyst

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9
Q

Where might unipotent stem cells be found?

A

Base of crypts of Lieberkühn

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10
Q

What is another term for multipotent stem cells?

A

Pluripotent

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11
Q

How does the propensity to regenerate vary?

A

Between cell types

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12
Q

Describe labile cells.

A

Normal state is active cell division
Usually proliferate rapidly
Constantly progressing through cell cycle

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13
Q

Give two examples of labile cells.

A

Epithelial

Haematopoietic

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14
Q

Describe stable cells.

A

Normal state is resting state

Speed of regeneration is variable

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15
Q

Give four examples of stable cells.

A

Hepatocytes
Osteoblasts
Fibroblasts
Renal tubule

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16
Q

Describe permanent cells.

A

Unable to divide

Cannot regenerate

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17
Q

Give two examples of permanent cells.

A

Neurones

Cardiac myocytes

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18
Q

What two mechanisms control regeneration?

A

Growth factors

Cross talk b/w basement membrane and adjacent cells

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19
Q

How does binding of growth factor to membrane-bound tyrosine kinase receptor cause cellular responses?

A

Receptor dimerises, forms kinase ability –> acts on membrane bound kinase –> increases transcription factors –> cellular responses

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20
Q

What is the membrane bound kinase acted upon by the dimerised receptor after growth factor binding?

A

ras

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21
Q

What two pathways can ras take to have effects on a cell exposed to growth factor?

A

ras –> raf –> mck –> erk –> transcription factors

ras –> P13k –> Akt –> survival, proliferation, migration

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22
Q

Which molecules act as growth factors?

A

Proteins: EGF, PDGF, FGF
Hormones: oestrogen, testosterone, GH
Autocrine, paracrine and endocrine signals from many cell types

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23
Q

Where does epidermal growth factor come from?

A

Keratinocytes
Macrophages
Inflammatory cells

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24
Q

What is contact inhibition?

A

Signalling through adhesion molecules which inhibitis proliferation in intact tissues

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25
Q

What happens to cells that are isolated in culture?

A

Become motile and proliferate rapidly until a monolayer is formed

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26
Q

What abnormalities of regeneration are seen in cancer?

A

Abnormalities in growth factors and contact inhibiton

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27
Q

How can contact inhibition be lost in cancer?

A

E-Catherine binds w/calcium to form a dimer –> allows activation of beta caterin which binds to actin filaments in cytoplasm preventing them from adhering

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28
Q

What is fibrous repair?

A

Replacement of functional tissue by scar tissue

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29
Q

What must occur for fibrous repair and scarring to be caused?

A

Necrosis of permanent cells

Necrosis of labile or stable cells with collagen framework damage

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30
Q

If the collagen framework of necrotised labile or stable cells remains intact, what happens?

A

Resolution of injury and inflammation

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31
Q

What are the key components of fibrous repair?

A

Cell migration
Angiogenesis
Extracellular production
Extracellular remodelling

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32
Q

What is granulation tissue?

A

Specialised type of tissue only seen in areas of chronic inflammation and fibrous repair

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33
Q

What cell types are seen in fibrous repair?

A

Inflammatory cells
Endothelial cells
Fibroblasts/myofibroblasts

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34
Q

What role do inflammatory cells carry out in fibrous repair?

A

Neutrophils and macrophages phagocytose debris

Lymphocytes and macrophages release chemical mediators

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35
Q

What role do endothelial cells carry out in fibrous repair?

A

Angiogenesis

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36
Q

What is the function of fibroblasts and myofibroblasts in fibrous repair?

A

Synthesise extracellular matrix proteins

Wound contraction

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37
Q

What characteristics do myofibroblasts have?

A

Smooth muscle qualities

Contractile fibres

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38
Q

What are the five steps of angiogenesis?

A

Endothelial proteolysis of BM
Migration of endothelial cells via chemotaxis
Endothelial proliferation
Endothelial maturation and tubular remodelling
Recruitment of periendothelial cells

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39
Q

What is released from an hypoxic site of injury to induce angiogenesis?

A

Growth factors e.g. VEGF

Platelets

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40
Q

What role do pre-existing unaffected blood vessels have in angiogenesis?

A

Sprout new vessels

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41
Q

What exploits angiogenesis so it is not limited by vascular supply?

A

Malignant cells

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42
Q

What are the functions of the extracellular matrix?

A 
Support and anchor cell
Separate tissue compartments
Sequester growth factors 
Allow communication b/w cells
Facilitate cell migration through tissues
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43
Q

What is the function of collagen in the extracellular matrix?

A

Provide extracellular framework

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44
Q

Which types of collagen are fibrillar and where are they found?

A

I-III

Everywhere

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45
Q

Which types of collagen are amorphous and where are they found?

A

IV-VI

Basement membrane

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46
Q

What are amorphous collagens quite resistant to?

A

Enzymes except specific collagenases used for remodelling

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47
Q

How many types of collagen are there?

A

28

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48
Q

How is fibrillar collagen formed?

A

Polypeptide alpha chain in ER –> enzymatic modification inc. vitamin C dependent hydroxylation –> alpha chains align and cross link –> soluble procollagen triple helix secreted –> cleaved to tropocollagen –> polymerises to form fibrils which bundle to form fibres –> slow remodelling by specific collagenases

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49
Q

Name three defects of collagen synthesis which cause defective fibrous proteins.

A

Scurvy
Ehlers-Danlos syndrome
Osteogenesis Imperfecta

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50
Q

Why does scurvy cause haemorrhage and skeletal changes in infants?

A

Inadequate hydroxylation of alpha chains causes defective helix formation –> collagen supporting BV especially is weak and vulnerable to enzymatic degradation

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51
Q

How does Ehlers Danlos syndrome cause skin laxity, hyper mobile joints and lens dislocation?

A

Defective conversion of procollagen to tropocollagen

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52
Q

How does the sclera appear in osteogenesis imperfecta?

A

Thin and blue

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53
Q

What defect of collagen synthesis causes defective amorphous proteins?

A

Alport syndrome

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54
Q

Why does Alport syndrome cause renal problems?

A

The basement membrane is disrupted

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55
Q

What maintains tissue integrity and resolution?

A

Extracellular matrix

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56
Q

What secretes the extracellular matrix?

A

Fibroblasts

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57
Q

What does the extracellular matrix contain?

A

Growth factor reservoir
Matrix glycoproteins
Proteoglycans
Elastin

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58
Q

What is the function of fibronectin, laminin and tenascin in the extracellular matrix?

A

To organise and orientate cells

Support cell migration

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59
Q

What is the function of elastin in the extracellular matrix?

A

Provide tissue elasticity

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60
Q

What are the three generalised changes sene in fibrous repair?

A

Tissue becomes more cellular
Increased vascularity
Decreased extracellular matrix

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61
Q

What are the three stages of fibrous repair?

A

Inflammatory cell infiltrate
Clot replaced by granulation tissue
Maturation

62
Q

What happens in the inflammatory cell infiltrate stage of fibrous repair?

A

Extravasation of blood –> clot forms w/ingress of neutrophils around edges causing chronic inflammation –> macrophages and lymphocytes move into clot

63
Q

What affect does inflammatory cell infiltration have on the area of fibrous repair?

A

Becomes more cellular

64
Q

How is a blood clot replaced by granulation tissue in fibrous repair?

A

Capillaries and lymphocytes sprout and infiltrate
Myofibroblasts and fibroblasts recruit, migrate and differentiate
Synthesis of ECM
Myofibroblasts synthesise glycoproteins

65
Q

Are granulomas present in granulation tissue?

A

Nope

66
Q

What happens during maturation in fibrous repair?

A

Cell population falls
More collagen is present which matures and remodels
Myofibroblasts contract to reduce volume of defect
Vessels differentiate and decrease in number
Fibrous scar is formed

67
Q

Comparatively, which stage of fibrous repair is the longest lasting?

A

Maturation

68
Q

What controls inflammatory cell recruitment in fibrous repair?

A

Chemotaxis

69
Q

What controls angiogenesis in fibrous repair?

A

Cytokines released by platelets and ECM in response to hypoxia

70
Q

Give three examples of pro-fibrotic cytokines.

A

IL-1
TNF-alpha
TGF-beta

71
Q

What type of cells release pro-fibrotic cytokines causing fibroblast proliferation and ECM synthesis?

A

Macrophages

72
Q

What are the two methods of regeneration and repair of the skin?

A

Primary and secondary intention

73
Q

When is primary intention used to heal the skin?

A

Incised wound with opposed edges

74
Q

How can the clot and granulation tissue seen in primary intention skin healing be described?

A

Minimal

75
Q

What causes epidermis regeneration in both primary and secondary intention skin healing?

A

Loss of contact inhibition

76
Q

What happens to the dermis in primary intention healing?

A

Undergoes fibrous repair

77
Q

When are sutures removed in primary intention skin healing?

A

~10 days

When skin is ~10% of normal strength

78
Q

What does vascular granulation tissue lead to after ~2 years in primary intention skin healing?

A

Scar tissue

79
Q

Why does primary intention skin healing have good tensile strength?

A

Minimal contraction and scarring

80
Q

What forms is infection is trapped in the skin during primary intention healing?

A

Abscess

81
Q

What causes a laceration?

A

Blunt trauma

82
Q

What causes primary intention skin healing?

A

Clean, sutured wound

83
Q

What skin insults will be healed by secondary intention?

A

Infarct
Ulcer
Abscess
Any large wound where edges are unapposed

84
Q

What happens to the large blood clot formed during healing by secondary intention?

A

Dries to form scab or eschar

85
Q

What is an eschar?

A

Slough or piece of dead tissue cast off from surface of skin

86
Q

In which direction does the epidermis regenerate in healing by secondary intention?

A

From the base up

87
Q

How much granulation tissue is produced in healing by secondary intention?

A

Lots

88
Q

Why is more contraction seen in healing by secondary intention than in primary?

A

To decrease the larger defect volume

89
Q

How does the scar formed in healing by secondary intention compare to that formed by primary intention?

A

Larger, not necessarily weaker

90
Q

What does skin healing by secondary intention have a higher risk of complications than healing by primary intention?

A

Takes longer

91
Q

Why does healing of bone fractures require modification of the repair seen at other sites?

A

It is a special environment

92
Q

How does the haematoma form in bone fracture repair?

A

Ruptured BV in marrow cavity and periosteum

93
Q

What does haematoma organisation allow in bone fracture healing?

A

Framework for macrophage, endothelial cell, fibroblast and osteoblast ingress

94
Q

What happens after the haematoma is organised in bone fracture healing?

A

Necrotic tissue is removed and capillaries develop to form soft callus

95
Q

How is woven bone laid down in bone fracture formation?

A

W/islands of cartilage

96
Q

What role does the external callus have in the bone during fracture healing when woven bone is being laid down?

A

Provide splint-like support

97
Q

What eventually happens to woven bone in fracture healing?

A

Replaced by lamellar bone and remodelled

98
Q

What are the stages of bone fracture healing?

A 
Haematoma forms
Haematoma organised
Soft callus formed
Woven bone laid down
Woven bone replaced by lamellar bone and remodelled
99
Q

Give examples of local wound healing factors.

A 
Blood supply
Lack of movement
Foreign material
Size/location/type
Infection
Apposition
Angiogenesis impairment effecting stimulation of (myo)fibroblasts
Radiation
100
Q

What is suppuration?

A

Infection of a wound causing pus formation

101
Q

Give examples of general wound healing factors.

A 
General CVS status
Age
Drugs e.g. steroids or hormones
Dietary deficiencies
General state of health e.g. chronic diseases
102
Q

What complications of repair can arise during wound healing?

A

Insufficient fibrosis
Excessive fibrosis
Excessive contraction

103
Q

What can loss of wound strength in insufficient fibrosis cause?

A

Dehiscence
Hernia
Ulceration

104
Q

What factors increase the risk of insufficient fibrosis?

A

Obesity
Old age
Malnutrition
Steroids

105
Q

Why does obesity increase the risk of insufficient fibrosis?

A

Due to increased intrabdominal pressure

106
Q

What is the difference between a hypertrophic scar and a keloid?

A 
Hypertrophic = w/in bounds of wound and regresses w/time
Keloid = outside wound borders and does not regress w/time
107
Q

Is surgery useful for treating keloids?

A

Not really, incision is likely to cause redevelopment

108
Q

Does the injury have to be severe for a keloid to form?

A

No, it can be innocuous

109
Q

Which population is at increased risk of keloid formation?

A

Afro-Caribbean

110
Q

How is cirrhosis caused by excessive fibrosis?

A

Exuberant fibrotic response creates fibrous surrounding to nodules of new cells in liver

111
Q

What are strictures?

A

When excessive contraction causes obstruction of tubes and channels

112
Q

What disease is oesophageal stricture seen in?

A

Chronic inflammation caused by gastro-oesophageal reflux disease

113
Q

How is inflammation caused in sigmoid colon leading to formation of a diverticular stricture?

A

Small herniations of unknown cause in mucosa trap faeces –> inflammation
Fibrous repair creates stricture

114
Q

In what group of people are diverticular strictures common?

A

Elderly

115
Q

If an elderly patient presents with a diverticular stricture, which two main diseases are considered?

A

Colon cancer

Sigmoid colon

116
Q

What is a contracture?

A

Limitation of joint movement due to fibrous scarring over the joint

117
Q

What wound location causes slow healing?

A

Over a joint

118
Q

If part of the liver is removed, how does the organ respond?

A

Compensatory growth occurs and mass is restored by enlargement of remaining lobes

119
Q

How do cells in the liver replicate during liver healing?

A

Almost all hepatocytes replicate during regeneration

Non-parenchymal cells replicate afterwards

120
Q

Why is there no fibrosis in acute liver damage?

A

Scaffolding architecture is maintained

121
Q

Why are nodules formed in chronic liver damage?

A

Over-exuberant wound healing process causes CT deposition around island of new cells

122
Q

How does nodule formation in chronic liver disease progress?

A

Initially can regress but w/increased time becomes permanent

123
Q

What can nodule formation in chronic liver disease lead to?

A

Portal hypertension

Cirrhosis

124
Q

Is chronic liver damage itself symptomatic?

A

Nope

125
Q

When do kidney cells heal completely by regeneration?

A

If collagen framework is maintained

126
Q

How are epithelial cells destroyed in acute tubular necrosis of the kidney?

A

Ischaemia

127
Q

What can cause the hypoperfusion of kidney epithelial cells associated w/hypovolaemia?

A 
Haemorrhage
Burns
Severe dehydration
Pump failure/MI/cardiac tamponade 
Peripheral vasodilation
Sepsis
Anaphylaxis
Toxins
128
Q

What toxins can cause hypovolaemia leading to acute tubular necrosis?

A

NSAIDs
Aminoglycoside antibiotics
Heavy metals
Endogenous filtered proteins

129
Q

How is the necrosis seen in acute tubular necrosis typically seen?

A

Epithelial patches still alive and collagen framework intact in some areas

130
Q

How can the kidney heal so that damage can be undetectable even microscopically?

A

Remaining epithelial cells replicate using BM as a guide

131
Q

How does myocyte necrosis progress in the heart?

A

Endocardium –> epicardium

132
Q

What percentage of necrotised tissue can be salvaged if the heart is reperfused within 3 hours of MI?

A

~40%

133
Q

What can happen to the heart if it is reperfused 6hrs or longer after MI?

A

Haemorrhage

Reperfusion arrhythmias

134
Q

What is the regenerative capacity of cardiac myocytes?

A

Limited if any

135
Q

What takes place in heart healing?

A

Fibrous repair for in scar and compromising function

136
Q

What is the special regenerative tissue used in bone healing?

A

Callus - woven bone w/islands of cartilage

137
Q

What is found in the medullary cavity of a healing bone?

A

Internal callus

138
Q

What is found at the periosteum of a healing bone?

A

External callus

139
Q

How does the callus become trabecular bone in bone healing?

A

Replaced by lamellar bone which is mineralised

140
Q

What does cartilage not heal well?

A

Lack of blood supply, lymphatic drainage and innervation

141
Q

What is Wallerian degeneration?

A

Distal portion of severed peripheral nerve swells due to proliferation of Schwann cells

142
Q

What happens to the proximal axon of a severed peripheral nerve?

A

Degenerated for 1-2 nodes

143
Q

If there is good alignment of severed peripheral nerves, what happens?

A

Axons regrow down previous channels occupied by proliferative Schwann cells

144
Q

What is unusual in peripheral nerve healing?

A

Full functional recovery

145
Q

What happens if there is poor alignment or amputation of peripheral nerve?

A

Cut ends proliferate disorderly –> tangled mass of axons and stroma called an amputation neuroma which can be painful and require removal

146
Q

What is the rate of axon growth in peripheral nerve healing?

A

1-3mm per day

147
Q

What is the replicative capacity of the CNS?

A

Evidence suggests it is low

148
Q

Can the CNS regenerate?

A

Not effectively

149
Q

Why can the CNS not regenerate?

A

It is a permanent tissue

150
Q

What occurs in CNS healing?

A

Gliosis

151
Q

What is gliosis?

A

Replacement of CNS neural tissues by proliferation of glial cells

152
Q

Give two examples of disease in which gliosis is seen.

A

Multiple sclerosis

Stroke

153
Q

What is the rabbit ear chamber model?

A

Insertion of plastic chamber allowed in vivo microscopic visualisation of healing and repair due to thin tissue bed development b/w layers of the chamber

Semester 2 (45 decks)

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