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Semester 2 > MoD Session 7 > Flashcards

MoD Session 7 Flashcards

0
Q

What regulates proliferation in physiological and pathological conditions?

A

Proto-oncogenes

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1
Q

What does the size of a cell population depend on?

A

Proliferation

Cell death

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2
Q

How are cells stimulated to divide?

A

Signal molecule binds to a receptor modulating gene expression and causing the cell to enter the cell cycle

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3
Q

How can increased cell growth arise?

A

Shortening of cell cycle

Conversion of quiescent cells

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4
Q

Where can receptors for signal molecules modulating gene expression be found in a cell?

A

Usually membrane but can be cytosol or nucleus

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5
Q

How can cell to cell signalling occur to cause cells to divide?

A

Hormones
Local mediators
Direct cell-cell/cell-stroma contact

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6
Q

How does endocrine signalling take place?

A

Cell secretes molecules into circulation which then act on a distant cell

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7
Q

How does autocrine signalling work?

A

Cell secretes molecules and expresses receptors for them on CSM

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8
Q

How does intracrine cell signalling work?

A

Cell synthesises signalling molecules but does not secrete it so it can act on receptors present in the cell

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9
Q

How does paracrine cell singling work?

A

Cell releases molecules that act on a nearby cell

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10
Q

What is G1?

A

Gap 1 stage in the cell cycle before DNA synthesis where the cell grows

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11
Q

What happens in the S stage of the cell cycle?

A

DNA synthesis

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12
Q

What is G2?

A

Gap 2 stage of the cell cycle where the cell prepares to divide

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13
Q

What happens in the M stage of the cell cycle?

A

Mitosis

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14
Q

Where are the checkpoints in the cell cycle located?

A

Between G1 and S

Between G2 and M

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15
Q

What distinctive processes occur during the M stage of the cell cycle that can be seen under the light microscope?

A

Mitosis

Cytokinesis

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16
Q

What regulates transition of a cell from G1 to S in the cell cycle?

A

Cyclin E

CDK2

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17
Q

What regulates transition of a cell from S to G2 in the cell cycle?

A

Cyclin A

CDK2

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18
Q

What regulates transition of a cell from G2 to M in the cell cycle?

A

Cyclin B

CDK1

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19
Q

What regulates transition of a cell from M to G1 in the cell cycle?

A

Cyclin D

CDK2

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20
Q

What is permanent exit from the cell cycle called?

A

Terminal differentiation

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21
Q

How long does it take for a cell to enter the cell cycle

A

A few hours

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22
Q

During which stages of the cell cycle does interphase occur?

A

G1
S
G2

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23
Q

Which is the most critical point in control of the cell cycle?

A

Restriction point towards the end of G1

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24
Q

What happens to the majority of cells that pass the restriction point?

A

Complete the full cell cycle

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25
Q

What can the restriction point towards the end of G1 also be considered as?

A

Point of no return

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26
Q

What is the most commonly altered checkpoint in cancer cells?

A

Restriction point

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27
Q

What can checkpoint activation trigger?

A

DNA repair

Apoptosis via p53

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28
Q

What action does p53 have when a checkpoint is activated?

A

Stops cell cycle and stimulates DNA repair which if not possible will then stimulate apoptosis

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29
Q

What are cells responsive to up until the restriction point?

A

Mitogenic growth factors

TGF-beta

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30
Q

How do cyclins tightly regulate the transition of cells from G to S?

A

Bind with enzymes needed causing phosphorylation of the substrate activating the cyclin dependent kinase

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31
Q

What tightly regulates the CDK-cyclin complex?

A

CDK inhibitors

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32
Q

What are growth factors?

A

Polypeptides that act on specific CSM receptors to regulate transcription of genes regulating entry and passage of the cell through the cell cycle

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33
Q

What effects do growth factors have on a cell?

A 
Proliferation
Inhibition
Locomotion
Contractility
Differentiation
Viability
Activation
Angiogenesis
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34
Q

Give four named examples of growth factors.

A

Epidermal growth factor
Vascular endothelial growth factor
Platelet derived growth factor
Granulocyte colony-stimulating factor

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35
Q

Why is GCSF given after chemotherapy?

A

Used pharmacologically to stimulate neutrophil release from bone marrow

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36
Q

What is the difference between adult and embryonic stem cells?

A

Adult have one mature type

Embryonic have multiple mature types

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37
Q

What replenishes loss of differentiated cells?

A

Tissue stem cells present in most but not all adult tissues

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38
Q

Compare the proliferation of labile, stable and permanent stem cells.

A

Labile: divide persistently to replenish losses
Stable: normally quiescent/slowly proliferating but proliferate persistently when needed
Permanent: cannot mount an effective proliferative response to significant cell loss

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39
Q

How long do labile mature cells live?

A

Short amount of time

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40
Q

Can stable mature cells proliferate if needed?

A

Yes

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41
Q

Can cell adaptation be reversed?

A

Yep as long as cell isn’t injured

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42
Q

What is regeneration?

A

Replacement of cell losses by identical cells to maintain tissue/organ size

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43
Q

How does the effectiveness of cells after regeneration change?

A

After a short delay they are as effective as the original cells

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44
Q

Why are immature respiratory epithelial cells immune to flu virus?

A

Lack receptors as not fully functional yet

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45
Q

What happens in regeneration if a harmful agent persists?

A

Causes extensive damage including to permanent cells leading to scar formation

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46
Q

What happens in regeneration if a harmful agent is removed?

A

Tissue damage is limited so regeneration can occur in non-permanent tissue causing a negligible scar which does not affect function therefore achieving resolution

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47
Q

What is the Hayflick number?

A

Number of regenerations cells can undergo dependent on species and its life expectancy

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48
Q

What is hyperplasia biologically similar to?

A

Regeneration

49
Q

What is characteristic about the increase in size seen in hyperplasia?

A

It is not uniform

50
Q

When can hyperplasia occur?

A

Only in labile or stable cell populations under reversible physiological control

51
Q

What can hyperplasia be in response to?

A

Normal response to abnormal condition

Secondary response to pathological cause

52
Q

What does hyperplasia expose a cell to?

A

Risk of mutations - neoplasia

53
Q

Why is hyperplasia seen physiologically in the endometrium and bone marrow?

A

To increase functionality of the tissue

54
Q

What stimulates physiological hyperplasia?

A

Hormones

55
Q

Give two examples of pathological hyperplasia.

A

Eczema

Goitre

56
Q

What is hyperplasia?

A

Increase in tissue/organ size due to increased cell number

57
Q

What is hypertrophy?

A

Increase in tissue/organ size due to increase in cell size

58
Q

What causes hypertrophy in permanent cells?

A

Increased workload by increased functional demand or hormonal stimulation

59
Q

Why do hypertrophied cells contain more structural components?

A

So workload is shared and therefore less likely to injure individual components

60
Q

What can hypertrophy occur alongside?

A

Hyperplasia

61
Q

In what tissues is physiological hypertrophy seen?

A

Skeletal muscle

Pregnant uterus

62
Q

In what tissues can pathological hypertrophy be seen?

A

Ventricular muscle

Bladder muscle due to compression by prostrate

63
Q

What is atrophy?

A

Shrinkage of a tissue/organ due to an acquired decrease in size and/or number of cells

64
Q

How does the reversibility of atrophy change with time?

A

Possible but becomes less so with increased time

65
Q

How are residual bodies formed in atrophy?

A

Cells get rid of what they can manage without

66
Q

In what order are tissues lost in atrophy?

A

Functional tissues are lost before connective tissue support

67
Q

In what order does pancreatic tissue atrophy?

A

Leaves islets of Langerhans in islands of CT as parenchyma lost before stroma

68
Q

What is metaplasia?

A

Reversible change of one differentiated cell type to another

69
Q

Is atrophy associated more with physiology or pathology?

A

Pathology

70
Q

What do many metaplasias represent?

A

Adaptive substitution

71
Q

What allows metaplasia to happen?

A

Altered stem cell differentiation

72
Q

How does metaplastic tissue differ from dysplastic and cancerous epithelium?

A

It is fully differentiated so is organised

73
Q

What can metaplasia sometimes prelude?

A

Dysplastia and cancer

74
Q

What cells can metaplasia happen in?

A

Only in cells that replicate

75
Q

What causes the new phenotype in metaplasia?

A

New genetic programme expression

76
Q

What is reconstitution?

A

Replacement of a lost part of the body

77
Q

How does reconstitution differ from proliferation?

A

Requires coordination of lots of different cell types not just one

78
Q

When is reconstitution seen in adults?

A

Angiogenesis

79
Q

Shay are scars hairless?

A

Hair follicles cannot reconstitute

80
Q

Why is physiological hypertrophy of cardiac muscle not dangerous?

A

There is a period of rest from the increased resistance to blood flow causing the hypertrophy

81
Q

When does physiological hypertrophy of the heart become pathological?

A

If the increased angiogenesis for the heart is insufficient and causes relative ischaemia

82
Q

What is compensatory hypertrophy?

A

Removal of one of a paired organ causes functional overstrain on the remaining organ thus causing hypertrophy

83
Q

What is seen in functional overstrain of the kidney?

A

Hypertrophy

Hyperplasia

84
Q

What happens if the functional overstrain is removed in compensatory hypertrophy?

A

Hypertrophy is resolved

85
Q

What can cause pathological atrophy?

A 
Loss of endocrine stimuli
Inadequate nutrition
Senile atrophy
Inadequate blood supply
Denervation
Persistent injury
Pressure
Disuse
86
Q

In what organs is senile atrophy seen in?

A 
Spleen
Liver
Heart
Brain
Kidneys
87
Q

Why does only partial or gradual inadequate blood supply cause pathological atrophy?

A

Sudden inadequate blood supply causes cell injury

88
Q

In what circumstances is physiological atrophy seen?

A

Post menopausal ovaries

Post childbirth

89
Q

What causes physiological atrophy?

A

Loss of endocrine stimuli

90
Q

Which disease is an example of cerebral pathological atrophy?

A

Alzheimer’s

91
Q

How can atrophy of disuse be reversed?

A

With activity

92
Q

Why does smoking cause metaplasia?

A

The end tissue is better able to withstand the irritating effects of smoke

93
Q

What change in phenotype is seen in metaplasia caused by cigarette smoking?

A

Bronchial pseudostratified ciliated epithelium to stratified squamous epithelium

94
Q

What is lost in metaplasia caused by cigarette smoke?

A

Mucociliratory escalator

95
Q

What metaplasia is seen in persistent acid reflux?

A

Stratified squamous to gastric/intestinal glandular epithelium

96
Q

What is metaplasia due to persistent acid reflux called?

A

Barrett’s oesophagus

97
Q

How does muscle injury lead to metaplasia?

A

Fibroblasts turn into osteoblasts so bone is laid down in muscle

98
Q

What causes metaplasia in muscle injury?

A

Returning to activity prematurely after injury

99
Q

What is hypoplasia?

A

Congenital condition in which there is an underdevelopment/incomplete development of a tissue/organ at the embryonic stage due to an inadequate number of cells

100
Q

Where might hypoplasia be seen?

A

Kidneys
Breasts
Testes in Klinefelter’s syndrome
Chambers of the heart

101
Q

Who discovered the function of platelets, described helicon acted pylori and classified cells by stheir ability to multiply?

A

Giulio Bizzozero

102
Q

What is aplasia?

A

Embryonic developmental disorder causing complete failure of a specific tissue/organ to develop

103
Q

What does thymic aplasia cause?

A

Infections and autoimmune problems

104
Q

What is seen in aplasia of a kidney?

A

Only one kidney present

105
Q

What term is used to describe an organ whose cells no longer proliferate?

A

Aplasia

106
Q

What is seen in aplastic anaemia?

A

Aplasia of bone marrow

107
Q

What is involution?

A

Normal programmed shrinkage of an organ

108
Q

When is involution seen?

A

Uterus after childbirth
Thymus in early life
Foetal organs (pro- and mesonephros)

109
Q

What is atresia?

A

Lack of an opening which can be seen in part of the gut/anus/vagina

110
Q

What is dysplasia?

A

Potentially reversible abnormal cells in a tissue

111
Q

What is dysplasia often seen before?

A

Cancer

112
Q

Why is the regenerative capacity of a tendon poor?

A

It is avascular

113
Q

Why is secondary rupture of a tendon common?

A

Due to abnormal use of other tendons to compensate

114
Q

What is the regenerative capacity of the skin?

A

Good

115
Q

What is the regenerative capacity of the liver?

A

Good

116
Q

What happens to transplant livers which demonstrates its good regenerative capacity?

A

It will regrow to almost the exact same size of the removed liver

117
Q

In what circumstances is peripheral nerve regeneration capacity not OK?

A

If injury is severe

If distance to be branched is too far

118
Q

Why is hypopigmentation seen in scars?

A

Poor regenerative capacity of melanocytes

119
Q

What causes a neuroma?

A

Disorganised regeneration of a peripheral nerve

120
Q

What does the CNS have instead of good regenerative capacity?

A

Plasticity to form alternative pathways around damage

121
Q

Why is improvement in symptoms seen following strokes with therapy?

A

CNS forms alternative pathways around the damage

Semester 2 (45 decks)

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