MoD Session 7 Flashcards
0
Q
What regulates proliferation in physiological and pathological conditions?
A
Proto-oncogenes
1
Q
What does the size of a cell population depend on?
A
Proliferation
Cell death
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
3
Q
How can increased cell growth arise?
A
Shortening of cell cycle
Conversion of quiescent cells
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
5
Q
How can cell to cell signalling occur to cause cells to divide?
A
Hormones
Local mediators
Direct cell-cell/cell-stroma contact
6
Q
How does endocrine signalling take place?
A
Cell secretes molecules into circulation which then act on a distant cell
7
Q
How does autocrine signalling work?
A
Cell secretes molecules and expresses receptors for them on CSM
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
9
Q
How does paracrine cell singling work?
A
Cell releases molecules that act on a nearby cell
10
Q
What is G1?
A
Gap 1 stage in the cell cycle before DNA synthesis where the cell grows
11
Q
What happens in the S stage of the cell cycle?
A
DNA synthesis
12
Q
What is G2?
A
Gap 2 stage of the cell cycle where the cell prepares to divide
13
Q
What happens in the M stage of the cell cycle?
A
Mitosis
14
Q
Where are the checkpoints in the cell cycle located?
A
Between G1 and S
Between G2 and M
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
16
Q
What regulates transition of a cell from G1 to S in the cell cycle?
A
Cyclin E
CDK2
17
Q
What regulates transition of a cell from S to G2 in the cell cycle?
A
Cyclin A
CDK2
18
Q
What regulates transition of a cell from G2 to M in the cell cycle?
A
Cyclin B
CDK1
19
Q
What regulates transition of a cell from M to G1 in the cell cycle?
A
Cyclin D
CDK2
20
Q
What is permanent exit from the cell cycle called?
A
Terminal differentiation
21
Q
How long does it take for a cell to enter the cell cycle
A
A few hours
22
Q
During which stages of the cell cycle does interphase occur?
A
G1
S
G2
23
Q
Which is the most critical point in control of the cell cycle?
A
Restriction point towards the end of G1
24
What happens to the majority of cells that pass the restriction point?
Complete the full cell cycle
25
What can the restriction point towards the end of G1 also be considered as?
Point of no return
26
What is the most commonly altered checkpoint in cancer cells?
Restriction point
27
What can checkpoint activation trigger?
DNA repair
| Apoptosis via p53
28
What action does p53 have when a checkpoint is activated?
Stops cell cycle and stimulates DNA repair which if not possible will then stimulate apoptosis
29
What are cells responsive to up until the restriction point?
Mitogenic growth factors
| TGF-beta
30
How do cyclins tightly regulate the transition of cells from G to S?
Bind with enzymes needed causing phosphorylation of the substrate activating the cyclin dependent kinase
31
What tightly regulates the CDK-cyclin complex?
CDK inhibitors
32
What are growth factors?
Polypeptides that act on specific CSM receptors to regulate transcription of genes regulating entry and passage of the cell through the cell cycle
33
What effects do growth factors have on a cell?
```
Proliferation
Inhibition
Locomotion
Contractility
Differentiation
Viability
Activation
Angiogenesis
```
34
Give four named examples of growth factors.
Epidermal growth factor
Vascular endothelial growth factor
Platelet derived growth factor
Granulocyte colony-stimulating factor
35
Why is GCSF given after chemotherapy?
Used pharmacologically to stimulate neutrophil release from bone marrow
36
What is the difference between adult and embryonic stem cells?
Adult have one mature type
| Embryonic have multiple mature types
37
What replenishes loss of differentiated cells?
Tissue stem cells present in most but not all adult tissues
38
Compare the proliferation of labile, stable and permanent stem cells.
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
39
How long do labile mature cells live?
Short amount of time
40
Can stable mature cells proliferate if needed?
Yes
41
Can cell adaptation be reversed?
Yep as long as cell isn't injured
42
What is regeneration?
Replacement of cell losses by identical cells to maintain tissue/organ size
43
How does the effectiveness of cells after regeneration change?
After a short delay they are as effective as the original cells
44
Why are immature respiratory epithelial cells immune to flu virus?
Lack receptors as not fully functional yet
45
What happens in regeneration if a harmful agent persists?
Causes extensive damage including to permanent cells leading to scar formation
46
What happens in regeneration if a harmful agent is removed?
Tissue damage is limited so regeneration can occur in non-permanent tissue causing a negligible scar which does not affect function therefore achieving resolution
47
What is the Hayflick number?
Number of regenerations cells can undergo dependent on species and its life expectancy
48
What is hyperplasia biologically similar to?
Regeneration
49
What is characteristic about the increase in size seen in hyperplasia?
It is not uniform
50
When can hyperplasia occur?
Only in labile or stable cell populations under reversible physiological control
51
What can hyperplasia be in response to?
Normal response to abnormal condition
| Secondary response to pathological cause
52
What does hyperplasia expose a cell to?
Risk of mutations - neoplasia
53
Why is hyperplasia seen physiologically in the endometrium and bone marrow?
To increase functionality of the tissue
54
What stimulates physiological hyperplasia?
Hormones
55
Give two examples of pathological hyperplasia.
Eczema
| Goitre
56
What is hyperplasia?
Increase in tissue/organ size due to increased cell number
57
What is hypertrophy?
Increase in tissue/organ size due to increase in cell size
58
What causes hypertrophy in permanent cells?
Increased workload by increased functional demand or hormonal stimulation
59
Why do hypertrophied cells contain more structural components?
So workload is shared and therefore less likely to injure individual components
60
What can hypertrophy occur alongside?
Hyperplasia
61
In what tissues is physiological hypertrophy seen?
Skeletal muscle
| Pregnant uterus
62
In what tissues can pathological hypertrophy be seen?
Ventricular muscle
| Bladder muscle due to compression by prostrate
63
What is atrophy?
Shrinkage of a tissue/organ due to an acquired decrease in size and/or number of cells
64
How does the reversibility of atrophy change with time?
Possible but becomes less so with increased time
65
How are residual bodies formed in atrophy?
Cells get rid of what they can manage without
66
In what order are tissues lost in atrophy?
Functional tissues are lost before connective tissue support
67
In what order does pancreatic tissue atrophy?
Leaves islets of Langerhans in islands of CT as parenchyma lost before stroma
68
What is metaplasia?
Reversible change of one differentiated cell type to another
69
Is atrophy associated more with physiology or pathology?
Pathology
70
What do many metaplasias represent?
Adaptive substitution
71
What allows metaplasia to happen?
Altered stem cell differentiation
72
How does metaplastic tissue differ from dysplastic and cancerous epithelium?
It is fully differentiated so is organised
73
What can metaplasia sometimes prelude?
Dysplastia and cancer
74
What cells can metaplasia happen in?
Only in cells that replicate
75
What causes the new phenotype in metaplasia?
New genetic programme expression
76
What is reconstitution?
Replacement of a lost part of the body
77
How does reconstitution differ from proliferation?
Requires coordination of lots of different cell types not just one
78
When is reconstitution seen in adults?
Angiogenesis
79
Shay are scars hairless?
Hair follicles cannot reconstitute
80
Why is physiological hypertrophy of cardiac muscle not dangerous?
There is a period of rest from the increased resistance to blood flow causing the hypertrophy
81
When does physiological hypertrophy of the heart become pathological?
If the increased angiogenesis for the heart is insufficient and causes relative ischaemia
82
What is compensatory hypertrophy?
Removal of one of a paired organ causes functional overstrain on the remaining organ thus causing hypertrophy
83
What is seen in functional overstrain of the kidney?
Hypertrophy
| Hyperplasia
84
What happens if the functional overstrain is removed in compensatory hypertrophy?
Hypertrophy is resolved
85
What can cause pathological atrophy?
```
Loss of endocrine stimuli
Inadequate nutrition
Senile atrophy
Inadequate blood supply
Denervation
Persistent injury
Pressure
Disuse
```
86
In what organs is senile atrophy seen in?
```
Spleen
Liver
Heart
Brain
Kidneys
```
87
Why does only partial or gradual inadequate blood supply cause pathological atrophy?
Sudden inadequate blood supply causes cell injury
88
In what circumstances is physiological atrophy seen?
Post menopausal ovaries
| Post childbirth
89
What causes physiological atrophy?
Loss of endocrine stimuli
90
Which disease is an example of cerebral pathological atrophy?
Alzheimer's
91
How can atrophy of disuse be reversed?
With activity
92
Why does smoking cause metaplasia?
The end tissue is better able to withstand the irritating effects of smoke
93
What change in phenotype is seen in metaplasia caused by cigarette smoking?
Bronchial pseudostratified ciliated epithelium to stratified squamous epithelium
94
What is lost in metaplasia caused by cigarette smoke?
Mucociliratory escalator
95
What metaplasia is seen in persistent acid reflux?
Stratified squamous to gastric/intestinal glandular epithelium
96
What is metaplasia due to persistent acid reflux called?
Barrett's oesophagus
97
How does muscle injury lead to metaplasia?
Fibroblasts turn into osteoblasts so bone is laid down in muscle
98
What causes metaplasia in muscle injury?
Returning to activity prematurely after injury
99
What is hypoplasia?
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
Where might hypoplasia be seen?
Kidneys
Breasts
Testes in Klinefelter's syndrome
Chambers of the heart
101
Who discovered the function of platelets, described helicon acted pylori and classified cells by stheir ability to multiply?
Giulio Bizzozero
102
What is aplasia?
Embryonic developmental disorder causing complete failure of a specific tissue/organ to develop
103
What does thymic aplasia cause?
Infections and autoimmune problems
104
What is seen in aplasia of a kidney?
Only one kidney present
105
What term is used to describe an organ whose cells no longer proliferate?
Aplasia
106
What is seen in aplastic anaemia?
Aplasia of bone marrow
107
What is involution?
Normal programmed shrinkage of an organ
108
When is involution seen?
Uterus after childbirth
Thymus in early life
Foetal organs (pro- and mesonephros)
109
What is atresia?
Lack of an opening which can be seen in part of the gut/anus/vagina
110
What is dysplasia?
Potentially reversible abnormal cells in a tissue
111
What is dysplasia often seen before?
Cancer
112
Why is the regenerative capacity of a tendon poor?
It is avascular
113
Why is secondary rupture of a tendon common?
Due to abnormal use of other tendons to compensate
114
What is the regenerative capacity of the skin?
Good
115
What is the regenerative capacity of the liver?
Good
116
What happens to transplant livers which demonstrates its good regenerative capacity?
It will regrow to almost the exact same size of the removed liver
117
In what circumstances is peripheral nerve regeneration capacity not OK?
If injury is severe
| If distance to be branched is too far
118
Why is hypopigmentation seen in scars?
Poor regenerative capacity of melanocytes
119
What causes a neuroma?
Disorganised regeneration of a peripheral nerve
120
What does the CNS have instead of good regenerative capacity?
Plasticity to form alternative pathways around damage
121
Why is improvement in symptoms seen following strokes with therapy?
CNS forms alternative pathways around the damage
