Cellular Adaptations - Hypertrophy/Hyperplasia/Atrophy etc

Question 1

Which 3 factors determine the size of a cell population?

Answer 1

Rate of proliferation, rate of death by apoptosis and cell differentiation

Question 2

What are proto-oncogenes?

Answer 2

Code for proteins that help to regulate cell growth and differentiation - can turn into oncogenes and have a role in cancer

Question 3

Broadly, how is cell proliferation controlled? Where are the receptors found?

Answer 3

By stimulus –> receptors –> turning on/off gene transcription of either stimulating or inhibitory chemical signals. Receptors usually on the cell membrane but can be on nucleus e.g. steroidogenic

Question 4

What 4 processes can the chemical signals make a cell do (inhibitory or stimulatory to cell proliferation)?

Answer 4

• Proliferate - divide
• Apoptosis
• Resist apoptosis - survive
• Differentiate

Question 5

Which two ways can a cell population increase its size?

Answer 5

• Shorten cell cycle

- Conversion of quiescent cells to prolif cells (e.g. G0 back into cell cycle)

Question 6

Can you see the cell cycle by light microscopy?

Answer 6

Yes

Question 7

Can cells with damaged DNA replicate? Where are the check points? Which is the ‘check point of no return’? When is this relevant in disease?

Answer 7

No. They are G1 before replication, G2 before mitosis and. The R point in G1 before replication is the most important cell check point - after this the cell will complete cell cycle. It is the most commonly altered check point in cancer.

Question 8

What occurs at checkpoint activation?

Answer 8

Checks DNA - if damaged, cell cycle can pause for repair or trigger apoptosis via p53

Question 9

What are cyclins and cyclin dependent kinases (CDKs)? When are the 4 different cyclins present during the cell cycle?

Answer 9

Control cell cycle - Cyclins bind to CDKs and activate them. CDKs phosphorylate important proteins needed for continuation of the cell cycle at certain points. Different cyclins are present at different points of the cell cycle. 
Cyclin D - G1
Cyclin E - G1-S
Cyclin A - S-G2
Cyclin B - G2- M

Question 10

How many times can a human cell divide?

Answer 10

61.3

Question 11

Which 4 ways can cells adapt? Which one is the least reversible?

Answer 11

Hyperplasia
Hypertrophy
Atrophy - least reversible
Metaplasia

Question 12

What is metaplasia?

Answer 12

Reversible change of one differentiated cell type to another. Eg. stem cells that produce this line of cell switch and produce another type. Is NOT one already differentiated cell to another

Question 13

Can hyperplasia occur in permanent cells? Which type of cells can it? What is the risk with increased hyperplasia? Why?

Answer 13

No only labile or stable

Risk of cancer as increased prolif exposes to more mutations

Question 14

Is hyperplasia in neoplasm (cancer) reversible? Why?

Answer 14

No as not under physiological control - is pathological

Question 15

Give two examples of physiological hyperplasia, and two pathological from the lectures?

Answer 15

Normal - endometrium, erythropoiesis

Pathological - Eczema, goitre

Question 16

Can hypertrophy occur in permanent cells? Does it occur in labile/stable?

Answer 16

Yes mostly in permanent, but also in the others

Question 17

What two processes can cause hypertrophy to occur (2)

Answer 17

Hormonal control or increased demand e.g. muscle

Question 18

Is the uterus in pregnancy hypertrophy hyperplasia or both?

Answer 18

Both

Question 19

Give 2 examples of pathological hypertrophy from the lecture

Answer 19

Myocardium in response to disease e.g. hypertension.

Bladder hypertrophy due to stricture

Question 20

Why don’t athletes get pathological hypertrophy?

Answer 20

Can do but mostly physiological as their hearts get a rest from increased demand in comparison with heart disease thats continuous –> pathological.

Question 21

Why is myocardium in hypertrophy sometimes hypoxic? What can this lead to?

Answer 21

Because angiogenesis may not be full thickness - so some hypertrophied areas go without blood supply –> fibrosis –> arrhythmias and sudden cardiac death.

Question 22

What is compensatory hypertrophy? give an example

Answer 22

Damage to one of a pair of organs - the other hypertrophies to compensate e.g. kidneys

Question 23

What is atrophy? Can you atrophy a whole organ? Do cells survive in atrophy?

Answer 23

Shrinkage of a tissue or organ by reducing size and/or number of cells. Yes can atrophy a whole organ - involves apoptosis too. Cell shrinkage is to a size that is still survivable - may eventually result in cell death

Question 24

Is tissue atrophy reversible?

Answer 24

Only up to a point - start to see fibrosis and this is irreversible.

Question 25

What have autophagosomes got to do with atrophy?

Answer 25

Atrophy removes cellular components/debris it can do without, that are then phagocytosed and you can see the residual bodies on microscopy - gives an indication cell is undergoing atrophy.

Question 26

Give two examples of physiological atrophy (think female)

Answer 26

Ovarian atrophy in post menopausal women | Uterus atrophy post partum

Question 27

Give examples of how the following can cause atrophy: 1) reduced demand 2) reduced blood flow 3) reduced nervous supply 4) malnutrition 5) Loss of endocrine stimuli 6) Persistent injury 7) Ageing 8) Pressure

Answer 27

- Skeletal muscle wasting - Skin thinning on legs with PVD - Thenar wasting e.g. median nerve damage - Wasting of muscles and eventually brain - Breast post menopause - loss of hormones - E.g. polymyositis (inflammation of muscle) - Brain/heart - also Alzheimers disease - Tissues around an enlarging benign tumour - maybe due to ischaemia due to pressure

Question 28

What is atrophy of extracellular matrix? Give an example

Answer 28

Loss of ECM - e.g. in osteoporosis loss of bone matrix

Question 29

What is the risk with metaplasia?

Answer 29

Can prelude dysplasia and cancer

Question 30

Give 2 examples of metaplasia

Answer 30

Pseudo stratified columnar w/villi respiratory - changing to stratified squamous in smokers Stratified squamous --> gastric glandular epithelium - Barretts oesophagus in response to reflux - oesophageal adenocarcinoma

Question 31

What is aplasia?

Answer 31

Failure of tissue/organ to form - e.g. fingers/kidney

Question 32

What is hypoplasia? Is this opposite to hyperplasia?

Answer 32

Underdevelopment/incomplete development of a tissue or organ - no not opposite to hyperplasia. E.g. renal, breast, chambers of heart, testicles in Kleinfelter's

Question 33

What is involution?

Answer 33

Fully developed then normal programmed shrinkage of an organ - e.g. thymus

Question 34

What is reconstitution? Does it occur in humans?

Answer 34

Complete reformation of a body part - e.g. lizard tail. Doesn't really happen in humans

Question 35

What is atresia? Give an example?

Answer 35

No orrifice - e.g. anal/vaginal - congenital malformation

Question 36

What is dysplasia? What can this lead to?

Answer 36

Abnormal maturation of cells in a tissue - sometimes reversible - can prelude cancer

Question 37

What is the most common metaplasia (cell type to cell type)

Answer 37

Columnar to squamous

Question 38

What is the importance of Retinoblastoma susceptibility protein in cell cycle?

Answer 38

Phosphorylated by cyclin dependent kinases and are a major control point of proceeding to the next stage of cell cycle. Particularly G1-S

Question 39

In terms of cell adaptation, what is regeneration?

Answer 39

Multiplication of cells to replace loses