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Pathology > Cellular Adaptations - Hypertrophy/Hyperplasia/Atrophy etc > Flashcards

Cellular Adaptations - Hypertrophy/Hyperplasia/Atrophy etc Flashcards

1
Q

Which 3 factors determine the size of a cell population?

A

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

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2
Q

What are proto-oncogenes?

A

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

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3
Q

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

A

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

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4
Q

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

A
  • Proliferate - divide
  • Apoptosis
  • Resist apoptosis - survive
  • Differentiate
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5
Q

Which two ways can a cell population increase its size?

A
  • Shorten cell cycle

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

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6
Q

Can you see the cell cycle by light microscopy?

A

Yes

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7
Q

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?

A

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.

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8
Q

What occurs at checkpoint activation?

A

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

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9
Q

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

A 
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
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10
Q

How many times can a human cell divide?

A

61.3

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11
Q

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

A

Hyperplasia
Hypertrophy
Atrophy - least reversible
Metaplasia

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12
Q

What is metaplasia?

A

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

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13
Q

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

A

No only labile or stable

Risk of cancer as increased prolif exposes to more mutations

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14
Q

Is hyperplasia in neoplasm (cancer) reversible? Why?

A

No as not under physiological control - is pathological

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15
Q

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

A

Normal - endometrium, erythropoiesis

Pathological - Eczema, goitre

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16
Q

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

A

Yes mostly in permanent, but also in the others

17
Q

What two processes can cause hypertrophy to occur (2)

A

Hormonal control or increased demand e.g. muscle

18
Q

Is the uterus in pregnancy hypertrophy hyperplasia or both?

A

Both

19
Q

Give 2 examples of pathological hypertrophy from the lecture

A

Myocardium in response to disease e.g. hypertension.

Bladder hypertrophy due to stricture

20
Q

Why don’t athletes get pathological hypertrophy?

A

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

21
Q

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

A

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

22
Q

What is compensatory hypertrophy? give an example

A

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

23
Q

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

A

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

24
Q

Is tissue atrophy reversible?

A

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

25
Q

What have autophagosomes got to do with atrophy?

A

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.

26
Q

Give two examples of physiological atrophy (think female)

A

Ovarian atrophy in post menopausal women

Uterus atrophy post partum

27
Q

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

A
  • 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
28
Q

What is atrophy of extracellular matrix? Give an example

A

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

29
Q

What is the risk with metaplasia?

A

Can prelude dysplasia and cancer

30
Q

Give 2 examples of metaplasia

A

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

31
Q

What is aplasia?

A

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

32
Q

What is hypoplasia? Is this opposite to hyperplasia?

A

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

33
Q

What is involution?

A

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

34
Q

What is reconstitution? Does it occur in humans?

A

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

35
Q

What is atresia? Give an example?

A

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

36
Q

What is dysplasia? What can this lead to?

A

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

37
Q

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

A

Columnar to squamous

38
Q

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

A

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

39
Q

In terms of cell adaptation, what is regeneration?

A

Multiplication of cells to replace loses

Pathology (13 decks)

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