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Pathological Processes > Session 7: Cellular Adaptations > Flashcards

Session 7: Cellular Adaptations Flashcards

1
Q

Cell cycle.

A

Mitosis->Cytokinesis->G1->S->G2->Mitosis

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2
Q

What happens in G1?

A

Cellular contents excluding chromosomes are duplicated.

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3
Q

What happens in S?

A

Each of the 46 chromosomes are duplicated by the cell.

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4
Q

What happens in G2?

A

The cell double checks the duplicated chromosomes for error making any needed repairs.

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5
Q

What is G0?

A

A state where the cell cycle is at arrest.

This can be restarted again by growth signals.

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6
Q

What does size of cell population depend on?

A

Rate of cell proliferation
Cell differentiation
Cell death by apoptosis and by necrosis

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7
Q

What is a consequence of G0?

A

G0 can undergo terminal differentiation which means that there is a permanent exit from the cell cycle.

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8
Q

How does increased growth of a tissue occur?

A

By either shortening the cell cycle or by conversion of quiescent cells to proliferating cells by making them enter the cell cycle.

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9
Q

What is cell cycle progression controlled by?

A

Three key checkpoints which sense damage to DNA and ensure cells with damaged DNA do not replicate.

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10
Q

What are the three checkpoints?

A

Restriction (R) point
G1/S transition point
G2/M transition point

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11
Q

What is the R point and where can it be found?

A

Found towards the end of G1 and is the most critical checkpoint. Majority of the cells that pass the R point will complete the full cycle.

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12
Q

What happens if the R point is activated? (and other checkpoints)

A

p53 protein becomes activated and will suspend the cell cycle and trigger DNA repair mechanisms or if the DNA can’t be repaired it will trigger apoptosis.

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13
Q

What does the G1/S transition point do?

A

Checks for DNA damage after DNA replication

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14
Q

What does the G2/M transition point do?

A

Check for DNA damage after DNA replication again.

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15
Q

What happens if the cell cycle checkpoints are not working correctly?

A

Defective cell cycle checkpoints are a major cause of genetic instability in cancer cells.

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16
Q

What is G1/S transition (and the others but in particular G1/S) regulated by?

A

By proteins called cyclins and their associated enzymes called cyclin-dependent kinases aka CDKs.

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17
Q

How are CDKs activated?

A

By binding to cyclin.

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18
Q

What is the purpose of CDKs?

A

When activated they drive the cell cycle by phosphorylating proteins. This means that they are critical in order for progression of the cell to the next stage of the cell cycle.

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19
Q

What is CDKs + cyclin regulated by?

A

By CDK inhibitors.

CDK inhibitors are an emerging cancer treatment market.

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20
Q

How do growth factors work together with CDKs + cyclin?

A

Some GFs stimulate production of cyclin.

Some GFs shut down the production of CDK inhibitors.

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21
Q

What is cell adaptation?

A

The state between a normal unstressed cell and and overstressed injured cell. This is usually reversible.

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22
Q

What are the four major important types of cell adaptations?

A

Hyperplasia
Hypertrophy
Atrophy
Metaplasia

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23
Q

What is hyperplasia?

A

Increase in number of cells above normal

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24
Q

What is hypertrophy?

A

Increase in the size of the cells

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25
Q

What is atrophy?

A

When the cells become smaller

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26
Q

What is metaplasia?

A

When the cells are replaced by a different type of cell.

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27
Q

What is hyperplasia a response to?

A

Increased functional demand an/or external stimulation.
It is a physiological response to either a physiological reaction, or a pathological reaction but it is still a physiological response.
Usually hormonal stimuli or reparation of tissue damage or increased functional demand.

28
Q

In what cell populations can hyperplasia occur?

A

Only in labile or stable populations and it remains under physiological control and is reversible compared to neoplasia which is not under physiological control and not reversible.

29
Q

Causes of physiological hyperplasia.

A

It is either hormonal to increase functional capacity or compensatory to increase tissue mass after tissue damage.

Examples such as bone marrow production of erythrocytes in response to hypoxia by the increase in EPO.

Such as proliferation of endometrium under the influence of oestrogen.

30
Q

Causes of pathological hyperplasia.

A

Usually occurs secondary to excessive hormonal stimulation or GF production.

Examples such as epidermal thickening in chronic eczema and psoriasis.
Enlargement of thyroid gland in response to iodine deficiency.

31
Q

What can pathological hyperplasia lead to?

A

Neoplasia as the repeated cell divisions that occur in hyperplasia expose the cell to the risk of mutations.

32
Q

What is hypertrophy a response to?

A

Similar to hyperplasia, usually hormonal or increased functional demand of the tissue.

33
Q

In what cell populations can hypertrophy be seen?

A

Usually in all cells but especially highlighted in permanent cell populations because these cells have little or no replicative ability which means in order to increase in organ size it must be due to hypertrophy.
Endocrine stimulation is usually both hypertrophic and hyperplasic stimulation.

34
Q

Why do hypertrophic cells have more structural components?

A

Because they are synthesising more cytoplasm. This means the cellular workload is spread by a greater mass of cellular components.

35
Q

Physiological hypertrophy examples.

A

Skeletal muscle hypertrophy in weight lifters.
Smooth muscle hypertrophy in the pregnant uterus.
Compensatory hypertrophy if a kidney is removed the other one will become larger.

36
Q

Examples of pathological hypertrophy.

A

Ventricular cardiac muscle hypertrophy in response to hypertension or valvular disease.

Smooth muscle hypertrophy above an intestinal stenosis meaning the intestines must push harder in order to get the contents through the narrowing.

Bladder smooth muscle hypertrophy in a bladder obstruction or enlarged prostate gland.

Hypertrophy is reversible.

37
Q

There are two perspectives of atrophy. Which?

A

Cellular atrophy and organ atrophy

38
Q

Explain cellular atrophy.

A

Shrinkage of cell size to a size which survival is still possible.
There will be reduced function. There is a limit to shrinkage because most cellular organelles are essential for survival.

39
Q

Why do atrophic organs usually contain a large amount of connective tissue?

A

Because during atrophy cell deletion by parenchymal cells usually happens first (the functional cells) and stroll cells will follow afterwards. This means that function will be lost before structure.

40
Q

Is atrophy reversible?

A

Yes. Up to a point but after years or months.

It becomes less reversible as parenchymal cells die and are replaced by connective tissue.

41
Q

Physiological causes of atrophy.

A

Ovarian atrophy in post-menopausal women

Decrease in size of uterus after parturition.

42
Q

Pathological causes of atrophy.

A 
Immobilisaton
Loss of innervation
Inadequate blood supply in peripheral vascular disease.
Loss of endocrine stimulation
Inadequate nutrition
Persistent injury
Aging
Pressure
Occlusion of secretory duct
Toxic agents and drugs
X-rays
Immunological mechanisms.
43
Q

What is metaplasia?

A

Reversible replacement of one adult differentiated cell type by another of a different type.

44
Q

Briefly explain how it occurs.

A

Cells of one phenotype are eliminated and replaced by cells of a different phenotype. The cells do not turn into another cell type, it is replacement.
Instead stem cells within the tissues are reprogrammed so the can start to produce a different cell type.

45
Q

Can metaplasia occur over germ layers?

A

No, not proven.

46
Q

In what cell population can metaplasia occur?

A

Only in those who divide so labile and stable but not permanent. It is not known to occur in adult striated muscle cells or in neurones.

47
Q

What is the purpose of metaplasia?

A

To change on cell type to another more suited to an altered environment.

48
Q

In what type of tissue is metaplasia most commonly present?

A

In epithelial and specifically columnar epithelium which is fragile is replaced by squamous epithelium which is more resilient.

49
Q

What is a major problem with metaplasia of epithelium?

A

The metaplastic epithelium might not be able to perform some of the functions that the original epithelium did. Like mucus secretion by columnar epithelium is lost when the columnar is replaced by squamous.

50
Q

What is the main difference between metaplastic and dysplastic epithelium?

A

Metaplastic epithelium is fully differentiated and shows no sign of a mixture of epithelium.

In dysplastic epithelium the epithelium is disorganised and the differentiation is abnormal meaning there might still be pieces of columnar epithelium left or something else.

51
Q

Give examples of when metaplasia is useful.

A

Myeloid metaplasia

Columnar epithelium lining ducts change to stratified squamous epithelium

52
Q

What is myeloid metaplasia?

A

When the bone marrow is destroyed by disease splenic tissue can undergo metaplasia in order to form bone marrow.

53
Q

Why is columnar epithelium lining ducts changing to stratified squamous epithelium beneficial?

A

When it happens in salivary glands, pancreas, bile ducts or the renal pelvis due to chronic irritation by stones it can be useful to have squamous stratified epithelium in order to preserve the structure of the ducts because this epithelium is more resistant to mechanical abrasion.

54
Q

Give examples of when metaplasia is of no apparent benefit and can even be harmful.

A

Transformation of bronchial pseudo stratified ciliated columnar epithelium to stratified squamous epithelium due to cigarette smoke.

Flat non-secreting epithelium replaced by secretory epithelium or glands in lower oesophagus (epithelium in lower oesophagus becomes the same as the intestinal type of epithelium) in Barrett’s oesophagus due to persistent acid reflux.

Traumatic myositis ossificans

55
Q

Explain traumatic myositis ossificans.

A

Fibroblasts within muscle tissue undergo metaplastic change to osteoblasts causing bone formation. This can often happen in young people after premature return to activity before proper healing has occurred.

56
Q

How does traumatic myositis ossificans resolve?

A

By metaplasia in opposite direction.

57
Q

What is the connection between metaplasia and dysplasia?

A

Metaplasia can be a prelude to dysplasia and cancer.
Like in Barrett’s this can often turn to dysplasia and neoplasia.
Also intestinal metaplasia of the stomach due to chronic infection by Helicobacter pylori can lead to intestinal cancer.

However how epithelial metaplasia can go to dysplasia and then neoplasia is not understood.

58
Q

What is aplasia? (Two uses of the word)

A

Complete failure of a specific tissue or organ to develop. This means that it is of embryonic development origin.

Also used to describe an organ whose cells have ceased to proliferate like aplastic anaemia due to aplasia of the bone marrow.

59
Q

What is hypoplasia?

A

Congenital underdevelopment or incomplete development of a tissue or organ. There is a subtle difference where underdevelopment means that everything that should be there is there but it’s not of the appropriate size. There are an inadequate number of cells within the tissue present in both types.

Incomplete development is when all the components are not present.

60
Q

Give examples of hypoplasia.

A

Renal hypoplasia
Breast hypoplasia
Testicular hypoplasia in Klinefelter’s syndrome

61
Q

Difference between atrophy and hypoplasia.

A

Atrophy is when an existing part wastes away.

Hypoplasia is when the part never existed to begin with.

62
Q

What is atresia?

A

No orifice where the congenital imperforation of an opening. Aka no opening formed.
Atresia of anus and vagina

63
Q

What is reconstitution?

A

Different to regeneration because it is replacement of a lost part of the body like a lizard’s tail or deer antlers.

64
Q

What is involution?

A

Term which overlaps with atrophy.
Normal programmed shrinkage of an organ like uterus after childbirth.
Thymus in early life
Temporary foetal organs

65
Q

What is dysplasia?

A

The abnormal maturation of cells within a tissue. It is potentially reversible but is often a pre-cancerous condition. The organ starts to lose its tissue structure.

Pathological Processes (14 decks)

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