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Semester 2 - PathPro > 11. Cellular adaptations > Flashcards

11. Cellular adaptations Flashcards

1
Q

What are the stages of cell cycle and what occurs in each?

A

G1: cellular contents, excluding chromosomes are duplicated
S: chromosomes are duplicated
G2: double checks duplicated chromosomes for error
Mitosis

G0: cell cycle arrest

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2
Q

At which stage of the cell cycle can cells undergo terminal differentiation?

A

Cells in G0 can undergo terminal differentiation where there is a permanent exit from the cell cycle

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3
Q

What determines the size of cell populations in adults?

A

The size of cell populations in adults depends on the rate of cell proliferation, cell differentiation and cell death by apoptosis.

You’ll get an increase in the number of cells if there’s increased cell proliferation or decreased cell death.

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4
Q

How can you increase growth of a tissue?

A

Increased growth of a tissue occurs either by shortening the cell cycle or by conversion of quiescent cells to proliferating cells by making them enter the cell cycle

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5
Q

What are the 3 major cell cycle checkpoints?

A
  • G1 checkpoint (between G1 and S phase)
  • G2 checkpoint (between G2 and mitosis)
  • The restriction point (before G1 checkpoint)
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6
Q

What does the G1 checkpoint check for?

A
  • is cell big enough
  • is environment favourable (nutrients, growth factors?)
  • is DNA damaged (checks for DNA damage before DNA replication)
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7
Q

What does the G2 checkpoint check for?

A
  • is all DNA replicated
  • is cell big enough
  • is DNA damaged (checks for DNA damage after DNA replication)

(not concerned with external environment)

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8
Q

During which period of the cell cycle are cells responsive to extracellular stimuli and which stimuli are they responsive to?

A

Between start of G1 and the restriction point.

- Growth factors and transforming growth factor beta

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9
Q

What happens to cells that pass the restriction point in the cell cycle?

A

Majority of cells that pass R point will complete cell cycle

  • point of no return
  • cannot respond to extracellular stimuli inhibiting growth
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10
Q

What is the most commonly altered checkpoint in cancer cells?

A

The restriction point

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11
Q

What happens if the restriction checkpoint is activated?

A

Delays cell cycle and triggers DNA repair mechanisms or apoptosis via p53

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12
Q

What stimuli can P53 respond to?

A
  • oxidative stress
  • nutrient deprivation
  • hypoxia
  • DNA damage
  • oncogene expression
  • ribosomal dysfunction
  • telomere attrition
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13
Q

What can P53 result in?

A
  1. cell cycle arrest - allows DNA repair
  2. Senescence - permanent cell cycle arrest
  3. Apoptosis
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14
Q

Describe the action of the p53 protein

A

The p53 protein is a tumour suppressor protein - function is to stop the formation of tumours.

DNA damage leads to increase in activated p53
It has 2 mechanism of action;
• if it notices abnormal cellular action it can induce apoptosis in a cell that can’t be repaired
• it also stimulates the formation of p21 protein.

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15
Q

what is the effect of p53 causing an increase in p21?

A

In the cell the p53 protein binds to DNA which in turn stimulates another gene to produce a protein called p21. p21 proteins prevent the phosphorylation of cycllins.

This leads to cell cycle arrest and thus allows DNA repair.

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16
Q

What are cyclins?`

A

Proteins that regulate the cell cycle

- different cyclins present at different times in different amounts during different parts of the cell cycle

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17
Q

How do cyclins control the cell cycle?

A

They bind to enzymes called cyclin dependant kinases which then become active and attach phosphate groups to other proteins in the cell
- This triggers other proteins to become active and carry out task specific to that phase of the cell cycle that are critical for progression of the cell to the next stage of the cell cycle

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18
Q

Give an examples of a protein that is regulated by cyclin/CDK complex

A

Retinoblastoma protein

• This protein usually acts to prevent DNA replication
• tumour suppressor gene
• It is inactivated by phosphorylation by cyclin D/CDK4
complex

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19
Q

What regulates the activity of cyclin-CDK complexes?

A

CDK inhibitors.

Some growth factors work by stimulating the production of cyclins and some work by shutting off production of CDK inhibitors.

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20
Q

What are teleomeres?

A

Repetitive nucleotide sequences at each end of a chromosome, which protects the end of the chromosome from deterioration or from fusion with neighboring chromosomes.
Gets shorter with each cell replication, dictates how many times a cell can divide.

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21
Q

What percentage of cancers are caused by p53 mutations?

A

70%

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22
Q

What is cell adaptation?

A

Reversible changes in number/size/phenotype/function

Cell adaptation is the state between a normal unstressed cell and an overstressed injured cell.

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23
Q

What are physiological adaptations?

A

response to normal stimulation by hormones or chemical mediators

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24
Q

What are pathological adaptations?

A

Responses to stress that allow cells to escape injury

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25
Q

What are the different types of adaptations?

A
  • hyperplasia
  • hypertrophy
  • atrophy
  • metaplasia
  • dysplasia
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26
Q

What is hyperplasia?

A

Increase in tissue or organ size due to increased cell numbers

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27
Q

In which tissues can hyperplasia occur?

A

Stable or labile tissues

28
Q

What are the 2 main causes of physiological hyperplasia?

A
  • Hormonal (when there is increase in functional demand)

- Compensatory (eg following injury)

29
Q

What causes pathological hyperplasia?

A

This is when hyperplasia occurs secondary to a pathological cause, so cellular proliferation will be a normal response to an abnormal cause.

Pathological hyperplasia usually occurs secondary to excessive hormonal overstimulation or excessive growth factor production.

30
Q

Why is Neoplasia a risk in hyperplastic tissue?

A

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

31
Q

What examples are there of physiological hyperplasia?

A
  1. Increased bone marrow production of erythrocytes in response to hypoxia resulting in increased erythropoietin
  2. The proliferation of the endometrium under the influence oestrogen
32
Q

What examples are there of pathological hyperplasia?

A
  1. Epidermal thickening in chronic eczema
  2. Psoriasis
  3. Enlargement of the thyroid gland in response to iodine deficiency.
33
Q

Is hyperplasia reversible?

A

YES

34
Q

What is hypertrophy?

A

increase in tissue or organ size due to increase in cell size

35
Q

In which types of tissue does hypertrophy occur?

A

All types but especially permanents as these cell

populations have little or no replicative potential and so any increase in organ size must occur via hypertrophy.

36
Q

What are the 2 main causes of hypertrophy?

A

caused by increased functional demand or hormonal stimulation

37
Q

Describe the microscopic characteristics of a hypertrophic cell

A

Hypertrophic cells will have more structural components e.g protein than a hyperplastic cell.
The intracellular organelles, cytoplasm and structural proteins all increase whilst the number of cells in the tissue stay the same

It will have a greater cellular workload which is why the increase in cellular components in needed

38
Q

Is it possible for hyperplasia and hypertrophy to occur at the same site?

A

In labile and stable tissues hypertrophy usually occurs along with hyperplasia

In this case the hyperplasia and the hypertrophy would be triggered by the same stimulus.

39
Q

Give physiological examples of hypertrophy.

A
  1. Skeletal muscle hypertrophy folowing exercise e.g of a bodybuilder
  2. The smooth muscle hypertrophy of a pregnant uterus (this also involves hyperplasia).
    This is triggered by hormonal changes.
40
Q

Give pathological examples of hypertrophy

A
  1. Ventricular cardiac muscle hypertrophy.
    This is in response to hypertension or valvular disease.
  2. Smooth muscle hypertrophic above an intestinal stenosis due to the extra work of pushing intestinal contents through the narrowing.
  3. Smooth muscle hypertrophy with bladder obstruction due to an enlarged prosthetic gland
41
Q

What is compensatory hypertrophy?

A

The enlargement of a remaining organ or tissue after a portion has been surgically removed or rendered inactive

42
Q

Give an example of compensatory hypertrophy.

A

Hypertrophy of one kidney due to failure of the other

43
Q

What is atrophy?

A

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

44
Q

Why does atrophy occur?

A

Shrinkage in the size of the cell to a size at which survival is still possible. The cell contains a reduced number of structural components and has reduced function however cell shrinkage has limits because most cellular organelles are essential for survival.

45
Q

What may cause atrophy?

A

It can be caused by a reduced supply of growth factors and/or nutrients.

46
Q

What are the two forms of atrophy?

A

Atrophy on a cellular level and atrophy on the level of the organ/tissue.

47
Q

Compare Atrophy on a cellular level and atrophy on the level of the organ/tissue.

A

Cellular atrophy is a decrease in cell size whilst organ/tissue atrophy is typically due to a combination of cellular atrophy and apoptosis and occurs when many cells in the tissue undergo atrophy and apoptosis.

48
Q

What is cell deletion?

A

certain cells are picked out and induced to undergo apoptosis. In organs undergoing atrophy by cell
deletion parenchymal cells will disappear before stromal cells and atrophic organs therefore often contain a large amount of connective tissue.

49
Q

How is atrophy best treated?

A

Atrophy is linked with disease and senescence.
It is a process that’s reversible to a point but the likelihood of reversal goes down as time passes (particularly when parenchymal cells are replaced by connective tissue). Atrophy is therefore best treated by the removal of the cause.

50
Q

Give examples of physiological atrophy.

A
  1. Ovarian atrophy in post-menopausal women

2. The decrease in the size of the uterus after childbirth (parturition)

51
Q

What are the 11 causes of pathological atrophy?

A
  1. Reduced functional demand/workload (atrophy of disuse)
  2. Loss of innervation (denervation atrophy)
    e. g. wasted striated muscle within the hand after median (motor) nerve damage.
  3. Inadequate blood supply, e.g.
    Sudden loss of blood supply results in tissue death however partial but prolonged inadequacy of blood flow results in tissue atrophy.
  4. Inadequate nutrition, e.g., wasting of muscles with malnutrition.
  5. Loss of endocrine stimulation, e.g., as occurs in the breast and reproductive organs with withdrawal of hormonal stimulation, wasting of the adrenal gland with loss of pituitary ACTH following hypophysectomy.
  6. Persistent injury, e.g., polymyositis (inflammation of muscle).
  7. Aging (senile atrophy), usually in permanent tissues e.g., the brain and heart
  8. Pressure, e.g., tissues around an enlarging benign tumour
  9. Occlusion of a secretory duct, this causes the parenchymal cells of the gland to undergo apoptosis,
  10. Toxic agents and drugs, e.g., on the bone marrow and testes.
  11. X-rays, by direct cellular damage and microcirculatory damage.
  12. Immunological mechanisms, e.g., atrophic gastric mucosa in pernicious anaemia where the body produces autoantibodies against parietal cells. The parietal cells produce intrinsic factor which is required for the absorption of vitamin B12. Lack of vitamin B12 results in anaemia.
52
Q

Give an example of atrophy of extracellular matrix.

A

Osteoporosis

53
Q

What is metaplasia?

A

Reversible replacement of one differentiated cell type to another

54
Q

In which cell types does metaplasia occur?

A

Labile or stable

55
Q

Why does metaplasia occur?

A

Stress causes genetic reprogramming of stem cells

56
Q

Which cells more commonly undergo metaplasia?

A

In adult mammals metaplasia only occurs within varieties of epithelia and within varieties of connective tissue.

57
Q

What is the aim of metaplasia?

A

to change one cell type to another more suited to an altered environment.

58
Q

Describe epithelial metaplasia and provide examples

A

Epithelial metaplasia is a very common form of metaplasia, it involves the replacement of one type of epithelium with another that will more likely tube better suited to withstand the stress it is faced with.

For example metaplasia resulting in the replacement of fragile columnar epithelia for squamous epithelia (more resilient).

Epithelial metaplasia is common on surface linings, probably because they are exposed to stress.

The metaplastic epithelium may lose functions that the original epithelium performed, e.g., mucus secretion is lost when columnar epithelium becomes squamous epithelium.

59
Q

Compare the differentiation of metaplastic epithelium, dysplastic epithelium and cancerous epithelia

A

Metaplastic epithelium is fully differentiated and the process is reversible.

Dysplastic epithelium has disorganised and abnormal differentiation and the process of formation is reversible.

Cancerous epithelial differentiation is disorganised, abnormal and irreversible.

60
Q

Give examples of when metaplasia can be adaptive and useful

A
  1. If the bone marrow is destroyed by disease, splenic tissue undergoes metaplasia to bone marrow (myeloid metaplasia).
  2. The columnar epithelium lining ducts such as those of salivary glands, pancreas, bile ducts or the renal pelvis can change to stratified squamous epithelium secondary to chronic irritation by stones.
    This is useful as squamous stratified epithelium is more resistant to mechanical abrasion.
61
Q

Give examples of when metaplasia can be detrimental/ lack usefulness

A
  1. bronchial pseudostratified ciliated columnar epithelium —> stratified squamous epithelium due to the effect of cigarette smoke.
    The squamous epithelium doesn’t produce mucus and lacks cilia to move the mucus along.
  2. Metaplasia can also be seen in connective tissue when it changes to bone.
  3. Metaplastic bone can develop in skeletal muscle following trauma (traumatic myositis ossificans) when fibroblasts within the muscle tissue undergo metaplastic change to osteoblasts.
  4. Barrett’s esophagus: Stratified squamous epithelium –> gastric glandular epithelium with persistent acid reflux

Metaplasia can also act as a precursor to dysplasia and cancer.
E.g Barrett’s epithelium and oesophageal adenocarcinoma

62
Q

What is aplasia?

A
  • Complete failure of a specific tissue or organ to
    develop
  • An embryonic developmental disorder
  • Also used to describe an organ whose cells
    have ceased to proliferate, e.g. aplasia of bone
    marrow in aplastic anaemia
63
Q

What is hypoplasia?

A

Underdevelopment or incomplete development of tissue or organ at embryonic stage, inadequate number of cells. - congenital disorder

64
Q

What is involution?

A
  • Normal programmed shrinkage of an organ

- Uterus after childbirth, thymus in early life, pro- and mesonephros

65
Q

What is reconstitution?

A

This is the replacement of a lost part of the body rather than a small group of cells.
It’s a process that requires coordinated regeneration of several types of cells.
E.g regrowth of lizards tail.

66
Q

What is atresia?

A
  • ‘No orifice’
  • Congenital imperforation of an opening
    e. g., atresia of the anus or vagina.
67
Q

What is dysplasia?

A
  • Abnormal maturation of cells within a tissue
  • Potentially reversible
  • Often pre-cancerous condition

Semester 2 - PathPro (16 decks)

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