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Path Pro 2023 > Cellular adaptations (Session 7) > Flashcards

Cellular adaptations (Session 7) Flashcards

1
Q

What does the size of cell populations in adults depend on? (3)

A

The rate of:
- Cell proliferation
- Cell differentiation
- Cell death by apoptosis

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2
Q

When are increased cell numbers seen? (2)

A

With either:
- Increased cell proliferation
- or decreased cell death

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3
Q

Why may cell proliferation occur?

A

As the result of physiological or pathological conditions. (benign prostatic hypertrophy - check lecture??)

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4
Q

What is responsible for regulating normal cell proliferation?

A

Proto-oncogenes

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5
Q

What happens when a cell receives an instruction to divide?

A

The cell enters the cell cycle

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6
Q

What are the phases of the cell cycle?

A

G1→S→G2→M

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7
Q

What does the cell do after cell cycle completion? (2)

A
  • The cell either re-starts the process from G1 or
  • Exits (G0) until further growth signals occur
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8
Q

What can cells in G0 do?

A

Can undergo terminal differentiation where there is a permanent exit from the cell cycle.

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9
Q

How does increased growth of a tissue occur?

A

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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10
Q

Which stage of the cell cycle is distinctive under a light microscope?

A

M phase (mitosis)

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11
Q

What does the M phase of the cell cycle consist of? (2)

A
  • Mitosis (nuclear division)
  • Cytokinesis (cell division to yield two daughter cells).
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12
Q

What do you call the rest of the cell cycle between successive M phases?

A

Interphase

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13
Q

What does interphase look like under a light microscope?

A

Deceptively uneventful.

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14
Q

Name the phases in interphase and state what happens in each one (3)

A
  • G1 (gap 1, presynthetic, where the cell grows)
  • S (DNA synthesis)
  • G2 (gap 2, premitotic where the cell prepares to divide)
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15
Q

What does interphase include?

A
  • DNA replication
  • Protein synthesis for growth in cell size
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16
Q

Identify the phases of the cell cycle in this image

A
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17
Q

1) What is cell cycle progression controlled by?
2) What do these do?
3) Name them

A

1) Three key “checkpoints”
2) Sense damage to DNA and ensure cells with damaged DNA do not replicate.
3) - The Restriction (R) point (towards the end of G1)
- checkpoint at G1/S transition
- checkpoint at G2/M transition

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18
Q

1) What is the most critical checkpoint in the cell cycle?
2) Where is this checkpoint found?
3) A majority of cells that pass this checkpoint will…

A

1) The Restriction (R) point
2) Towards the end of G1
3) The majority of cells that pass the R point will complete the full cell cycle.

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19
Q

Describe what happens if checkpoint activation occurs at the restriction point

A
  • The p53 protein comes into play.
  • This protein suspends the cell cycle and triggers DNA repair mechanisms or, if the DNA cannot be repaired, apoptosis.
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20
Q

Describe what happens at the other 2 less critical checkpoints of the cell cycle

A
  • Checkpoint at G1/S transition - checks for DNA damage before DNA replication
  • Checkpoint at G2/M transition - checks for DNA damage after DNA replication
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21
Q

What are defective cell cycle checkpoints a major cause of?

A

A major cause of genetic instability in cancer cells.

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22
Q

1) What is progression through the cell cycle tightly regulated by? (2)
2) Which transition is particularly regulated by these things?

A

1) - Proteins called cyclins and
- Associated enzymes called cyclin-dependent kinases (CDKs).

2) The G1/S transition

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23
Q

Describe how cyclin-dependant kinases work

A
  • CDKs become active by binding to and complexing with cyclins.
  • Activated CDKs drive the cell cycle by phosphorylating proteins, e.g., retinoblastoma susceptibility (RB) protein, that are critical for progression of the cell to the next stage of the cell cycle.
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24
Q

What tightly regulates the activity of cyclin-CDK complexes?

A

CDK inhibitors

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25
Q

How do some growth factors work?

A
  • Some work by stimulating the production of cyclins
  • Some work by shutting off production of CDK inhibitors.
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26
Q

1) How can cells respond to challenges that are not severe enough to cause injury?

2) What is the risk of this?

A

1) By adaptations that are not truly pathologic

2) This may open the door to disease

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27
Q

What is cell adaptation? What is it usually like?

A
  • The state between a normal unstressed cell and an overstressed injured cell.
  • It is usually reversible
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28
Q

Describe the 4 important types of cell adaptation

A
  • Increase in number above normal (hyperplasia)
  • Increase in size (hypertrophy)
  • Become smaller (atrophy)
  • Be replaced by a different type of cell (metaplasia).
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29
Q

1) What is hyperplasia?

2) What is it a response to?

3) Which cell population types can hyperplasia only occur in?

A

1) an increase in tissue or organ size due to increased cell numbers

2) a response to increased functional demand and/or external stimulation.

3) labile or stable cell populations

30
Q

1) What kind of control does hyperplasia remain under?

2) Compare this to neoplasia

A

1) Physiological control, and it is reversible

2) Neoplasia is not under physiological control and is usually irreversible

31
Q

1) What is hyperplasia biologically similar to?

2) How is it different to this thing?

A

1) Regeneration

2) It leads to an increase in the size of the tissue or organ

32
Q

1) Name and describe the 2 types of physiological hyperplasia

A
  • Hormonal, when the result is an increase in functional capacity,

or

  • Compensatory, when there is an increase in tissue mass after tissue damage
33
Q

1) What can hyperplasia occur secondary to?

2) In these cases, what is a normal response?

b) Compare this to neoplasia

A

1) To a pathological cause

2) The cellular proliferation is a normal response to another abnormal condition

3) In neoplasia, the proliferation in itself is abnormal

34
Q

Why does pathological hyperplasia usually occur?

A

Secondary to excessive hormonal stimulation or growth factor production.

35
Q

What is hyperplastic tissue at risk of? Why?

A
  • Neoplasia
  • as the repeated cell divisions that occur in hyperplasia expose the cell to the risk of mutations (which commonly occur during DNA replication).
36
Q

Describe 2 examples of physiological hyperplasia

A
  • increased bone marrow production of erythrocytes in response to hypoxia and the resulting increased erythropoietin
  • The proliferation of the endometrium under the influence of oestrogen.
37
Q

Describe 2 examples of pathological hyperplasia

A
  • Epidermal thickening in chronic eczema or psoriasis
  • Enlargement of the thyroid gland in response to iodine deficiency.
38
Q

1) What is hypertrophy?

2) Hypertrophy can occur in many tissues but what cell populations is it seen most in?

3) Why?

A

1) an increase in tissue or organ size due to an increase in cell size without an increase in cell numbers.

2) Permanent cell populations

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

39
Q

Describe how it is important to know the regenerating capacity of each cell type

A
  • Enables you to predict the type of response to increased functional demand
  • Cells that cannot multiply have no option but to become larger.
40
Q

What is hypertrophy a response to? (2)

A
  • Response to increased functional demand and/or hormonal stimulation.
41
Q

1) What are cells undergoing hypertrophy synthesising more of?

2) What do hypertrophic cells contain more of?

3) Thus…

A

1) More cytoplasma ie protein

2) more structural components

3) hence the cellular workload is shared by a greater mass of cellular components.

42
Q

Describe hyperplasia in cells where division is possible

A
  • Hypertrophy may still occur but often occurs alongside hyperplasia.
  • In such cases both hyperplasia and hypertrophy are triggered by the same stimulus
43
Q

Give an example of something that results in a combo of hypertrophy and hyperplasia

A

Endocrine stimulation

44
Q

Describe 2 examples of physiological hypertrophy

A
  • The skeletal muscle hypertrophy of a bodybuilder
  • The smooth muscle hypertrophy of a pregnant uterus (which also involves hyperplasia). In pregnancy under the influence of oestrogen the body of the uterus enlarges approximately 70 fold.
45
Q

Describes 3 examples of pathological hypertrophy

A
  • Ventricular cardiac muscle hypertrophy in response to hypertension or valvular disease
  • Smooth muscle hypertrophy above an intestinal stenosis due to the extra work of pushing the intestinal contents through the narrowing
  • Bladder smooth muscle hypertrophy with bladder obstruction due to an enlarged prostate gland (which has undergone both hypertrophy and hyperplasia).
46
Q

Describe a simple way to study the effect of functional overstrain

A
  • By removing one of two paired organs, e.g., if one kidney is removed the other enlarges = compensatory hypertrophy (in this case actually a combination of hypertrophy and hyperplasia)
  • When the stimulus for hypertrophy and hyperplasia disappears, the cells and organs become normal size once again.
47
Q

1) What is atrophy?

2) What will cause atrophy?

A

1) This is shrinkage of a tissue or organ due to an acquired decrease in size and/or number of cells.

2) A reduced supply of growth factors and/or nutrients

48
Q

1) How many perspectives can atrophy be considered from?

2) Describe them

A

1) 2

2) at the level of the cell and at the level of the organ/tissue.

49
Q

1) What is cellular atrophy?

2) What is tissue/organ atrophy usually due to?

A

1) Decrease in cell size

2) a combination of cellular atrophy and apoptosis and occurs when many cells in the tissue undergo atrophy and apoptosis.

50
Q

Describe cellular atrophy

A
  • Involves 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.
51
Q

1) What happens in cell deletion ?

2) What happens in organs undergoing atrophy by cell deletion?

3) Thus what do tropic organs contain a large amount of?

A

1) certain cells are picked out and induced to commit suicide (by apoptosis).

2) Parenchymal cells will disappear before stromal cells

3) Connective tissue

52
Q

What is atrophy often linked with?

Give an everyday example of senescence

A

1) Disease

2) Senescence

(an everyday example of senescence is baldness in adult males – atrophy of hair follicles)

53
Q

1) Describe the reversibility of atrophy

2) Thus, what is the best treatment for atrophy?

A

1) Atrophy is reversible up to a point but after years or months it is less so particularly when parenchymal cells are replaced by connective tissue.

2) Atrophy is therefore best treated by removal of the cause.

54
Q

Give 2 physiological examples of Atrophy

A
  • Ovarian atrophy in post-menopausal women
  • The decrease in size of the uterus after parturition.
55
Q

Describe 5 pathological causes of atrophy

A
  • Reduced functional demand/workload (atrophy of disuse), e.g., muscle atrophy after disuse due to immobilisation in a plaster cast (this is reversible with activity).
  • Inadequate nutrition, e.g., wasting of muscles with malnutrition.
  • Persistent injury, e.g., polymyositis (inflammation of muscle).
  • Aging (senile atrophy), usually in permanent tissues e.g., the brain and heart although the
    weight of the liver, kidneys and spleen is also reduced in old age
  • Toxic agents and drugs, e.g., on the bone marrow and testes.
56
Q

What is shown in this image?

A
  • Atrophy of muscle cells
  • N = Normal
  • A = trophy from denervated motor unit.
57
Q

1) What is metaplasia?

2) Describe what happens in metaplasia

3) What happens to the stem cells in the tissue?

4) What can it be considered as?

A

1) This is the reversible replacement of one adult differentiated cell type by another of a different type.

2) Cells of one phenotype are eliminated and replaced by cells of a different phenotype.

3) The stem cells within the tissue are reprogrammed and switch to producing a different type of progeny.

4) It can be considered as ‘abnormal regeneration’.

58
Q

Describe the actual science behind metaplasia

A
  • Metaplasia involves expression of a new genetic programme (i.e., turning certain genes on and certain genes off) which results in cells assuming a different structure and a different function.
  • The end result of metaplasia is to change one cell type to another more suited to an altered environment.
59
Q

1) What types of cells can metaplasia only occur?

2) In adult mammals, where does metaplasia only occur?

3) Despite the fact that what?

4) What cell types is it most commonly seen in?

A

1) In cells that can replicate

2) occurs only within varieties of epithelia and within varieties of connective tissue.

3) Despite the fact that all cells have the same full complement of genetic material and therefore the potential to form any cell type

4) epithelial tissues and often in columnar epithelium (fragile) which undergoes metaplasia to become squamous epithelium (more resilient).

60
Q

There is no proof of metaplasia occurring in the following areas:

A
  • Across germ layers (e.g., bone to nerve) or from a connective tissue (mesenchyme) to epithelium
  • it is not known to occur in adult striated muscle cells or in neurones.
61
Q

Describe epithelial metaplasia

A
  • Epithelial metaplasia is common on surface linings, probably because they are exposed to insults.
  • The metaplastic epithelium may lose functions that the original epithelium performed, e.g., mucus secretion is lost when columnar epithelium becomes squamous epithelium.
  • Metaplastic epithelium is fully differentiated.
  • In contrast, dysplastic epithelium has disorganised and abnormal differentiation, while cancerous epithelial differentiation is also disorganised and abnormal and, in addition, irreversible.
62
Q

Give 2 examples of how metaplasia can be adaptive and useful

A
  • If the bone marrow is destroyed by disease, splenic tissue undergoes metaplasia to bone marrow (myeloid metaplasia).
  • 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.
63
Q

2 Examples of where neoplasia may be detrimental

A
  • The transformation of bronchial pseudostratified ciliated columnar epithelium to stratified squamous epithelium due to the effect of cigarette smoke.
  • The squamous epithelium doesn’t produce cleansing mucus and lacks cilia to move the mucus along.
  • Flat, non-secreting epithelium can also be replaced by secretory epithelium or glands such as in the lower oesophagus when the oesophageal stratified squamous epithelium changes to gastric or intestinal type epithelium with persistent acid reflux (Barrett’s oesophagus).
64
Q

1) Metaplasia can also be seen in connective tissue when it…

2) Why might metaplasia bone develop?

3) What is this called?

4) When is this commonly seen?

5) How does trauma myositis disappear?

A

1) changes to bone

2) In skeletal muscle following trauma when fibroblasts within the muscle tissue undergo metaplastic change to osteoblasts.

3) Traumatic myositis ossificans

4) often seen in young people and usually after a premature return to activity before proper healing has occurred

5) often disappears by metaplasia in the opposite direction

65
Q

1) What might metaplasia sometimes be a prelude to?

2) Name some epithelial metaplasia that predispose to malignant epithelial cancers

3) What does intestinal metaplasia of the stomach occur with?

4) Why can epithelial metaplasia progress to dysplasia and then neoplasia?

A

1) To dysplasia and cancer

2) Barrett’s epithelium and intestinal metaplasia of the stomach

3) occurs with chronic infection by Helicobacter pylori

4) Not understood

66
Q

1) What is aplasia?

2) What kind of disorder is it?

3) Give 2 examples of aplasia

4) State what one of them results in

5) What is the term aplasia also used to describe?

6) Give an example of this

A

1) the complete failure of a specific tissue or organ to develop.

2) It is an embryonic developmental disorder

3) Thymic aplasia and aplasia of a kidney.

4) Thymic aplasia results in infections and auto-immune problems

5) The term aplasia is also used to describe an organ whose cells have ceased to proliferate

6) e.g., aplasia of the bone marrow in aplastic anaemia.

67
Q

1) What is hypoplasia?

2) Why does it occur?

3) What kind of disorder is it?

4) What is it in spectrum with?

5) Give examples of hypoplasia (4)

6) Is hypoplasia the opposite of hyperplasia?

7) Why?

8) What can is be more closely compared with?

A

1) the congenital underdevelopment or incomplete development of a tissue or organ.

2) Because there are an inadequate number of cells within the tissue which is present.

3) An embryonic developmental disorder

4) Aplasia

5) - Renal hypoplasia
- Breast hypoplasia
- Testicular hypoplasia in Klinefelter’s syndrome
- Hypoplasia of the chambers of the heart.

6) NO

7) HYPOPLASIA is a congenital condition.

8) Compare it with atrophy which occurs when an existing part wastes away.

68
Q

What is atresia?

Give 2 examples of atresia

A

‘no orifice’, the congenital imperforation of an opening,

e.g., atresia of the anus or vagina.

69
Q

1) What is reconstitution?

2) How is it different to regeneration?

3) What does reconsitution require?

4) Give 2 examples of reconstitution

5) In mammals, what can many cell types do?

6) But what is minimal?

7) What can’t most mammals do?

A

1) the replacement of a lost part of the body

2) Regeneration is the replacement of a small group of cells.

3) the coordinated regeneration of several types of cells.

4) regrowth of a lizard’s tail and the growth of deer antlers

5) Can regenerate well

6) The ability to reconstitute a body part

7) can’t even reconstitute a lost nail bed or the root of a hair (note that scars are hairless).

70
Q

1) What is involution?

2) What does it overlap with?

3) Give 3 examples of involution

A

1) The normal programmed shrinkage of an organ

2) Atrophy

3) Shrinkage of:
- Uterus after childbirth
- Thymus in early life
- Temporary foetal organs such as the pro- and mesonephros.

71
Q

1) What is dysplasia?

2) What is it potentially like?

3) However dysplasia is often…

A

1) The abnormal saturation of cells with a tissue

2) Reversible potentially

3) often a pre-cancerous condition

Path Pro 2023 (21 decks)

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