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Pathological Processes > Cellular Adaptations > Flashcards

Cellular Adaptations Flashcards

1
Q

What determines the size of a cell population?

A
  • Depends on rate of cell proliferation, cell differentiation and cell death by apoptosis
  • Increased numbers are seen with increased proliferation or decreased cell death
  • Cell proliferation occurs in physiological and pathological conditions
  • Excessive physiological stimulation can become pathological, e.g., prostatic hypertrophy
  • Proto-oncogenes regulate normal cell proliferation
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2
Q

How is cell proliferation controlled?

A
  • Largely by chemical signals from the microenvironment which either stimulate or inhibit cell proliferation
  • When a signalling molecule binds to a receptor it results in the modulation of gene expression
  • Receptors usually in cell membrane but can be in the cytoplasm or nucleus (e.g., steroid receptors)
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3
Q

What can chemical signals make a cell do?

A
  • Survive (resist apoptosis)
  • Divide (enter cell cycle)
  • Differentiate (take on specialised from and function)
  • Die (undergo apoptosis)
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4
Q

How can a cell population increase it’s numbers?

A

Increased growth occurs by:

  • Shortening the cell cycle
  • Conversion of inactive cells to proliferating cells by making them enter the cell cycle.
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5
Q

Can you see the cell cycle by microscopy?

A

Interphase cannot be seen but mitosis and cytokinesis can be.

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6
Q

Can cells with damaged DNA replicate?

A
  • Mutation produces other cells with these changes (cancer) = not in normal state
  • Checkpoints within cell cycle (before M and S phase)
  • If there is damaged DNA cells try to fix it, if they can’t then the cell enters apoptosis
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7
Q

What is the restriction (R) point?

A
  • Most critical checkpoint
  • Majority of cells that pass R point will complete cell cycle
  • Most commonly altered checkpoint in cancer cells
  • Checkpoint activation delays cell cycle and triggers DNA repair mechanisms or apoptosis via p53 (guardian of the genome)
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8
Q

How is the cell cycle controlled?

A
  • Cyclins and cyclin dependant kinases (CDK’s)
  • CDK’s become active by binding with cyclins
  • CDK phosphorylates target proteins.
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9
Q

How many times can cells divide?

A

61.3 (due to telomere length etc)

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10
Q

How can cells adapt?

A

Hyperplasia
Hypertrophy
Atrophy
Metaplasia

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11
Q

What is hyperplasia?

A

Increase in tissue or organ size due to increased cell numbers

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12
Q

What is hypertrophy?

A

Increase in tissue or organ size due to increased cell size

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13
Q

What is atrophy?

A

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

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14
Q

What is metaplasia?

A

Reversible change of one differentiated cell type to another

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15
Q

In which types of tissues does hyperplasia occur?

A
  • Labile or stable tissues
  • Caused by increased functional demand or hormonal
    stimulation
  • Remains under physiological control and is reversible
  • Can occur secondary to a pathological cause but the proliferation itself is a normal response
  • Repeated cell divisions exposes the cell to the risk of mutations and neoplasia
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16
Q

Give an example of physiological hyperplasia

A
  • Proliferative endometrium under the influence of oestrogen

- Bone marrow produces erythrocytes in response to hypoxia

17
Q

Give a pathological example of hyperplasia

A
  • Eczema

- Thyroid goitre in iodine deficiency

18
Q

In which types of tissue does hypertrophy occur?

A
  • Labile, stable but especially permanent tissues
  • Like hyperplasia, caused by increased
    functional demand or hormonal stimulation
  • Cells contain more structural components – workload is shared by a greater mass of cellular components
  • In labile and stable tissues hypertrophy usually occurs along with hyperplasia
19
Q

Give an example of physiological hypertrophy

A
  • Skeletal muscle

- Pregnant uterus (hypertrophy and hyperplasia)

20
Q

Give an example of pathological hypertrophy

A
  • Hypertrophy of cardiac muscle to combat hypertension
  • Proximal to a bowel stricture = hypertrophy of smooth muscle to push things through stricture
  • Smooth muscle of bladder due to enlarged prostate gland (push harder to pass urine)
21
Q

What is compensatory hypertrophy?

A

Damage to one of two paired organs (e.g. kidney) or part of an organ. Small kidney at birth/ if one is removed the other undergoes hypertrophy and hyperplasia.

22
Q

What is happening in the cell in atrophy?

A
  • Shrinkage in the size of the cell to a size at which survival is still possible
  • Reduced structural components of the cell
  • May eventually result in cell death
23
Q

Is tissue atrophy only a result of cell atrophy?

A
  • Organ/tissue atrophy typically due to combination of cellular atrophy and apoptosis
  • Is reversible but only up to a point
24
Q

Give an example of physiological atrophy

A
  • Decrease in size of uterus after child birth

- Ovarian atrophy in post menopausal women

25
Q

Give an example of pathological atrophy

A
  • Reduced functional demand/workload = atrophy of disuse: muscle atrophy after disuse, reversible with activity
  • Loss of innervation = denervation atrophy: wasted hand muscles after median nerve damage
  • Inadequate blood supply: thinning of skin on legs with peripheral vascular disease
  • Inadequate nutrition: wasting of muscles with malnutrition
  • Loss of endocrine stimuli: breast, reproductive organs
  • Persistent injury: polymyositis (inflammation of muscle)
  • Aging = senile atrophy: brain, heart
  • Pressure: tissues around an enlarging benign tumour (probably secondary to ischaemia)
26
Q

What is atrophy of extracellular matrix?

A

Lack of actual bone matrix (not just lack of calcium)

Due to immobility/ bed rest

27
Q

What is metaplasia?

A
  • Due to altered stem cell differentiation
  • May represent adaptive substitution of cells that are sensitive to stress by cell types better able to withstand the adverse environment
  •  Metaplastic cells are fully differentiated and the process is reversible (cf dysplasia and cancer)
  • Sometimes a prelude to dysplasia and cancer
  • No metaplasia across germ layers
  • Occurs only in labile or stable cell types
  •  Involves expression of a new genetic programme
28
Q

Give an example of metaplasia

A
  • Bronchial pseudo stratified ciliated epithelium -> stratified squamous epithelium due to the effect of cigarette smoke
  • Stratified squamous epithelium -> gastric glandular epithelium with persistent acid reflux (Barrett’s oesophagus)
29
Q

Does metaplasia predispose to cancer?

A
  • Epithelial metaplasia can be a prelude to dysplasia and cancer.
    = Barrett’s epithelium and oesophageal adenocarcinoma
    = Intestinal metaplasia of the stomach and gastric adenocarcinoma
30
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
31
Q

What is hypoplasia?

A
  • Underdevelopment or incomplete development of
    tissue or organ at embryonic stage, inadequate number of cells.
  • In a spectrum with aplasia
  • Not opposite of hyperplasia as it is a congenital
    condition.
32
Q

What is involution?

A
  • Overlaps with atrophy

- Normal programmed shrinkage of an organ

33
Q

What is reconstitution?

A

Replacement of a lost part of the body

34
Q

What is atresia?

A
  • ‘No orifice’

- Congenital imperforation of an opening

35
Q

What is dysplasia?

A
  • Abnormal maturation of cells within a tissue
  • Potentially reversible
  • Often pre-cancerous condition
36
Q

Give an example of involution

A
  • Uterus after childbirth

- Thymus in early life

37
Q

Does reconstitution occur in humans?

A
  • Development of blood vessels
  • Children under 4.5 can grow back tip of finger (if cleanly cut off)
  • Scars are generally hairless, pale and stretched = no
38
Q

Give an example of atresia

A

 Examples:

  •  Anus
  • Vagina
  • Small bowel

Pathological Processes (13 decks)

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