sell gwoth Flashcards

1
Q

What is cell growth

A

• Increase in size of cell without division

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2
Q

What is coupled cell growth and proliferation known as

A

Hyperplasia

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3
Q

Where does hyperplasia occur

A
Renewing tissue (e.g. stem cells in epidermis)
Resting tissue: thyoid or liver
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4
Q

Why are cell growth and proliferation coupled

A

• This is because to go through cell cycle, cells must pass checkpoints influenced by growth, so growth can drive cell cycle.

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5
Q

What does growth drive

A

• Growth drives cell cycle: If you increase growth, increase rate of cell cycle

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6
Q

Increasing rate of cell cycle doesn’t necessarily make cells

A

Grow…they just keep dividing

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7
Q

When can cell growth and proliferation uncouple

A
  • Cleavage: proliferation but no growth
  • Hypertrophy: growth but no proliferation (e.g. skeletal muscle, more proteins made)
  • Growth and DNA replication but no cytokinesis (e.g. some myocardial cells, 4N/tetraploid)
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8
Q

What is morphogenesis

A
  • biological process that causes an organism to develop its shape.
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9
Q

What is morphogenesis induced by

A

Hormones, chemicals etc

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10
Q

Why is cell growth important

A
  • • Maintenance of normal tissue structure and function requires controlled cell growth and proliferation
  • . Cell growth is the basic mechanism by which proliferation occurs
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11
Q

How is cell growth controlled

A

regulated by extracellular growth factors/inhibitors + contact with ECM. Effects of cell growth can be countered by cell death/apoptosis/necrosis

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12
Q

What does cell growth determine

A

• Major determinant of organ and body size. Under normal growth conditions, organ grows to fixed size (intrinsic control of growth).

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13
Q

How can organ growth be modulated

A

educed/excess extrinsic growth factors (endocrine like molecules – global nutrient regulation)

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14
Q

What happens in cancer with regards to cell growth

A

• Regulation of cell growth defective in diseases such as cancer (neoplasia – abnormal growth leads to tumour)

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15
Q

Requirements for cell growth

A
  • Increase in cell mass and volume (macromolecular synthesis, e.g. protein, polysaccharide, lipids)
  • Movement at cell surface
  • (maybe change in shape) - .eg. neurone sends out axon/dendrite, different from initial rounded precursor.
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16
Q

Growth factors drive proliferation so known as m…

A

mitogen

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17
Q

3 ways GF end up at cells

A

1) Autocrine
2) Paracrine
3) Endocrine

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18
Q

What is autocrine route for growth factor

A

Factor produced by cell itself but acts back on it to stimulate growth. Indicates metabolic well being of cell, and suggesting room for more similar cells

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19
Q

Describe paracrine route

A

short range soluble molecules produced by cells near affected cell

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20
Q

Describe endocrine route

A

GF produced at far distance to affected cells and carried to it by blood

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21
Q

Example of endocrine method for GF

A

thyroid stimulating hormone produced by pituitary stimulates growth of thyroid epithelial cells and production of thyroxine.

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22
Q

Example of local factors

A

Autocrine or paracrine

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23
Q

What do local growth factors do

A

): control growth of specific organs E.g. NGF (nerve growth factor) so don’t diffuse in blood

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24
Q

What is a global factor

A

Endocrine

25
Q

What do global factors do

A

can regulate coordinated growth (nutrition dependent) of many organs

26
Q

What allows proportional growth of organism in development

A

Combination of local factors (paracrine)controlling individual organs and global factors that allows coordinated growth

27
Q

How does GF work

A
  • GF binds specific transmembrane cell surface receptor
  • Cell surface receptor either has intrinsic enzyme (e.g. kinase) activity on its intracellular domain, or is linked to second messenger molecule which has activity
  • Sets off signal transduction chain to nucleus, where TF activated (e.g. by phosphorylation), so increased macromolecular synthesis,, stimulates growth, more cells pass into and through cell cycle. So GF drives growth of cell
28
Q

Example of GF

A

Insulin like growth factor: stimulates formation of macromolecules by increasing number and activity of ribosomes in cell, more proteins, stimulates growth .

29
Q

How do growth inhibitors work

A

similar mechanism as GF but cause increased transcription of genes which code for inhibitors of cell cycle

30
Q

Organ size under autonomous control , true or false

A

Twue

31
Q

How is growth coordinated with patterning

A

Localised expression of GF

32
Q

What happens to cels in skin

A

basal cell layer contains stem cells which proliferate and move through layers of skin. Stem cells and transient amplifying cells lie in crypts These multipotent cells move through states of gene expression towards terminal differentiation. Cells expressing different keratin proteins as they progressively differentiate to replace cells sloughed off at surface after 30 days

33
Q

What happens to skin stem cells in basal layer

A

Give rise to keratinocytes

34
Q

What do follicular stem cells (base of hair follicle) give rise to

A

Hair follicle and epidermis

35
Q

Describe how SI renews itself

A

Multipotent stem cells in crypts divide to form absorptive, goblet, and enteroendocrine cells (which migrate upwards) and Paneth cells (which migrate downwards)

36
Q

What do absorptive/brush border/enterocytes do

A

Absorb nutrients with microvilli

37
Q

What do goblet cells do

A

Secret mucus

38
Q

What do enteroendocrine cells do

A

Serotonin and peptide hormone

39
Q

What do Paneth cells do

A

innate immune cells

40
Q

What happens to stem cells in SI

A

Cells reach tip of villus 2-5 days after emerging from crypt

At the tip, cells undergo apoptosis and shed into gut lumen

41
Q

3 types of growth after birth

A

1) renewing tissue e.g. skin, gut epithelium
2) resting tissue: e.g. liver - cells only multiply to repair damage 3) 3) non dividing tissue - e.g. neurones don’t multiply after birth

42
Q

Where do blood cells derive from

A

Common stem cell in bone marrow (haematopoietic stem cell)

43
Q

when do cells multiply in resting tissue

A

To repair damage

44
Q

Why are hepatocytes unipotent stem cells

A

high capacity for cell division - can repair tissue in liver

45
Q

How does skeletal muscle repair

A

: satellite cells are stem cells activated by hepatocyte growth factor released by damaged myofibres upon injury, they proliferate and fuse to form myofibres

46
Q

Describe examples of non dividing tissues,

A

Neurones, cardiac muscle (no regenerative capacity)

47
Q

What does non dividing tissue mean

A

post mitotic cells that don’t multiply after birth

48
Q

What is apoptosis

A

• Regulated/programmed cell death affecting individual cells

49
Q

Differnece between apoptosis and necrosis

A
  • Unlike necrosis, which is death of many adjacent cells due to factor extrinsic to them (e.g. ischaemia)
  • unlike necrosis is not pro-inflammatory
50
Q

Morphology of apoptosis

A
  • Membrane blebbing (bulge in membrane)
  • Cell shrinkage
  • Condensation of chromatin
  • Fragmentation of DNA
  • Phagocytosis of neighbouring cells
51
Q

Initiators of apoptosis

A
  • Deprivation of survival factors (e.g. interleukin-1)
  • Proapoptotic cytokines – promote apopotsis (e.g. Fas, tumour necrosis factor)
  • Irradiation (e.g. Gamma and UV light)
  • Anti cancer drugs
52
Q

Intracellular regulators of apoptosis

A
  • P53 – induces apoptosis in case of irreplacable DNA damage

* bcl-2: suppresses the apoptotic pathway

53
Q

Effectors of apoptosis

A

• Caspases: enzymes that cleave proteins close to aspartate residues. They have specific intracellular targets such as protein of nuclear lamina and cytoskeleton

54
Q

Physiological roles of apoptosis, give example

A

• Growth and development: loss of redundant tissue during organ development.
Eg. Interdigital webs, apoptosis needed for tissue patterning and digit formation. Distal part of limb forms a plate, In order to make digits, degeneration of tissue between digits hence individual digits

55
Q

Describe apoptosis of neuronal cells, why this is needed

A

Over half of of human neuronal cells produced duringnervous system development also die during development because they don’t form right connections in brain, ensure correct neurone connectivity in fully developed brain

56
Q

2 roles of apoptosis

A
  • Growth and development: loss of redundant tissue during organ development.
  • Control of cell number in adult life: regulation of balance between proliferation and cell death
57
Q

How is apoptosis altered in disease

A
  • Increased apoptosis: aquire immune deficiency syndrome (AIDs), neurodegenerative diseases, post ischaemic injury, graft vs host disease
  • Decreased apoptosis: malignancies, autoimmune disorders (e.g. systemic lupus erythematosus)
58
Q

Anticancer cells/radiotherapy induces apoptosis in normal and tumour tissue, true of false

A

True