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Mechanisms of Disease > Session 7 - Cellular adaptations > Flashcards

Session 7 - Cellular adaptations Flashcards

0
Q

How do cell populations increase in cell number?

A
  • Increased proliferation

- Decreased death

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1
Q

What determines the size of cell populations?

A
  • The rate of cell proliferation
  • The rate of cellular differentiation
  • The rate of apoptosis
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2
Q

What are proteo-oncogenes?

A

-Genes which regulate cellular cellular proliferation

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3
Q

What are the final possible outcomes of cellular signalling?

A
  • Survive
  • Divide
  • Differentiate
  • Die
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4
Q

How does cell-cell signalling occur?

A
  • Hormones
  • Local mediators
  • Direct cell-cell contact or cell-stroma contact
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5
Q

What is intracrine signalling?

A

-Cells synthesise a factor but does not secrete it and it binds to its own intracellular receptors

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6
Q

What are growth factors?

A

-Polypeptides which work through cell-surface receptors to act as local mediators for cellular proliferation

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7
Q

What genes encode for growth factors?

A

-Proto-oncogenes

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8
Q

How do growth factors effect cellular proliferation?

A

-Bind specific receptors and stimulate the transcription of genes which regulate entry into the cell cycle

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9
Q

Other than cellular proliferation, briefly name a few events which are controlled by growth factors

A
  • Differentiation
  • Contractilitty
  • Angiogenesis
  • Migration
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10
Q

What is EGF?

A
  • Epidermal growth factor
  • Mitogenic for epithelial cells, hepatocytes and fibroblasts
  • Produced by macrophages and keratinocytes
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11
Q

What is VEGF?

A
  • Vascular endothelial growth factor

- Potent inducer of BV development and angiogenesis in wound healing, chronic inflammation and tumours

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12
Q

What is PDGF?

A
  • Platelet-derived growth factor
  • Stored in platelet a-granules and released upon activation
  • Causes migration of fibroblasts, smooth muscle cells and monocytes
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13
Q

What is GCSF?

A
  • Granulocyte colony-stimulating factor
  • Stimulates BM to produce blood cells, especially neutrophils
  • Used after chemotherapy
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14
Q

Briefly describe the cell cycle

A

G0- resting phase
G1 -Gap 1, presynthetic, cell grows,check point after
S-DNA replication
G2 - gap 2, premitotic, cell prepares to divide, check point after
M-> mitosis

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15
Q

How does increased proliferation occur in terms of cell cycle?

A
  • Shortening the cycle (can take a few hours)

- Conversion of G0 cells to proliferating cells through making them enter the cel cycle

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16
Q

Which check point is most significant?

A
  • R after G1
  • Majority of cells which pass the point of R will complete the full cell cycle-> point of no return
  • Most commonly altered check point in cancer cells
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17
Q

If a cell is damaged and detected by R, what happens?

A

-The cell cycle is delayed, DNA repair mechanisms are triggered or apoptosis through p53 is induced

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18
Q

What are cyclins?

A

-A family of proteins which control the progression of cells through the cell cycle by activating cyclin-dependant kinase enzymes

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19
Q

How do cyclins activate CDK?

A

-Bind to it and induce its phosphorylation to become fully activated

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20
Q

What do activated CDK do?

A

-Control other enzymes which are responsible for progression through the phases of the cell cycle

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21
Q

What cells are responsible for cellular proliferation?

A

-Stem cells

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22
Q

What is self-renewal during stem cell division?

A

-Stem cell undergoes asymmetric division so one daughter cell differentiates and the other remains a stem cell

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23
Q

What is a labile population?

A

-Population of cells in which stem cells divide persistently to replenish loss

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24
Q

What is a stable cell population?

A

-Population of cells which is normally stable, but quiescent cells can proliferate persistently when required

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25
Q

What are permanent cell populations?

A

-Stem cells present but cannot mount an effective proliferative response to significant cell loss

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26
Q

Give an example of labile populations

A
  • Epidermis
  • Gut epithelia
  • BM
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27
Q

Give an example of stable cell populations

A
  • Hepatocytes

- Osteoblasts

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28
Q

Give an example of permanent cell population

A
  • Brain neurones (replaced by glial cells)

- Cardiac and skeletal muscle

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29
Q

What are the 5 important types of cell adaption?

A
  • Regeneration
  • Hyperplasia
  • Hypertrophy
  • Atrohpy
  • Metaplasia
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30
Q

What is regeneration?

A

-The replacement of cell losses by identical cells to maintain tissue or organ size (cells multiply to replace losses)

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31
Q

What are the two possible outcomes of regeneration?

A
  • Resolution with negligible scar tissue

- Scarring

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32
Q

When does resolution occur in regeneration?

A
  • Removal of harmful agent

- Limited tissue damage

33
Q

When does scarring occur in regeneration?

A
  • Persistent harmful agent
  • Extensive tissue damage
  • Permanent cell populations
34
Q

Is regeneration always due to injury?

A

-No occurs physiologically eg RBC replacement, epithelia

35
Q

What is the main factor which determines the outcome of regeneration?

A

-The regenerative capacity of the tissue, ie whether it is a labile/permanent population eg epithelial vs CNS

36
Q

Do tendons have good regenerative capacity?

A

-No, there are few/if any BVs in them so regeneration is often poor and leads to secondary rupture

37
Q

If CNS neurones cannot regenerate, how is it possible to recover from a stroke?

A
  • Regeneration is replacement by identical cells

- The plasticity of neurones means alternative pathways are generated, it is not the same

38
Q

Are regenerated cells as good as the original cells? Why may this be beneficial?

A
  • Usually but not always-> can take weeks/years to reach morphological maturity
  • When exposed to certain viruses which infect mature cells eg influenzae, immature endothelia do not have influenzae receptor and so are protected
39
Q

What is the role of retinoblastoma susceptibility protein in cell cycle?

A

-Restricts the cells ability to replicate its DNA by preventing progression from G1

40
Q

How is RB protein inhibited?

A

-Phosphorylation by activated CDK

41
Q

Describe the regeneration capacity of the following tissues:

Bone, Cartilage, Adipocytes, Epithelia, Liver, Melanocytes, Smooth muscle, Striated muscle, peripheral nerves, CNS

A

Bone-> Very good; Cartilage -> Poor; Adipocytes-> nil; Epithelia -> very good; Liver -> Very good; Melanocytes -> Tend to regenerate too little (hypopigmentation); Smooth muscle -> very well; Striated muscle -> Limited (regenertaion from satellite cells); Peripheral nerves -> predicatble (sprouts 1-3mm/day); CNS -> none

42
Q

When does a neuroma form?

A

-When regenerating axons of peripheral nerves have to cross a wide gap and a disordered tangle forms

43
Q

What induces cells to regenerate?

A
  • Growth factors

- Cell-cell communication

44
Q

What is reconstitution?

A

-The replacement of a lost part of the body eg blood vessels in wound healing

45
Q

What is hyperplasia?

A

-Increase in tissue/organ size due to increased cell number in response to increased functional demand or external stimulation

46
Q

Does hyperplasia occur in all tissues?

A

-No only in labile and stable populations

47
Q

Is hyperplasia physiological or pathological?

A
  • It is under physiological control
  • Can be secondary to pathological cause, however the proliferation itself is a normal response to another abnormal condition
48
Q

What are the disadvantages of repeated cell divisions in hyperplasia?

A

-Exposes cells to the risk of mutations and neoplasia

49
Q

Give a physiological example of hyperplasia?

A
  • Proliferative endometrium influenced by oestrogen

- BM producing more RBC in response to hypoxia (altitude)

50
Q

Give a pathological example of hyperplasia?

A
  • Thyroid goitre

- Epidermal thickening in eczema/psoriasis

51
Q

Is hyperplasia reversible?

A

-Yes

52
Q

What is hypertrophy?

A

-Increase in tissue/organ size due to increased cell size

53
Q

Does hypertrophy occur in all cells?

A

-Yes, but especially permanent cell populations as they cannot divide

54
Q

What are the main causes for hypertrophy?

A
  • Increased functional demand

- Increased hormonal stimulation

55
Q

What happens on a cellular level in hypertrophy?

A
  • Cell increases in size

- Organelles increase in number

56
Q

Give physiological examples of hypertrophy

A
  • Pregnant uterus (Hypertrophy+hyperplasia)

- Skeletal muscle

57
Q

Give pathological examples of hypertrophy

A
  • Ventricular hypertrophy (hypertension/abnormal valves/pulmonary)
  • Urinary bladder during prostate enlargement -> bladder has to work harder to empty as urethra narrows
58
Q

Is hypertrophy of cardiac muscle always pathological?

A

-No, can occur in athletes without the pathological consequences as the heart is not constantly working hard as in hypertension

59
Q

What is compensatory hypertrophy?

A

-Occurs in paired organs when one is removed or hypoplastic; the other organ hypertrophies due to extra work load

60
Q

Define hypoplasia

A

-The underdevelopment of an organ or tissue at the embryonic stage eg heart, kidneys, breasts

61
Q

Define aplasia

A

-Total failure of development of an organ or tissue at the embryonic stage

62
Q

Is hypertrophy reversible?

A

-Yes

63
Q

What is atrophy?

A

-Shrinkage of a tissue or organ due to an acquired decrease in cell size or number

64
Q

Why is cardiac hypertrophy a problem?

A

-The number of capillaries increase but not enough to satisfy the increased muscle mass, leads to anoxia and fibrosis. This decreases compliance and effectiveness and can eventually lead to myocardial exhaustion

65
Q

What are the main causes of atrophy?

A
  • Reduced functional demand

- Reduced hormonal stimulation

66
Q

How do cells reduce in size?

A
  • Reduce the number of structural components by eliminating organelles into residual bodies which are digested.
  • Removal of proteins by ubiquitin binding and targeting them for destruction
67
Q

How do organs/tissue reduce in cell number?

A
  • Cells are picked to undergo apoptosis
  • If they are situated on an external surface then cell remnants are lost into the lumen or from the surface of the body
  • Otherwise they will be removed by phagocytosis by macrophages or neighbouring cells
68
Q

In organs undergoing atrophy, why part of the organ is effected first?

A

-Parenchyma thus atrophic tissues contain large amounts of connective tissue

69
Q

Is atrophy reversible?

A

-Upto a point, after that it becomes permanent with reduced function

70
Q

Give a physiological example of atrophy

A
  • Decrease in uterus after parturition

- Ovarian atrophy in post-menopausal women

71
Q

Provide examples of pathological atrophy

A
  • Dis-use atrophy (reduced functional demand/workload)
  • Denervation atrophy (loss of innervation)
  • Inadequate blood supply
  • Inadequate nutrition
  • Loss of hormonal stimulation
  • Persistant injury
  • Ageing
72
Q

What is metaplasia?

A

-The reversible change of one cell type to another

73
Q

What happens in metaplasia to change the cell type present to a different one?

A

-Original cells die due to stress -> altered stem cell differentiation and they produce another fully differentiated cell more capable of withstanding the stress

74
Q

Where is metaplasia the most adaptive?

A

-Epithelia

75
Q

Does metaplasia occur in all tissues?

A

-No, only those which can replicate

76
Q

Give an example of metaplasia in the bronchi

How does this affect function?

A
  • Psuedostratified ciliated epithelia -> stratified squamous epithelia due to cigarette smoking
  • No mucocilliary esculator
77
Q

What can result from metaplasia in the bronchi to stratified squamous epithelia?

A

-Squamous cell carcinoma

78
Q

Give an example of metaplasia in the oesaphagus, what it can mead to and what causes it?

A
  • Stratified squamous epithelium -> gastric glandular epithelium
  • Oesophageal adenocarcinoma
  • Persistent acid reflux
79
Q

What is involution?

A
  • Normal programmed shrinkage of an organ (overlaps with atrophy)
  • Uterus after child birth
  • feotal organs (Pro- and mesonephros)
80
Q

Define atresia

A

-No development of an orifice eg anus, vagina, gut

81
Q

Define dysplasia

A

-Premalignant lesions of irregular and disorganised epithelia

Mechanisms of Disease (11 decks)

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