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Pathology > Cell Proliferation / Cell Death > Flashcards

Cell Proliferation / Cell Death Flashcards

1
Q

what is cell proliferation?

A

a process that results in an increase in the number of cells

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2
Q

what is cell proliferation characterised by?

A

by balance between cell division and cell death/differentiation

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3
Q

when is cell proliferation increased?

A

in tumours

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4
Q

when does cell death occur?

A

in response to injury

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5
Q

what is cell death essential for?

A

essential part of development

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6
Q

what are the 2 forms of cell death?

A

apoptosis

necrosis

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7
Q

what is increased proliferation achieved by?

A

Shortening cell cycle

Recruiting quiescent cells into cell cycle

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8
Q

what is cell proliferation controlled by?

A

Controlled by cell contact or soluble signals

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9
Q

what are the stimuli for cell proliferation?

A

May involve physiological or pathological stimuli

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10
Q

what are labile cells?

A

cells that are constantly dividing, regenerate rapidly

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11
Q

what are examples of labile cells?

A

skin cells

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12
Q

what are stable cells?

A

cells that have low level of replication; can rapidly divide in response to stimuli

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13
Q

what are examples of stable cells?

A

hepatocytes

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14
Q

what are permanent cells?

A

non-dividing cells, terminally differentiated; unable to re-enter cell cycle

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15
Q

what are examples of permanent cells?

A

neurons

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16
Q

what controls organ/tissue growth?

A

Balance between increase cell number due to proliferation

& decrease in cell numbers due to cell death

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17
Q

what is cell growth?

A

Response of cells to increased functional demands

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18
Q

what are examples of physiological hypertrophy?

A

skeletal muscles in athletes

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19
Q

what are examples of pathological hypertrophy?

A

myocardium - outflow obstruction, hypertension

Arterial smooth muscle - hypertension

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20
Q

what are physiological examples of hyperplasia?

A

Bone Marrow: RBC at altitude

Breast: puberty, pregnancy

Thyroid: puberty, pregnancy

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21
Q

what are pathological examples of hyperplasia?

A

Prostate: epithelial & connective tissue

Thyroid: Grave’s Disease

Adrenal cortex: ACTH secreting pituitary tumour

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22
Q

what are physiological examples of combined hypertrophy and hyperplasia?

A

Uterine smooth muscle: puberty, pregnancy

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23
Q

what is hyperplasia?

A

Increase in number of cells

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24
Q

what is hypertrophy?

A

Increase in size of cells

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25
Q

what is cell cycle?

A

A series of highly regulated steps that governs cell proliferation

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26
Q

what part of the cell cycle are in interphase?

A

G1, S, G2

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27
Q

what is G1?

A

pre-synthesis gap

cells differentiate, perform specialist function as part of tissue

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28
Q

what is the duration of G1?

A

10 hours -

highly variable duration – several days/weeks

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29
Q

what is the S stage?

A

“synthesis” – DNA replication

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30
Q

how long does the S phase last?

A

9 hours

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31
Q

what is the G2 phase?

A

post-synthesis gap

cells prepare for mitosis

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32
Q

how long does G2 last?

A

4 hours

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33
Q

how long does mitosis last?

A

1 hour

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34
Q

what is G0?

A

Differentiated cells

Continuous differentiated function

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35
Q

when do chromosomes first become visible in nucleus?

A

prophase

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36
Q

what happens in prophase?

A
  • Chromosomes first become visible in nucleus & become condensed
  • Nucleoli disappear
  • Dissolution of nuclear envelope
  • Microfilaments & microtubules disaggregate into protein subunits
  • Centrioles migrate to opposite poles of cells
  • Spindle of microtubules forms between centrioles
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37
Q

what happens in metaphase?

A
  • Mitotic spindle moves into nuclear area
  • Duplicated chromosomes attached at kinetochore (AKA chromosome microtubule)
  • Chromosomes aligned along metaphase plate
  • Mitosis cannot progress until all chromatid pairs aligned (metaphase checkpoint)
38
Q

what happens in anaphase?

A
  • Splitting of centromere which bind chromatids of duplicated chromosomes
  • Mitotic spindle lengthened
  • Centrioles pulled apart
  • Chromatids of each duplicated chromosome pulled to opposite ends of spindle
  • Two groups of identical chromosomes at opposite ends of cell
39
Q

what is the final phase of mitosis?

A

telophase

40
Q

what happens in telophase?

A

Chromosomes uncoil
Nuclear membrane reassembles & nucleoli become apparent
Cytokinesis
Plasma membrane around spindle equator indents – cleavage furrow
Cells cleave

41
Q

how is the cell cycle controlled?

A
  • check points
  • cyclins & cyclin dependent kinases (CDK) - promote cell cycle progression
  • CDK inhibitors - stop cell cycle progression
42
Q

what happens at the G2 checkpoint?

A

if DNA synthesis has been done correctly

43
Q

what happens at the metaphase checkpoint?

A

if the sister chromatids can separate correctly

44
Q

what happens at G1 checkpoint?

A

if DNA synthesis can begin

45
Q

what do cyclin and CDK control?

A

transition from

G1-S and G2-M

46
Q

what are the cyclin-CDK complexes do?

A

Phosphorylate protein substrates

47
Q

what do Cyclin-CDK complexes do at S-phase?

A

proteins that initiate DNA replication

48
Q

what do Cyclin-CDK complexes do at M-phase?

A

proteins needed for chromosomal condensation; nuclear membrane stabilisation

49
Q

what is the objective of Cyclin & Cyclin Dependent Kinases?

A

Correct DNA synthesis & mitosis

50
Q

what is the M-phase Cyclin*/CDK complex phosphorylated by?

A

CAK

51
Q

when is the M-phase Cyclin*/CDK complex activated?

A

Activated at end of G2 by phosphatase - Cdc25 (removes inhibitory phosphates)

52
Q

what is p53?

A

multifunctional protein

53
Q

what is the function of p53?

A

regulates cell-cycle & apoptosis

54
Q

what does p53 do?

A

Recognises & binds damaged DNA

55
Q

what is the transcription factor for p21?

A

p53

56
Q

what is p21?

A

CDK inhibitor

57
Q

where is a p53 mutation found?

A

Mutation found in Li-Fraumeni Syndrome

58
Q

when are cyclins degraded?

A

Cyclins are degraded after mitotic division

59
Q

what are active CDK complexes regulated by?

A

CDKIs
Kinases
Phosphatases

60
Q

when are checkpoints activated?

A

Problems with DNA replication, repair

61
Q

what do cell cycle checkpoints allow?

A

Allowing time for repair

62
Q

what is pRb?

A

Retinoblastoma protein

63
Q

what does pRb do?

A

Recognises damaged DNA

Prevents progression from G1-S

Binds & inhibits E2F (transcription factor)

64
Q

what does pRb mutation lead to?

A

Mutation leads to retinoblastoma

65
Q

what can lead to increased cell proliferation?

A 
high growth factors 
high oncogenes 
low tumour suppressors 
high ECM stiffness
low cell density
66
Q

what can lead to increased cell cycle arrest?

A 
low growth factors
low oncogenes
high tumour suppressors
low ECM stiffness
high cell density
67
Q

what is necrosis?

A

collapse of membrane integrity & death of a cell or tissue

68
Q

what can lead to necrosis?

A

cell death by injury

69
Q

how does necrosis occur?

A

Swelling of cells & organelles
Release of lysosomal enzymes
Membrane breaks down
Nuclear changes

70
Q

what is karyolysis?

A

loss of staining

71
Q

what is karyorrhexis?

A

fragmentation

72
Q

true or false necrosis is associated with inflammation?

A

true

73
Q

is necrosis active or passive cell death?

A

passive cell death

74
Q

what is apoptosis?

A

programmed cell death

75
Q

what is meant by active process?

A

Requires energy

RNA & protein synthesis

76
Q

what is the characteristic morphology of apoptosis?

A

Chromatin condenses
Cells shrinks
Formation of apoptotic bodies
Cleared by phagocytosis

77
Q

is apoptosis associated with inflammation?

A

apoptosis has no inflammatory response

78
Q

is apoptosis or necrosis part of normal homeostasis?

A

apoptosis

79
Q

how is apoptosis induced?

A

Physiological or pathological stimuli

80
Q

how is necrosis induced?

A

usually due to pathological injury

81
Q

to what extent does apoptosis effect cells?

A

only affects single cells

82
Q

what extent does necrosis effect cells?

A

usually affects cell groups

83
Q

what are the biochemical events in apoptosis?

A

Engergy-dependent fragmentation of DNA by endogenous endonucleases
Lysosomes intact

84
Q

what are the biological events in necrosis?

A

Energy failure
Impairment/cessation of homeostasis
Lysosomes leak lytic enzymes

85
Q

what happens to cell membrane integrity in apoptosis?

A

it is maintained

86
Q

what happens to cell membrane integrity in necrosis?

A

it is lost

87
Q

what is the morphology of apoptosis?

A

Cell shrinkage & fragmentation to form apoptotic bodies

88
Q

what is the morphology of necrosis?

A

Cell swelling and lysis

89
Q

what is the fate of dead cells in apoptosis?

A

Ingested by neighbouring cells

90
Q

what is the fate of dead cells in necrosis?

A

Ingested by neutrophils & macrophages

91
Q

what is the outcome of apoptosis?

A

cell elimination

92
Q

what is the outcome of necrosis?

A

defence & preparation for repair

Pathology (17 decks)

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