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Principles: Pathology > Pathology: Cell Injury > Flashcards

Pathology: Cell Injury Flashcards

1
Q

Prior to damage/death, how do body cells cope with changes (stress)?

A

Adaptations

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2
Q

What are examples of adaptions of body cells due to stress?

A
  • Increased demand on cells - hyperplasia, hypertrophy
  • Decreased demand - atrophy
  • Altered stimulus - metaplasia
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3
Q

In which 2 ways does the body grow?

A
  • Hypertrophy - cells get bigger

* Hyperplasia - cells increase in number

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4
Q

Do hyperplasia and hypertrophy occur randomly?

A

No, they require specific instructions to grow

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5
Q

How are signals for growth (hypertrophy) produced?

A
  • Produce more growth factors

* Produce more growth factor receptors

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6
Q

What are the 3 categories of growth receptors?

A
  • Receptors with intrinsic tyrosine kinase activity
  • 7 transmembrane G-protein coupled receptors
  • Receptors without intrinsic tyrosine kinase activity
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7
Q

Does hyperplasia and hypertrophy occur in a disordered fashion?

A

No, occurs in a stepwise progression

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8
Q

What can mistakes in signals for growth and cell division lead to?

A

Cancer

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9
Q

What are the stages of the cell cycle (G1, S, G2, M) controlled by?

A

Cyclin dependent kinases (CDKs)

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10
Q

What do CDKs do?

A

Activate each other and other enzymes in a stepwise fashion

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11
Q

What are CDKs activated by?

A

A specific cyclin

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12
Q

Do cyclins and CDKs vary in concentration throughout the cell?

A
  • Cyclins vary in concentration throughout the cell

* CDKs do not

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13
Q

What are the 4 types of cyclin?

A
  • Cyclin D
  • Cyclin E
  • Cyclin A
  • Cyclin B
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14
Q

What is G1?

A

Growth phase

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15
Q

What happens in G1?

A
  • Cell increases in size and synthesises proteins
  • CDK4 is activated by cyclin D
  • CDK4 phosphorylates retinoblastoma protein
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16
Q

What is the role of activated CDK4?

A

Phosphorylates Rb, which means it cannot bind to EF2 - allows cell cycle to progress

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17
Q

What is retinoblastoma?

A

Protein that is important in cell growth and malignancy

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18
Q

How does Rb inhibit the cell cycle?

A

Normally bound to EF2, which prevents EF2 from stimulating cell division

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19
Q

What is EF2?

A

A protein that stimulates cell cycle

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20
Q

What is the S phase?

A

Synthesis - DNA replication

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21
Q

What happens in the S phase?

A
  • EF2 initiates DNA replication
  • EF2 increases levels of cyclin A
  • Cyclin A activates CDK2
  • CDK2 also promotes DNA replication
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22
Q

How many copies of the genome are there at the end of the S phase?

A

2 copies of the genome

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23
Q

What is G2?

A

Second growth phase

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24
Q

What happens in G2?

A
  • More cell growth and protein synthesis
25
Q

Where does the main checkpoint of the cell cycle occur?

A

End of G2 (G2 checkpoint - P53)

26
Q

What is the role of P53 at the G2 checkpoint?

A
  • Checks for DNA damage
27
Q

What happens if mistake in DNA is found by P53?

A
  • Pauses cell cycle and attempts repair
  • If repair successful = cell cycle progresses
  • If repair unsuccessful = P53 triggers apoptosis
28
Q

How do cancer cells avoid apoptosis at the G2 checkpoint?

A

They avoid checking by P53 - they can keep dividing despite faults in DNA

29
Q

What checkpoint is present in the mitotic phase?

A

Mitotic checkpoint - checks chromosomes are correctly aligned on the spindle

30
Q

What happens once mitotic checkpoint is passed?

A
  • Nucleus divides

* Cytokinesis can then occur

31
Q

What is replicative senescence?

A

Cells which cannot/can no longer divide

32
Q

What does it mean if a cell is terminally differentiated?

A

Once specialised, lose ability to replicate e.g. neurones

33
Q

How do people recover from brain damage if neurones are terminally differentiated?

A
  • New cells are not formed in response to damage

* Instead, undamaged areas of the brain take on the function of the damaged area

34
Q

Do cells divide less in younger people than in older people?

A

No

  • Young people - cells divide lots of times
  • Older people - fewer times
35
Q

Why can cells only divide a certain number of times?

A

Due to telomere repeats at the end of chromosomes

* With every division, number of telomere repeats gets smaller until you can’t divide anymore

36
Q

What is the function of telomeres?

A

Provide protection and stop chromosome ends from degrading or fusing

37
Q

What are TTAGGG repeats?

A

Telomere repeats

38
Q

What must be present for hyperplasia to occur?

A

External stimulus - growth signals

39
Q

What will happen to hyperplasia if growth signals are withdrawn?

A

Hyperplasia will regress

40
Q

Is hyperplasia pathological?

A

Can be pathological or physiological

41
Q

What are examples of physiological hyperplasia?

A
  • Hormonal - puberty (breast tissue growth), pregnancy (hyperplasia of endometrium)
  • Compensatory - occurs after loss of tissues (not common in many tissues) e.g. liver, bone marrow
42
Q

What are examples of pathological hyperplasia?

A
  • Hormonally-induced - excess oestrogen leads to endometrial hyperplasia and abnormal menstrual bleeding (e.g. postmenopausal bleeding), prostatic hyperplasia in response to androgens
  • Infection - lymph nodes undergo hyperplasia in response to infection
43
Q

Is hyperplasia reversible?

A

Yes, upon withdrawal of stimulus

44
Q

Does cancer require an external stimulus?

A

No, cancer can keep growing even when stimulus is withdrawn

45
Q

What is hyperplasia a risk factor for?

A

Hyperplastic tissue is at risk for development of cancer

46
Q

What is hypertrophy?

A

Increase in cell size

47
Q

What does hypertrophy often occur in response to?

A

Mechanical stress - increased demand e.g. athletes have a big heart

  • However, big heart can also occur in response to pathology (hypertension) - heart has to work harder to pump blood
48
Q

When does compensatory hypertrophy of the heart become pathologic?

A

When heart is pushed too hard

  • Can no longer function
  • Requires more blood than is supplied
49
Q

What can pathologic hypertrophy of the heart result in?

A

Heart failure - inability of heart to pump normally

50
Q

What is atrophy?

A

Reduction in cell size

51
Q

Is atrophy pathological?

A

Can be pathological or physiological

52
Q

What are examples of physiological atrophy?

A
  • Embryological structures - if remain, can become pathological
  • Uterus undergoes rapid atrophy after child birth (parturition)
53
Q

What are examples of pathological atrophy?

A
  • Decreased demand (workload) e.g. broken limb immobilised in cast
  • Loss of innervation
  • Blocked blood supply
  • Loss of hormonal stimulation
  • Inadequate nutrition
  • Ageing
  • Pressure - endogenous (internal) or exogenous (external) structures, often seen in tissues adjacent to tumours
54
Q

What does loss of blood supply to 1 kidney result in?

A
  • Atrophy of the affected kidney

* Other kidney then undergoes compensatory hyperplasia due to increased demand

55
Q

What are the mechanisms of atrophy?

A
  • Reduced cellular components
  • Protein degradation

Both result in a decrease in cell size

56
Q

How are proteins degraded in atrophy?

A
  • ‘Digested’ by enzymes

* degraded by ubiquitin proteasome pathway

57
Q

Which hormones promote degradation and atrophy?

A
  • Glucocorticoids

* Thyroid hormone

58
Q

Which hormone opposes atrophy and promotes growth?

A
  • Insulin
59
Q

Why must atrophy and growth be balanced?

A

To maintain homeostasis

Principles: Pathology (4 decks)

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