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Principles: Everything Else, Histology, Radiology & Embryology > Pathology: Tissue and Cell Injury, and Cell Cycle > Flashcards

Pathology: Tissue and Cell Injury, and Cell Cycle Flashcards

1
Q

List the ways that cells can adapt

A
  • Hyperplasia
  • Hypertrophy
  • Atrophy
  • Metaplasia
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2
Q

How could a tissue adapt to increased demand?

A
  • Hyperplasia

- Hypertrophy

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3
Q

How could a tissue adapt to increased demand?

A
  • Atrophy
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4
Q

How could a cells adapt to an altered stimulus?

A

Metaplasia

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5
Q

Define hypertrophy

A

Cells get bigger

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6
Q

Define hyperplasia

A

More cells are produced

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7
Q

List the 3 categories of growth receptor

A
  • Receptors with intrinsic tyrosine kinase activity
  • 7 transmembrane G protein-coupled receptors
  • Receptors without intrinsic tyrosine kinase activity
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8
Q

What aspect of the pathways started by the activation of growth receptors make them susceptible to aiding the development of malignancy?

A

Lots of steps in pathway, so lots of chance for a mutation

The pathways govern cell proliferation so important in malignancy

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9
Q

Name the phases of the cell cycle in order (including those of the interphase)

A
  • Gap 1 (G1) phase
  • Synthesis (S) phase
  • Gap 2 (G2) phase
  • Mitotic (M) phase
  • Cytokinesis
  • Gap 0 (G0) phase
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10
Q

Explain the role of CDKs and cyclins at cell cycle checkpoints

A
  • Cyclins accumulate
  • Cyclins combine with Cyclin Dependant Kinases (CDKs)
  • This activates the CKD
  • Activated CDKs
    phosphorylate other proteins
  • Stimulating the move to the next phase of the cell cycle
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11
Q

Describe the G1 phase

A
  • Cell gets bigger, increased protein synthesis

- Cyclin D accumulates

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12
Q

Describe how the G1 progresses to the S phase

A
  • Cyclin D accumulates
  • CDK4 activated by cyclin D
  • Activated CDK4 phosphorylates (inactivates) retinoblastoma (Rb)
  • Usually Rb is bound to E2F, preventing E2F from staring the S phase
  • When Rb is phosphorylated E2F is free to start the S phase
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13
Q

Describe E2F

A
  • Transcription factor

- When free from Rb it initiates the S phase

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14
Q

Describe the S phase

A
  • DNA synthesis to produce 2 copies of the cells genome
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15
Q

Which cell cycle phases make up the interphase?

A

G1, S, G2

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16
Q

Describe the G2 phase

A
  • Second growth phase
  • Cells get bigger, more protein synthesis
  • Main checkpoint occurs at the end of the G2 phase
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17
Q

Describe the G2 checkpoint

A
  • p53 is activated if DNA damage s detected
  • If there is a mistake then the cell cycle arrests
  • Repair is attempted
  • If successful then the cell progresses to the M phase, if unsuccessful then apoptosis
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18
Q

Describe the M phase

A
  • Prophase, Metaphase, Anaphase, Telophase
    (*The four wonders)
  • Ends up with a cell with 2 discrete nuclei
19
Q

Describe cytokinesis

A

The connecting cytoplasm is severed, leaving 2 identical daughter cells

20
Q

Describe the G0 phase

A

A resting state where cells can stay if there is no need for cell division

21
Q

Define replicative senescence

A

When a cell is prevented or is is incapable of dividing

22
Q

Explain the importance of replicative senescence

A

Cancer suppression:

  • Gives all cells max number of divisions
  • Cancers have to overcome this

Keeps cells that need to not divide from doing so
e.g. Neurons

23
Q

Describe telomeres

A
  • The “caps” on the end of chromosomes
  • Prevent degradation and fusion of the chromosome
  • Consist of TTAGGG repeats
  • Get smaller every division
24
Q

Describe telomerase

A
  • An enzyme expressed by stem cells

- Regenerates the telomeres

25
Q

Describe physiological hormonal hyperplasia

A
  • Due to hormones

e. g. female breast during puberty, uterine lining during pregnancy

26
Q

Describe compensatory hyperplasia

A

After tissue loss

Not common in most tissues

Liver and bone marrow are good examples

27
Q

List the types of physiological hyperplasia

A
  • Hormonal

- Compensatory

28
Q

List the types of pathological hyperplasia

A
  • Hormonal

- Infection

29
Q

Describe pathological hormonal hyperplasia

A
  • Hormonally induced
  • Will regress on withdrawal of the stimulus

e.g.
Prostatic hyperplasia

30
Q

Give an example of pathological hyperplasia due to infection

A

Lymph nodes undergo hyperplasia during infection

31
Q

Describe the cancer risk of hyperplastic tissue

A

At a higher risk of cancer

32
Q

Describe hyperplasia

A

More cells are produced

  • Happens due to specific external signalling
  • Will regress on withdrawal of stimulus
  • Can be physiological or pathological
33
Q

Describe hypertrophy

A
  • Cells get bigger
  • Often occurs along with hyperplasia
  • Common in non-dividing cells
    e. g. skeletal muscle, cardiac myocytes
  • Often in response to mechanical stress
34
Q

Give an example of pathogenic hypertrophy

A

In response to increased workload cardiac myocytes undergo hypertrophy

This becomes pathological when the heart can no longer function as requires more blood than it is provided

35
Q

Give a difference between cancer and hyperplasia

A

Hyperplasia regresses at stimulus withdrawal

Cancer doesn’t

36
Q

Define atrophy

A

A reduction in cell size

37
Q

Give an example of physiological atropy

A

Cells in many embryological structures

38
Q

List causes of pathological atrophy

A
  • Decreased workload
  • Loss of function due to loss of innervation
  • Lack of adequate perfusion
  • Loss of hormonal
    stimulation
  • Inadequate nutrition
  • Aging
  • Pressure (endogenous or exogenous)
39
Q

Where are common places to see atrophy due to endogenous pressure?

A
  • Besides tumours

- Besides abscesses

40
Q

Describe the mechanism of atrophy

A
  • Reduced cellular components
  • Proteins degraded by lysosomes
  • Often by ubiquitin protease pathway
  • Some hormones promote atrophy
41
Q

Which hormones promote degradation and atrophy?

A
  • Glucocorticoids

- Thyroid hormone

42
Q

Which hormones oppose atrophy, and support growth?

A

Insulin

43
Q

A balance of growth and atrophy maintains homeostasis

A

Yep

Principles: Everything Else, Histology, Radiology & Embryology (7 decks)

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