Pathology: Tissue and Cell Injury, and Cell Cycle Flashcards

(43 cards)

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
Describe physiological hormonal hyperplasia
- Due to hormones | e. g. female breast during puberty, uterine lining during pregnancy
26
Describe compensatory hyperplasia
After tissue loss Not common in most tissues Liver and bone marrow are good examples
27
List the types of physiological hyperplasia
- Hormonal | - Compensatory
28
List the types of pathological hyperplasia
- Hormonal | - Infection
29
Describe pathological hormonal hyperplasia
- Hormonally induced - Will regress on withdrawal of the stimulus e.g. Prostatic hyperplasia
30
Give an example of pathological hyperplasia due to infection
Lymph nodes undergo hyperplasia during infection
31
Describe the cancer risk of hyperplastic tissue
At a higher risk of cancer
32
Describe hyperplasia
More cells are produced - Happens due to specific external signalling - Will regress on withdrawal of stimulus - Can be physiological or pathological
33
Describe hypertrophy
- 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
Give an example of pathogenic hypertrophy
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
Give a difference between cancer and hyperplasia
Hyperplasia regresses at stimulus withdrawal Cancer doesn't
36
Define atrophy
A reduction in cell size
37
Give an example of physiological atropy
Cells in many embryological structures
38
List causes of pathological atrophy
- 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
Where are common places to see atrophy due to endogenous pressure?
- Besides tumours | - Besides abscesses
40
Describe the mechanism of atrophy
- Reduced cellular components - Proteins degraded by lysosomes - Often by ubiquitin protease pathway - Some hormones promote atrophy
41
Which hormones promote degradation and atrophy?
- Glucocorticoids | - Thyroid hormone
42
Which hormones oppose atrophy, and support growth?
Insulin
43
A balance of growth and atrophy maintains homeostasis
Yep