Pathology: Tissue and Cell Injury, and Cell Cycle Flashcards
List the ways that cells can adapt
- Hyperplasia
- Hypertrophy
- Atrophy
- Metaplasia
How could a tissue adapt to increased demand?
- Hyperplasia
- Hypertrophy
How could a tissue adapt to increased demand?
- Atrophy
How could a cells adapt to an altered stimulus?
Metaplasia
Define hypertrophy
Cells get bigger
Define hyperplasia
More cells are produced
List the 3 categories of growth receptor
- Receptors with intrinsic tyrosine kinase activity
- 7 transmembrane G protein-coupled receptors
- Receptors without intrinsic tyrosine kinase activity
What aspect of the pathways started by the activation of growth receptors make them susceptible to aiding the development of malignancy?
Lots of steps in pathway, so lots of chance for a mutation
The pathways govern cell proliferation so important in malignancy
Name the phases of the cell cycle in order (including those of the interphase)
- Gap 1 (G1) phase
- Synthesis (S) phase
- Gap 2 (G2) phase
- Mitotic (M) phase
- Cytokinesis
- Gap 0 (G0) phase
Explain the role of CDKs and cyclins at cell cycle checkpoints
- 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
Describe the G1 phase
- Cell gets bigger, increased protein synthesis
- Cyclin D accumulates
Describe how the G1 progresses to the S phase
- 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
Describe E2F
- Transcription factor
- When free from Rb it initiates the S phase
Describe the S phase
- DNA synthesis to produce 2 copies of the cells genome
Which cell cycle phases make up the interphase?
G1, S, G2
Describe the G2 phase
- Second growth phase
- Cells get bigger, more protein synthesis
- Main checkpoint occurs at the end of the G2 phase
Describe the G2 checkpoint
- 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
Describe the M phase
- Prophase, Metaphase, Anaphase, Telophase
(*The four wonders) - Ends up with a cell with 2 discrete nuclei
Describe cytokinesis
The connecting cytoplasm is severed, leaving 2 identical daughter cells
Describe the G0 phase
A resting state where cells can stay if there is no need for cell division
Define replicative senescence
When a cell is prevented or is is incapable of dividing
Explain the importance of replicative senescence
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
Describe telomeres
- The “caps” on the end of chromosomes
- Prevent degradation and fusion of the chromosome
- Consist of TTAGGG repeats
- Get smaller every division
Describe telomerase
- An enzyme expressed by stem cells
- Regenerates the telomeres
Describe physiological hormonal hyperplasia
- Due to hormones
e. g. female breast during puberty, uterine lining during pregnancy
Describe compensatory hyperplasia
After tissue loss
Not common in most tissues
Liver and bone marrow are good examples
List the types of physiological hyperplasia
- Hormonal
- Compensatory
List the types of pathological hyperplasia
- Hormonal
- Infection
Describe pathological hormonal hyperplasia
- Hormonally induced
- Will regress on withdrawal of the stimulus
e.g.
Prostatic hyperplasia
Give an example of pathological hyperplasia due to infection
Lymph nodes undergo hyperplasia during infection
Describe the cancer risk of hyperplastic tissue
At a higher risk of cancer
Describe hyperplasia
More cells are produced
- Happens due to specific external signalling
- Will regress on withdrawal of stimulus
- Can be physiological or pathological
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
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
Give a difference between cancer and hyperplasia
Hyperplasia regresses at stimulus withdrawal
Cancer doesn’t
Define atrophy
A reduction in cell size
Give an example of physiological atropy
Cells in many embryological structures
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)
Where are common places to see atrophy due to endogenous pressure?
- Besides tumours
- Besides abscesses
Describe the mechanism of atrophy
- Reduced cellular components
- Proteins degraded by lysosomes
- Often by ubiquitin protease pathway
- Some hormones promote atrophy
Which hormones promote degradation and atrophy?
- Glucocorticoids
- Thyroid hormone
Which hormones oppose atrophy, and support growth?
Insulin
A balance of growth and atrophy maintains homeostasis
Yep
