Cellular adaptations Flashcards
what factors could affect cell population?
- cell proliferation, differentiation, apoptosis.
- an increase in number with greater proliferation and decreased apoptosis or both.
- could be pathological or physiological with excessive physiological becoming pathological.
what controls cell proliferation?
- proto-oncogenes and tumours supressor genes.
- chemical mediators/ signals from microenvironment.
- signalling molecules that bind to receptors.
briefly describe the stages of the cell cycle and what the possible destinations could be for a cell upon completion.
- G1 : cellular contents duplicate.
- S : chromosomes duplicate.
- G2 : cell double checks and repair errors.
- mitosis and cytokinesis : daughter cells.
*G0 which is cell arrest for stable cells, differentiate permanent cells.
differentiate between mitosis and cytokinesis.
- mitosis is nuclear division whereas cytokinesis is cell division.
what are the 3 main cellular checkpoints within the cell cycle?
- restriction point : via P53 at end of G1.
- G1 check point : to see if env, cell size viable.
- G2 check point : DNA replication check.
what is the significance of the P53 ‘guardian of the genome’ ?
- once this activated the cell cycle delayed and DNA repair/ apoptosis triggered.
- repair via increasing P21 which prevents phosphorylation of cyclins, arresting cell via CDK inhibitors until repair.
what are cyclins and CDK?
- cyclins and CDK are proteins that regulate the transition of phase S to G1 and others.
- CDK is activated by cyclin attachment which phosphorylates proteins.
- can be inhibited by CDK inhibitors.
*eg: retinoblastoma susceptibility protein acts to prevent DNA replication and when acted upon by cyclin and CDK inactivated.
so in summary what factors regulate the cell cycle?
differentiate between those that inhibit and stimulate.
- inhibiting : tumour suppressor genes like retinoblastomas, P53 and CDK inhibitors.
- stimulating : oncogenes, cyclins, CDK complexes, growth factors.
define hyperplasia.
*increase in tissue or organ size due to cells increase in number above normal.
- in labile and stable tissue due to increase in demand or hormonal effects or normal proliferation secondary to pathology.
- repeated hyperplasia high risk of mutations and neoplasia.
give causes of pathological vs physiological hyperplasia.
- physiological : endometrium due to oestrogen, BM and erythrocytes due to hypoxia.
- pathological : hyperkeratonic skin in eczema and thyroid goitre.
what is hypertrophy?
*increase in tissue or organ size due to increase in cell size due to more structural components to share greater workload.
- can be in labile and stable (usually with hyperplasia) but mostly in permanent tissue.
- can be compensatory incase of kidneys.
- athletes may have hypertrophies hearts nut physiological functions still normal.
give causes of pathological vs physiological hypertrophy.
- physiological : skeletal muscle, pregnant uterus along with hyperplasia.
- pathological : heart hypertrophy, bladder due to obstruction, intestinal stenosis pressure causes.
what is atrophy?
- shrinkage of tissue or organ (to size when survival still possible) due to an acquired decrease in size and or number of cells.
- tissue atrophy can be due to a combo of cellular atrophy and apoptosis.
- reduced structural components, may eventually lead to cell death.
- matrix can undergo in astronauts for an example.
give causes of pathological vs physiological atrophy.
- physiological : ovarian in post menopausal women, uterus after delivery.
- pathological : muscle atrophy due to decreased use, loss innervation/ denervation atrophy, inadequate blood supply, inadequate nutrition, loss of endocrine stimuli like post pregnancy breasts, aging, persistent injury, pressure from tumours.
what is metaplasia?
*reversible change of one differentiated cell type to another.
- in labile/ stable, with altered stem cell differentiation.
- can be adaptive to suit environment better.
- reversible.
- no metaplasia across germ layers.
- can lead to dysplasia and cancer.
