Cell injury 🗸 Flashcards
Homeostasis
steady state
closely maintained
stress on cells results in an attempt at adaptation
three adaptations to increased demand
hyperplasia
hypertrophy
growth receptors
hyperplasia
increase in cell number in response to external stimulus
can be physiological or pathological
reverses on withdrawal of stimulus
physiological example of hyperplasia
breast tissue in puberty
response to loss of tissue
pathological example of hyperplasia
hormonally induced e.g. excess of oestrogen = endometrial hypoplasia
hyperplasia of lymph nodes in response to infectiom
what happens if cells keep growing in a lack of stimulus?
could be cancerous
hypertrophy
increase in cell size
when does hypertrophy often occur?
in conjunction with hyperplasia
in isolation in non-dividing cells (e.g. skeletal muscle)
in response to mechanical stress
when does hypertrophy become pathological?
when heart/muscle cannot function
requires more blood supply
can cause heart failure
growth receptors
stress growth factors lead to cell division
to increase cell division…
produce more growth factors and growth factor receptors
three categories of growth factor receptor
receptors with intrinsic tyrosine kinase activity
7 transmembrane G protein coupled receptors
receptors without intrinsic tyrosine kinase receptors
Atrophy
reduction in cell size, can be physiological or pathological
physiological examples of atrophy
embryological structures
post-menopausal uterus
pathological examples of atrophy
decreased workload
blocked blood supply
loss of innervation
mechanisms of atrophy
reduced cellular components
protein degradation
some hormones promote degradation (thyroid hormone), others promote growth (insulin)
Cell cycle overview
tightly controlled with checkpoints
faulty cells may not perform function
each stage of the cell cycle is controlled by CDKs which are activate by a specific cyclin
G1
cells get bigger, increased protein synthesis
Cyclin D activates CDK4 with phosphorylates Rb protein
Rb is normally bound to E2F, stopping it from initiating cell division
when Rb is phosphorylated it is unable to bind to E2F and E2F will initiate cell division
p53 can cause cell arrest between G1 and S
S phase
E2F initiates DNA replication and increases levels of cyclin A
Cyclin A activates CDK2 also promoting DNA replication
ends with two copies of the genome
G2
Cell gets bigger, more protein synthesis
main p53 checkpoint occurs at the end of G2
- checks for mistakes
- pauses cell and attempts to repair, if its a success, the cycle continues and if it fails, the cell dies
if cells can avoid p53, the can keep dividing whilst being faulty
M phase
mitosis
Variations in the cell cylce
not all cells divide - some are terminally differentiated (neurons etc.)
Telomeres get smaller with each division, the cells can only divide a limited number of times
telomeres
caps which protect the chromosome ends from degradation and fusion
