Revision: Cellular Adaptations Flashcards
Chemical signal types for the control of cellular growth
1 Hormones
2 Local mediators (including GFs): paracrine, autocrine
3 direct cell->cell/stroma contact
Growth Factors
a type of local chemical mediator
stimulates cell prolif., also locomotion, contractility, differentiation, angiogenesis
Eg: Epidermal GF: made by keratinocytes, macrophages and other inflamm. cells, mitogenic for fibroblasts, hepatocytes, epith.
- Vascular Endothelial GF: role in vasculogenesis (development of vessels) and angiogenesis (new vessel growth), acts in tumours, CIRs, wound healing
- PDGF: stored in platelet alpha granules, also released by macrophages, endoth., SMCs and tumour cells, causes migration and prolif. of fibroblasts, SMCs and monocytes
Epidermal GF synth. by, acts on
made by keratinocytes, macrophages and other inflamm. cells, mitogenic for fibroblasts, hepatocytes, epith.
Vascular Epidermal GF role, acts in
role in vasculogenesis (development of vessels) and angiogenesis (new vessel growth), acts in tumours, CIRs, wound healing
PDGF released by, causes
stored in platelet alpha granules, also released by macrophages, endoth., SMCs and tumour cells, causes migration and prolif. of fibroblasts, SMCs and monocytes
Control of the cell cycle
R (restriction) point: towards the end of G1, most commonly altered checkpoint in cancerous cells, activation leads to a delay in the cell cycle, followed by either DNA repair mech.s or apoptosis initiated by p53
CDK (cyclin dependant kinase): activated by binding to cyclin, leads to phosphorylation of proteins involved in the cycle eg retinoblastoma susceptibility prot. that then allows passage past the R point, GFs can stim. production of cyclins and some can shut off production of cyclin-CDK inhibitors
Types of cellular adaptations
1 Regeneration: regeneration of cell losses by new cells to maintain tiss/organ size
2 Hypertrophy: inc. in tiss/organ size due to inc. cell size
3 Hyperplasia: inc. in tiss/organ size due to inc. cell no.s
4 Atrophy: dec. in tiss/organ size due to dec. cell no.s/size
5 Metaplasia: reversible change of one differentiated cell type to another
Regeneration outcome of cellular adaptation
Leads to the replacement of lost cells by new cells to maintain organ/tiss. size
If harmful agent is removed, the tiss. damage is not too severe and labile/stable cells are affected then it can lead to RESOLUTION eg liver cells can regenerate v. well
If any of these conditions are not met then it can lead to a scar eg on cardiac muscle, on skin with a severe burn
Hyperplasia outcome of cellular adaptations
Inc. in organ/tiss. size due to inc. cell no.s
Can be physiological, but this is when the proliferation is a NORMAL response to an ABNORMAL stimulus:
- eg endometrium thickening in response to oestrogen
- or bone marrow inc. erythropoiesis rate in response to hypoxia (eg high altitude)
If it is pathological, this is because it is an ABNORMAL response to a stimulus:
- eg epidermis thickening in eczema/psoriasis
- or thyroid goitre in response to iodine deficiency
Hypertrophy outcome of cellular adaptations
inc. in tiss./organ size due to inc. cell size
occurs esp. in permanent cells, though can appear in other types alongside hyperplasia, can be due to a functional demand/hormonal stimulus, contains more structural components to deal w/ the workload
Eg. physiological: skel. muscle in a bodybuilder, SMCs of pregnant uterus
pathological: ventricular cardiac muscle due to hypertension, SMCs of bladder due to obstruction from enlarged prostrate gland
Atrophy outcome of cellular adaptations
Dec. in tiss/organ size due to dec. cell no.s/size
if it is cellular atrophy it is due to cell size, if it is organ/tiss. atrophy it is due to both, leads to chrinkage where survival is still possible but may unintentionally result in death
Physioogical: ovarian atrophy in post-menopausal women
Pathological: denerv., inadeq. blood/nutrient supply -> muscle atrophy, loss of hormonal stim. -> breasts, reproductive organs, age -> senile atrophy of heart, brain
Metaplasia outcome of cellular adaptations
Reversible alteration of one differentiated cell type to another
most clearly seen in epith, can be a prelude to dysplasia and cancer
metaplasia is fully differentiated, dysplasia is disorganised and abnormal differentiation, cancerous is irrversible, disorganised and abnormal differentiation
eg bronchial pseudostratified ciliated -> stratified squamous epith. (due to cig. smoke)
stratified squam -> gastric glandular epith. w/ persistent acid reflux (aka Barrett’s oesophagus)
Aplasia
complete failure of org/tiss. to develop, an embryonic development disorder eg thymic aplasia, leading to AImmune problems and infections
hypoplasia
incomplete development of organ.tiss due to inadequate no. of cells, in a spectrum w. aplasia, NOT the opposite of hyperplasia as it occur at embryonic stage
eg testes in Klinefelter’s, chambers of the heart in congenital heart problems
dysplasia
disorganised and abnormal maturation of cells w/in tissues, potentially reversible but can be pre-cancerous
