Neoplasia I Flashcards
What is cellular hypertrophy?
The cell gets bigger.
What is cellular atrophy?
Fewer and/or smaller cells.
What is hypotrophy?
Not a word!!!
What is hyperplasia?
More cells
Do tissues/organs undergo hypertrophy or hyperplasia?
They can undergo both, where they can have more and/or larger cells.
What is the opposite of hyperplasia?
Hypoplasia (less cell division resulting in less cells in tissue)
Atrophy can also be an opposite
What is the opposite of hypertrophy?
Atrophy
What is aplasia?
Lack of cell division, cell hasn’t grown. The same as agenesis.
What is metaplasia?
The cells are different looking than normal, often more cells.
Define cardiomyopathy
diseased heart muscle
Define cardiomegaly
enlarged heart (organ)
Define myocardial hypertrophy
More myocardial tissue due to cell enlargement (cells in heart don’t usually divide)
Define endocrinopathy
Disease of an endocrine tissue/system
Define adrenomegaly
Enlarged adrenal gland
Define adrenocortical hyperplasia
Enlargement of adrenal cortex due to increased number of cells
Define renal hypoplasia
Kidney didn’t grow to normal size, smaller than normal kidney.
Define renal agenesis
Also called renal aplasia. No kidney as didn’t grow
What is segmental aplasia of the ureter?
Would have been a full ureter but discontinued.
Define renomegaly
One of the kidneys is larger than it should be.
Define atresia
Absence or abnormal narrowing of an opening or passage.
Intestinal aplasia could mean that ingest doesn’t pass through.
Can proliferative rates differ among cell types/age?
Yes, they differ among cell types and may decline with age. For many tissues, the proliferation depends on the age/stage of life.
What kinds of cells constantly proliferate to maintain cell populations?
Bone marrow, intestine
What kinds of cells have a low proliferation but can increase if needed, such as when damaged?
Liver and kidney
What kind of cells have little or no capacity for proliferation?
Muscle and brain
What can cells do in addition to proliferation?
Differentiate to have more specialized functions or less proliferative capacity.
True or false: stem cells have a higher proliferation rate than pluripotent cells?
False, pluripotent cells have a higher proliferation rate than stem cells.
How does the epidermis differentiate?
- basal layer at bottom is proliferative
- spinous layer has cells that are still alive, keratin and lipid synthesis
- granular layer is for lipid extrusion and programmed cell death
- cornified layer is dead cells, assembly of keratin and lipid
What regulates cell number and size?
- hormones
- local growth factors and nutrition
- demands on the tissue
What kind of signalling do hormones do?
Endocrine signalling
What kind of signalling do local growth factors (cytokines) and nutrition do?
Paracrine signalling.
What happens to cells with a lack of proper nutrition?
atrophy
What are some examples of demands on tissue that may interfere with regulation of proliferating cells?
workload (harder the muscle works, the bigger it gets-hypertrophy), nerve stimulation (if you lack, atrophy), hypoxia
compensation for loss of tissue
What are the steps involved in receptor control of cell proliferation and differentiation?
Growth factors bind to membrane receptors bind to signal transducers -> transcription factors -> response elements
the proteins made drive the cell response
What are the steps in nuclear receptor signalling?
ligand binds to nuclear receptor, transporter takes to nucleus. transcriptional response elements such as estrogen response element lead to altered gene expression
How does hepatocyte growth factor work with paracrine signalling?
- HGF is bound as a protein to ECF so is ready to go when needed
- HGF binds to c-met which activates receptor kinases which phosphorylate mTOR and lead to proliferation
- phosphatases such PTEN inhibit phosphorylation
How does IL-6 (cytokine signalling) work with endocrine signalling?
Il-6 from macrophages in another tissue (or local) binds to IL6R, which activates receptor kinases, causes phosphorylation of STAT3 and leads to proliferation.
-phosphatases like PTEN inhibit this
When blood oxygen is at an ok level, what happens with the number of RBCs and how?
- ok amount of O2 sensed by kidney
- kidney makes a basal amount of erythropoietin
- EPO travels through blood to bone marrow
- bone marrow produces basal number of RBCs
When blood oxygen is low, what happens with the number of RBCs and how?
- low O2 sensed by kidney
- kidney makes an increased amount of EPO
- EPO travels through blood, causing bone marrow to make an increased number of RBCs
How are EPO and VEGF regulated by hypoxia?
- hypoxia increases expression of EPO in kidney when renal blood flow or O2 carrying capacity is reduced
- In peripheral tissues and brain, hypoxia also increases expression of vascular endothelial growth factor (VEGF) that stimulates the production of new blood vessels in a paracrine manner
- thus, the cells that produce the growth factors can directly sense a low oxygen condition
- hypoxia inducible factor alpha (HIF-1a) is degraded by an oxygen dependent pathway which stops stimulation of EPO and VEGF when oxygen supply is adequate
- usual state is proper oxygenation and low activity, so labile HIF 1 a leads to ubiquitinylation and degradation
What does dysregulation of proliferative cells lead to?
Hyperplasia
What can damage to proliferative cells cause?
Atrophy
What other issue can result from hyperthyroidism and how?
Hyperthyroidism -> increased thyroid hormone -> myocardial hypertrophy as the cells have to enlarge (don’t divide) in heart -> cardiac dysfunction (so many cells, can’t fill enough with blood to properly pump
What is the pathogenesis of nutritional hyperparathyroidism and fibrous osteodystrophy?
High dietary phosphorus -> parathyroid chief cell hyperplasia and PTH secretion -> bone resorption and hyperplasia of periosteal and endosteal fibroblasts
How can endocrine effects cause atrophy?
Congenital portosystemic shunt and hepatic atrophy:
Portal-caval shunt (portal vein -> caudal vena cava) -> hepatotrophyic factors bypass liver -> hepatocellular atrophy (small cells in liver)
What is an example of compensatory hypertrophy?
When part of the liver is lost, the remaining hepatocytes replicate to replace the liver mass (other lobes get bigger)
What are the requirements for a tissue to return to normal?
- mitotically active epithelium (doesn’t happen in cardiac myocytes)
- Intact connective tissue framework
- adequate vascular supply
What does the suffix -megaly mean?
enlargement of an organ without specifying what contributed to the increase in size
How does cellular hypertrophy occur?
-cells increase amount of cytoplasmic components by increasing the expression of genes that supply these cellular components
