Neoplasia I

Question 1

What is cellular hypertrophy?

Answer 1

The cell gets bigger.

Question 2

What is cellular atrophy?

Answer 2

Fewer and/or smaller cells.

Question 3

What is hypotrophy?

Answer 3

Not a word!!!

Question 4

What is hyperplasia?

Answer 4

More cells

Question 5

Do tissues/organs undergo hypertrophy or hyperplasia?

Answer 5

They can undergo both, where they can have more and/or larger cells.

Question 6

What is the opposite of hyperplasia?

Answer 6

Hypoplasia (less cell division resulting in less cells in tissue)
Atrophy can also be an opposite

Question 7

What is the opposite of hypertrophy?

Answer 7

Atrophy

Question 8

What is aplasia?

Answer 8

Lack of cell division, cell hasn’t grown. The same as agenesis.

Question 9

What is metaplasia?

Answer 9

The cells are different looking than normal, often more cells.

Question 10

Define cardiomyopathy

Answer 10

diseased heart muscle

Question 11

Define cardiomegaly

Answer 11

enlarged heart (organ)

Question 12

Define myocardial hypertrophy

Answer 12

More myocardial tissue due to cell enlargement (cells in heart don’t usually divide)

Question 13

Define endocrinopathy

Answer 13

Disease of an endocrine tissue/system

Question 14

Define adrenomegaly

Answer 14

Enlarged adrenal gland

Question 15

Define adrenocortical hyperplasia

Answer 15

Enlargement of adrenal cortex due to increased number of cells

Question 16

Define renal hypoplasia

Answer 16

Kidney didn’t grow to normal size, smaller than normal kidney.

Question 17

Define renal agenesis

Answer 17

Also called renal aplasia. No kidney as didn’t grow

Question 18

What is segmental aplasia of the ureter?

Answer 18

Would have been a full ureter but discontinued.

Question 19

Define renomegaly

Answer 19

One of the kidneys is larger than it should be.

Question 20

Define atresia

Answer 20

Absence or abnormal narrowing of an opening or passage.

Intestinal aplasia could mean that ingest doesn’t pass through.

Question 21

Can proliferative rates differ among cell types/age?

Answer 21

Yes, they differ among cell types and may decline with age. For many tissues, the proliferation depends on the age/stage of life.

Question 22

What kinds of cells constantly proliferate to maintain cell populations?

Answer 22

Bone marrow, intestine

Question 23

What kinds of cells have a low proliferation but can increase if needed, such as when damaged?

Answer 23

Liver and kidney

Question 24

What kind of cells have little or no capacity for proliferation?

Answer 24

Muscle and brain

Question 25

What can cells do in addition to proliferation?

Answer 25

Differentiate to have more specialized functions or less proliferative capacity.

Question 26

True or false: stem cells have a higher proliferation rate than pluripotent cells?

Answer 26

False, pluripotent cells have a higher proliferation rate than stem cells.

Question 27

How does the epidermis differentiate?

Answer 27

- 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

Question 28

What regulates cell number and size?

Answer 28

- hormones - local growth factors and nutrition - demands on the tissue

Question 29

What kind of signalling do hormones do?

Answer 29

Endocrine signalling

Question 30

What kind of signalling do local growth factors (cytokines) and nutrition do?

Answer 30

Paracrine signalling.

Question 31

What happens to cells with a lack of proper nutrition?

Answer 31

atrophy

Question 32

What are some examples of demands on tissue that may interfere with regulation of proliferating cells?

Answer 32

workload (harder the muscle works, the bigger it gets-hypertrophy), nerve stimulation (if you lack, atrophy), hypoxia compensation for loss of tissue

Question 33

What are the steps involved in receptor control of cell proliferation and differentiation?

Answer 33

Growth factors bind to membrane receptors bind to signal transducers -> transcription factors -> response elements the proteins made drive the cell response

Question 34

What are the steps in nuclear receptor signalling?

Answer 34

ligand binds to nuclear receptor, transporter takes to nucleus. transcriptional response elements such as estrogen response element lead to altered gene expression

Question 35

How does hepatocyte growth factor work with paracrine signalling?

Answer 35

- 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

Question 36

How does IL-6 (cytokine signalling) work with endocrine signalling?

Answer 36

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

Question 37

When blood oxygen is at an ok level, what happens with the number of RBCs and how?

Answer 37

- 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

Question 38

When blood oxygen is low, what happens with the number of RBCs and how?

Answer 38

- 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

Question 39

How are EPO and VEGF regulated by hypoxia?

Answer 39

- 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

Question 40

What does dysregulation of proliferative cells lead to?

Answer 40

Hyperplasia

Question 41

What can damage to proliferative cells cause?

Answer 41

Atrophy

Question 42

What other issue can result from hyperthyroidism and how?

Answer 42

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

Question 43

What is the pathogenesis of nutritional hyperparathyroidism and fibrous osteodystrophy?

Answer 43

High dietary phosphorus -> parathyroid chief cell hyperplasia and PTH secretion -> bone resorption and hyperplasia of periosteal and endosteal fibroblasts

Question 44

How can endocrine effects cause atrophy?

Answer 44

Congenital portosystemic shunt and hepatic atrophy: Portal-caval shunt (portal vein -> caudal vena cava) -> hepatotrophyic factors bypass liver -> hepatocellular atrophy (small cells in liver)

Question 45

What is an example of compensatory hypertrophy?

Answer 45

When part of the liver is lost, the remaining hepatocytes replicate to replace the liver mass (other lobes get bigger)

Question 46

What are the requirements for a tissue to return to normal?

Answer 46

- mitotically active epithelium (doesn't happen in cardiac myocytes) - Intact connective tissue framework - adequate vascular supply

Question 47

What does the suffix -megaly mean?

Answer 47

enlargement of an organ without specifying what contributed to the increase in size

Question 48

How does cellular hypertrophy occur?

Answer 48

-cells increase amount of cytoplasmic components by increasing the expression of genes that supply these cellular components