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Pathology > Neoplasia I > Flashcards

Neoplasia I Flashcards

1
Q

What is cellular hypertrophy?

A

The cell gets bigger.

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2
Q

What is cellular atrophy?

A

Fewer and/or smaller cells.

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3
Q

What is hypotrophy?

A

Not a word!!!

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4
Q

What is hyperplasia?

A

More cells

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5
Q

Do tissues/organs undergo hypertrophy or hyperplasia?

A

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

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6
Q

What is the opposite of hyperplasia?

A

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

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7
Q

What is the opposite of hypertrophy?

A

Atrophy

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8
Q

What is aplasia?

A

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

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9
Q

What is metaplasia?

A

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

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10
Q

Define cardiomyopathy

A

diseased heart muscle

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11
Q

Define cardiomegaly

A

enlarged heart (organ)

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12
Q

Define myocardial hypertrophy

A

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

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13
Q

Define endocrinopathy

A

Disease of an endocrine tissue/system

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14
Q

Define adrenomegaly

A

Enlarged adrenal gland

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15
Q

Define adrenocortical hyperplasia

A

Enlargement of adrenal cortex due to increased number of cells

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16
Q

Define renal hypoplasia

A

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

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17
Q

Define renal agenesis

A

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

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18
Q

What is segmental aplasia of the ureter?

A

Would have been a full ureter but discontinued.

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19
Q

Define renomegaly

A

One of the kidneys is larger than it should be.

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20
Q

Define atresia

A

Absence or abnormal narrowing of an opening or passage.

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

21
Q

Can proliferative rates differ among cell types/age?

A

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

22
Q

What kinds of cells constantly proliferate to maintain cell populations?

A

Bone marrow, intestine

23
Q

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

A

Liver and kidney

24
Q

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

A

Muscle and brain

25
Q

What can cells do in addition to proliferation?

A

Differentiate to have more specialized functions or less proliferative capacity.

26
Q

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

A

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

27
Q

How does the epidermis differentiate?

A
  • 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
28
Q

What regulates cell number and size?

A
  • hormones
  • local growth factors and nutrition
  • demands on the tissue
29
Q

What kind of signalling do hormones do?

A

Endocrine signalling

30
Q

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

A

Paracrine signalling.

31
Q

What happens to cells with a lack of proper nutrition?

A

atrophy

32
Q

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

A

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

33
Q

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

A

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

34
Q

What are the steps in nuclear receptor signalling?

A

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

35
Q

How does hepatocyte growth factor work with paracrine signalling?

A
  • 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
36
Q

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

A

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

37
Q

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

A
  • 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
38
Q

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

A
  • 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
39
Q

How are EPO and VEGF regulated by hypoxia?

A
  • 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
40
Q

What does dysregulation of proliferative cells lead to?

A

Hyperplasia

41
Q

What can damage to proliferative cells cause?

A

Atrophy

42
Q

What other issue can result from hyperthyroidism and how?

A

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

43
Q

What is the pathogenesis of nutritional hyperparathyroidism and fibrous osteodystrophy?

A

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

44
Q

How can endocrine effects cause atrophy?

A

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

45
Q

What is an example of compensatory hypertrophy?

A

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

46
Q

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

A
  • mitotically active epithelium (doesn’t happen in cardiac myocytes)
  • Intact connective tissue framework
  • adequate vascular supply
47
Q

What does the suffix -megaly mean?

A

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

48
Q

How does cellular hypertrophy occur?

A

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

Pathology (12 decks)

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