Exam 1: Cellular Adaptations & Accumulations I Flashcards

1
Q

What is adaptation?

A

State between the normal unstressed cell & the injured over-stressed cell; the new but altered steady state

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2
Q

List some reversible changes that are seen in response to cellular damage.

A
  • Changes in size
  • Changes in number
  • Phenotype
  • Metabolic activity
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3
Q

What is physiologic adaptation?

A

Responses of cells to normal stimulation by hormones or endogenous chemical mediations

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4
Q

What is patholgoic adaptation?

A

Underlying disease mechanisms that allows cells to modulate their environment and escape injury

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5
Q

What is hypertrophy?

A

Increase in cell size & consequent increase in the size of the organ

  • No new cells
  • Increased synthesis of structural proteins & organelles
  • Opposite of atrophy

*Note that this can coexist with hyperplasia (increase in #) and physiologic or pathologic

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6
Q

What is hyperplasia?

A

Increase in number of cells in response to a stimulus or persistent cell injury, which usually results in increased size & weight of an organ or tissue

  • Frequently occurs in conjunction with hypertrophy
  • Can be physiologic or pathologic

*Cells must be capable of replication

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7
Q

What is atrophy?

A

Decrease in size of a tissue or organ due to a decrease in cell size & organelles

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8
Q

What is metaplasia?

A

A reversible change in cell type i.e. change in which on differentiated cell type is replaced by another cell type
- Cells sensitive to a particular stress are replaced by cells better able to withstand the stress

*Through to arise through “reprogramming”

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9
Q

How does the hypertrophy of weight lifting and pregnancy differ?

A
  • Weight lifting= hypertropy without hyperplasia

- Pregnancy= uterus hypertrophies and undergoes hyperplasia

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10
Q

Describe an example of pathologic hypertrophy.

A
  • Cardiac enlargement that occurs with HTN or aortic valve disease
  • Enlargement of individual cardiac fibers following a MI

*Note that cardiac cells DO NOT enter the cell cycle; thus, they can only get larger

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11
Q

What is the difference between concentric hypertrophy & dilated hypertrophy seen in CHF?

A
  • Concentric hypertrophy

Limited ability to enlarge, then degeneration

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12
Q

What happens structurally in cardiac hypertrophy? What are the microscope indications of hypertrophy?

A
  • Increased nucleus to make more proteins (“boxcar” nuclei)
  • Increased cytoplasm
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13
Q

What are the mechanisms that induce hypertrophy?

A

1) Mechanical stress
2) Vasoactive agents (alpha-adrenergic)
3) Growth factors (TGF-B)

*****There is a limit in the enlargement that can occur and you reach a point where the muscle can no longer compensate, which leads to cardiac failure

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14
Q

What changes in expression of genes and proteins occurs in hypertrophy? Are these changes reversible?

A
  • Early embryonic genes are turned on
  • Increased synthesis of contractile proteins (actin & myosin filaments)
  • Increased production of growth factors that have an autocrine effect

*Yes, these changes are reversible

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15
Q

What are the types of physiologic hyperplasia?

A
  • Homronal hyperplasia= increase in functional capacity of a tissue when needed e.g female breast tissue during puberty and pregnancy, and proliferation of the endometrium that is induced by estrogen
  • Compensatory hyperplasia= increased tissue mass after damage or resection e.g. liver begins to regenerate in as little as 12 hours
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16
Q

What causes most forms of pathologic hyperplasia? List common examples of pathologic hyperplasia.

A

Most forms of pathologic hyperplasia are due to excessive hormones or growth factors acting on target cells

  • E.g. Endometrial hyperplasia due to estrogen/progesterone imbalance
  • BPH due to an increase in androgens

Grave’s disease (antibody stimulation, NOT hormonal)

17
Q

What is the mechanism of hyperplasia?

A

Result of growth factor-driven proliferation of mature cells, & in some cases by increased output of new cells from tissue stem cells

18
Q

What causes atrophy?

A
  • Decreased workload (disuse atrophy)
  • Loss of innervation (denervation atrophy)
  • Decreased blood supply, called “senile” atrophy
  • Inadequate nutrition
  • Loss of endocrine stimulation
  • Pressure (tissue compression)
19
Q

What are the mechanisms of atrophy?

A

1) Decreased protein synthesis & increased protein degradation in cells
2) Degradation occurs mainly by ubiquitinaton
3) Autophagy
4) May see increased number of autophagic vacuoles & membrane-bound residual bodies (lipofuscin)

20
Q

What is lipofuscin an indication of?

A

Age

- Residual bodies that result from being unable to completely digest the phospholipid membrane

21
Q

How is metaplasia seen in smokers?

A

Replacement of pseudostratified ciliated columnar epithelial cells with stratified squamous epithelial cells

*This is to try and increase the number of cells for the mucociliary escalator & referred to as “squamous metaplasia”

22
Q

Why is metaplasia considered a “double-edged sword?”

A

Important protective mechanisms are lost; it is more likely that metaplastic cells will transition to dysplastic

23
Q

What happens in Barrett’s esophagus?

A

Metaplasia of normal squamous mucosa in esophagus to columar mucosa in esophagus

*This is an attempt to deal with the acid in the esophagus

24
Q

What is the typical cause of metaplasia in the connective tissue?

A

Necrosis leads to formation of cartilage, bone, or adipose tissue in tissue that does NOT normally contain these elements

  • E.g.
  • Bone formation in muscle after intramuscular hemorrhage
  • **Note that this may be result of tissue injury & healing rather than true metaplasia
25
Q

Describe the mechanism of metaplasia.

A

Metaplasia is the result of reprogramming stem cells that exist in normal tissues

26
Q

What is dysplasia?

A

Disordered growth

- Farther “down the road” to neoplasia than metaplasia

27
Q

What are the morphological changes that are seen in dysplasia?

A
  • Variations in size & shape of the cell
  • Disroderly arrangement within the epithelium
  • Nuclear changes, consisting of enlargement, irregular borders, hyperchromasia, or individual cell nuclei