Flashcards in Exam 1: Cellular Adaptations & Accumulations I Deck (27):
What is adaptation?
State between the normal unstressed cell & the injured over-stressed cell; the new but altered steady state
List some reversible changes that are seen in response to cellular damage.
- Changes in size
- Changes in number
- Metabolic activity
What is physiologic adaptation?
Responses of cells to normal stimulation by hormones or endogenous chemical mediations
What is patholgoic adaptation?
Underlying disease mechanisms that allows cells to modulate their environment and escape injury
What is hypertrophy?
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
What is hyperplasia?
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
What is atrophy?
Decrease in size of a tissue or organ due to a decrease in cell size & organelles
What is metaplasia?
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"
How does the hypertrophy of weight lifting and pregnancy differ?
- Weight lifting= hypertropy without hyperplasia
- Pregnancy= uterus hypertrophies and undergoes hyperplasia
Describe an example of pathologic hypertrophy.
- 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
What is the difference between concentric hypertrophy & dilated hypertrophy seen in CHF?
- Concentric hypertrophy
Limited ability to enlarge, then degeneration
What happens structurally in cardiac hypertrophy? What are the microscope indications of hypertrophy?
- Increased nucleus to make more proteins ("boxcar" nuclei)
- Increased cytoplasm
What are the mechanisms that induce hypertrophy?
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
What changes in expression of genes and proteins occurs in hypertrophy? Are these changes reversible?
- 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
What are the types of physiologic hyperplasia?
- 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
What causes most forms of pathologic hyperplasia? List common examples of pathologic hyperplasia.
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)
What is the mechanism of hyperplasia?
Result of growth factor-driven proliferation of mature cells, & in some cases by increased output of new cells from tissue stem cells
What causes atrophy?
- Decreased workload (disuse atrophy)
- Loss of innervation (denervation atrophy)
- Decreased blood supply, called "senile" atrophy
- Inadequate nutrition
- Loss of endocrine stimulation
- Pressure (tissue compression)
What are the mechanisms of atrophy?
1) Decreased protein synthesis & increased protein degradation in cells
2) Degradation occurs mainly by ubiquitinaton
4) May see increased number of autophagic vacuoles & membrane-bound residual bodies (lipofuscin)
What is lipofuscin an indication of?
- Residual bodies that result from being unable to completely digest the phospholipid membrane
How is metaplasia seen in smokers?
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"
Why is metaplasia considered a "double-edged sword?"
Important protective mechanisms are lost; it is more likely that metaplastic cells will transition to dysplastic
What happens in Barrett's esophagus?
Metaplasia of normal squamous mucosa in esophagus to columar mucosa in esophagus
*This is an attempt to deal with the acid in the esophagus
What is the typical cause of metaplasia in the connective tissue?
Necrosis leads to formation of cartilage, bone, or adipose tissue in tissue that does NOT normally contain these elements
- Bone formation in muscle after intramuscular hemorrhage
*****Note that this may be result of tissue injury & healing rather than true metaplasia
Describe the mechanism of metaplasia.
Metaplasia is the result of reprogramming stem cells that exist in normal tissues
What is dysplasia?
- Farther "down the road" to neoplasia than metaplasia