2. N Cellular Adaptations

8/8/2019 2. N Cellular Adaptations

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Cells in homeostasisPreserve intracellular and immediately

surrounding environment within anarrow range of physiologic parameters





Cells respond byAdaptation

intracellular accumulationssub-cellular alterationsinjury







Cellular AdaptationsPhysiologic: responses of cell to normalstimulation by hormones or endogenouschemical mediators.

Pathologic: same underline mechanism, cellmodulate their environmentMechanisms:



Cellular Adaptations- Mechanisms :Receptor binding, signal transduction,transcription, translation and transport of

proteins

Up or down regulation of specific cellular receptorsInduction of new protein synthesis by target

cell e.g. heat shock proteinsSwitching from one to another type of

protein or over production



Adaptation

hypertrophy hyperplasia atrophy metaplasia

adaption





CAUSES OF ATROPHYDecreased work load (atrophy of disuse)Loss of innervation (denervation atrophy)Diminished blood supplyInadequate nutritionLoss of endocrine stimulation

Aging (senile atrophy)Pressure



There are some muscle fibers here that show atrophy.

Thenumber of cells is the same as before the atrophy

occurred, but the size of some fibers is reduced. T his is aresponse to injury by "downsizing" to conserve the cell.In this case, innervation of the small fibers in the center

was lost. T his is a trichrome stain.





A trophy

decrease synthesis increase degradationD egradation: 2 proteolytic systems

LysosomesUbiquitin- proteosome pathway ± cytosolic and nuclear

proteins, conjugation, degradation in proteosome(cancer, activation molecules)Outcome:-

less cytoplasm/organelles

Autophagic vacuolesleft-over deposits ± membrane bound residual bodies(lipofuscin)less metabolism



METAPLASIA

A reversible change in which one adult cell type isreplaced by another cell type

Cells sensitive to a particular stress are replaced byother cell types which are better able to withstand theadverse environment

Smokers; ciliated columnar epithelial cells of thetrachea and bronchi are replaced by«.

Reversible



F ig 2.6 (R bi ' )



METAPLASIACancer can arise in the metaplastic epithelium; eg

squamous cell carcinoma of lung.

In chronic gastric reflux; the normal epithelial lining of lower esophagus may undergo metaplastictransformation to ««.Important to know clinically! Why?

Fibroblasts may be transformed to osteoblasts orchondroblasts to produce bone or cartilage





Metaplasia of laryngeal respiratory epithelium has occurredhere in a smoker. The chronic irritation has led to anexchanging of one type of epithelium (the normal respiratory

epithelium at the right) for another (the more resilients uamous e ithelium at the left .



Metaplasia of esophageal squamous mucosa has occurred

here, with gastric type columnar mucosa at the left.



MetaplasiaC hange from one type of mature/differentiated

cells into another mature/diff typeCharacteristics:

1.new tissue is structurally normal2.cellular organization is maintained3.is reversiblecause:changed differentiation of stem cells in

response to environmental changeoccurrence/types:epithelial and connective tissue



E pithelial

Columnar to squamous ( respiratory tract)Squamous to columnar (esophagus)

Transitional to squamous (bladder)



MesenchymalOsseous/chondroid : e.g. in scarsmyeloid: blood-forming cells in liver or

spleen



Outcome of metaplasiaAdvantagesdisadvantages,: loss of protectivemechanisms, neoplastic transformationD ysplasia / tumor development

3



T he prominent folds of endometrium in this uterus openedto reveal the endometrial cavity are an example of hyperplasia. Cells forming both the endometrial glands andthe stroma have increased in number. As a result, the size of the endometrium has increased. T his increase is physiologic

with a normal menstrual cycle.





T his is an example of prostatic

hyperplasia. T he normal prostate is about3 to 4 cm in diameter. T he number of prostatic glands, as well as the stroma, hasincreased. T he pattern of increase here isnot uniform, but nodular. T his increase isin response to hormonal manipulation , butin this case is not a normal physiologic

process.



H ere is one of the nodules of hyperplasic prostate. T he cells makingup the glands are normal in appearance, there are just too many of them.



hyperplasia

I ncrease in the size of a tissue due to increased number of component cells

occurrence:increased demand in tissues of

labile/stable cellscauses: physiological-eg bone marrow hyperplasiaat high altitudes

pathological:usually occurs when there is anincrease in trophic hormones,eg endometrial H

in states of estrogen excess

outcome:more cells more work



T his is cardiac hypertrophy involving the left ventricle. T henumber of myocardial fibers does not increase, but their size canincrease in response to an increased workload, leading to themarked thickening of the left ventricle in this patient withsystemic hypertension.



hypertrophy I

ncreased size of a tissue due to increase in the sizeof individual cells .Occurrence:permanent cells,or with hyperplasiawhen demand is increasedCauses:physiological,like in the muscles of body

builders pathological:like in failing heart(CCF)

outcome:increased cytoplasm/organellessecretory cells:more E R,golgi com.,ribosomes

contractile cells:more myofibrils



H earts, hypertrophied,normal (middle), and dilated- Gross, cross sections



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2. N Cellular Adaptations