PATHOLAB Cellular Growth and Differentiation

8/6/2019 PATHOLAB Cellular Growth and Differentiation

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Case Study: 60 y/o female that underwent hysterectomy

Nulliparous: 30-40g

parous: 75-100g

Adaptive Mechanism seen in the picture:

o Atrophy

Cause of Atrophy

a. Decreased workload

b. Denervation

c. Decrease hormone stimulation

d. Pressure

e. Inadequate nutrition

f. Hypoxia

Reversible injury can revert back to its original form

Injury progressively introduced to the cell will lead to irreversible injury and then cell death

hallmark of reversible injury:

Cell Swelling

decrease oxidative phosphorylation

fatty change- microscopic change and not a hallmark of reversible injury

Subject: Pathology LABTopic: Cellular Growth and DifferentiationLecturer: Dr. Renan NavarroDate of Lecture: 06/23/2011Transcriptionist: Desiree TimtimanPages: 8 S

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Case study: 50 y/o with Chronic HPN

Myocardium

Adaptive Mechanism seen in the picture:

o Hyperthropied myocardium

o Based on the history you can expect that the myocardium are enlarged

o Microscopic description: Notice the enlarged, box-shaped nucleus

Case Study: from a heart of a known hypertensive 45 y/o female with a diagnosis of intracerebral hemorrhage

Pictograph shows an Old myocardial infarction No acute inflammation

o Acute inflammation is characterized by infiltration of PMNs

Intensed fibrosis; notice the pink wavy collagen at the picture

Increased Vascular proliferation

tissue damaged exemplified by the loss of striation and nucleus of the myocardium

This is an irreversible damage

fibrosis

Myocardium: notice that there’s no nucleus and striations

Vascular proliferation



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Case Study: 45 y/o male with a history of subternal chest pain for 4 hours

Dx: Acute Myocardial InfarctionIncrease infiltration of PMNs

Some of the myocardium still have nucleus

Cardiac Markers: CKMB, Troponin-I, Troponin T

o Note for the onset because markers have different peak time:

CKMB for 4 hours and less

Troponin I and T- for 4 hours and more

Case Study: taken from a 70 y/o female’s uterus

Artery is thicker than vein

Metabolic alteration: Dystrophic Calcification

Dystrophic calcification will not cause ischemia or infarction because the artery cannot constrict and cause

an obstruction of the lumen

This is a physiologic calcification based on the history.



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Case Study: 65 y/o male with dysuria

Take note of the history

Organ: Prostate Gland

notice the corpora amylacea(C), a distinct feature of prostate gland

Notice the increase in glands and see how closely packed it is.

o This is therefore a Hyperplastic change

Adaptive Mechanism: Hyperplasia

o Increase in cells, in this case there’s an increase in glands

o This is increase in glands, therefore an increase in the size of the organ

Dx: Nodular Prostatic Hyperplasia

glands



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Case Study: 70 y/o complaining of vaginal spotting/ bleeding

Endometrium

You expect the endometrium of a 70 y/o to be thinned out, atrophic and inactive.

Adaptive Change: Hyperplasia

This is pathologic; you don’t expect bleeding from a 70 y/o.

In normal lining epithelium, nuclei are basally located while in neoplastic lining, nuclei are stratified (not

seen in the picture above)



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Case Study:

Transitional zone in cervix: from simple tall columnar to stratified squamous epi.

Adaptive Change: Metaplasia

Notice that the endocervical gland, which is normally beneath the simple columnar epithelium,is already

beneath the stratified squamous epithelium, indicating that metaplasia has taken place probably due toirritation.

If metaplasia persist, it can lead to malignant transformation

o Ex. Barret’s Esophagus

Endocervical

glands

Non-keratinized Stratified Squamous Epithelium

Transition

zone

Simple Columnar

Epithelium

Non-keratinized Stratified Squamous Epithelium



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Case Study: taken from the cervical mass of a 7 y/o male

From Lymph node(ok so the picture [I think] is from the lungs, but you get the point, right?)

This a granuloma, typically seen in a tuberculous infection

Caseous Necrosis

o Grossly: yellow cheesy/chalky material

o Acellular pink amorphous material

o Presence of Epitheloid cells surrounded by lymphocytes

Chronic granulomatous inflammation

o Inflammation seen in necrosis



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Necrosis

Cell death with inflammatory reaction in the host

Apoptosis

cell death by this pathway does not elicit an inflammatory reaction in the hostnuclear changes:

Karyorrhexis

pyknotic nucleus undergoes fragmentation.

Pyknosis

characterized by nuclear shrinkage and increased basophilia

Karyolysis

change that presumably reflects loss of DNA because of enzymatic degradation by

endonucleases.

Metaplasia

reversible change in which one differentiated cell type (epithelial or mesenchymal) is replaced by another

cell type

End of transcription

Pictures from laboratory(thank you Joyce), internet, Wheater’s and Robbin’s.

Study hard.

“I am the light of the world. Whoever follows me will not walk in darkness but will have the light of life.” John

8:12

Adaptive Mechanism Stimuli

Metaplasia Chronic irritation

Hypertrophy/Hyperplasia Increased demand, increased stimulation

Atrophy Decreased nutrients, decreased stimulation

Intracellular Accumulation METABOLIC ALTERATIONS, GENETIC OR ACQUIRED; CHRONIC INJURY

Karyorrhexis

Pyknosis

Karyolysis



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PATHOLAB Cellular Growth and Differentiation