Subject: Pathology LAB Topic: Cellular Growth and Differentiation Lecturer: Dr.

Renan Navarro Date of Lecture: 06/23/2011 Transcriptionist: Desiree Timtiman Pages: 8

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

SY 2011-2012

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
Myocardium: notice that theres no nucleus and striations

fibrosis

Vascular proliferation 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

Case Study: 45 y/o male with a history of subternal chest pain for 4 hours Dx: Acute Myocardial Infarction Increase 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 females 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.

glands

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 theres an increase in glands o This is increase in glands, therefore an increase in the size of the organ Dx: Nodular Prostatic Hyperplasia

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 dont 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)

Endocervical glands

Non-keratinized Stratified Squamous Epithelium

Simple Columnar Epithelium

Transition zone Non-keratinized Stratified Squamous Epithelium

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 to irritation. If metaplasia persist, it can lead to malignant transformation o Ex. Barrets Esophagus

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

Karyolysis

Karyorrhexis

Pyknosis Necrosis Cell death with inflammatory reaction in the host Apoptosis cell death by this pathway does not elicit an inflammatory reaction in the host nuclear 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. Adaptive Mechanism Metaplasia Hypertrophy/Hyperplasia Atrophy Intracellular Accumulation Stimuli Chronic irritation Increased demand, increased stimulation Decreased nutrients, decreased stimulation
METABOLIC ALTERATIONS, GENETIC OR ACQUIRED; CHRONIC INJURY

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, Wheaters and Robbins. 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