File:IPLab2Atrophy2.jpg|This is a low-power photomicrograph of an atrophic testis. Attached to the testis are several vessels (arrow) which are part of the epididymis and the vas deferens.File:IPLab2Atrophy3.jpg|This is a higher-power photomicrograph of an atrophic testis. In this section there are seminiferous tubules with viable cells (1) although there are no visible spermatocytes. Other seminiferous tubules are completely acellular and have a pale pink hyaline appearance (2).File:IPLab2Atrophy4.jpg|This is a higher-power photomicrograph indicating loss of testicular parenchymal tissue. There are very few recognizable spermatic cells in this tissue. The cluster of cells in the upper right is a focus of interstitial or Leydig cells (arrow). These cells are not affected by the hormone-induced atrophy process.File:IPLab2Atrophy5.jpg|A seminiferous tubule is shown on the left containing remnants of spermatocytes (1). There are no mature sperm present. On the right-hand portion of the slide are remnants of other spermatic tubules which have completely atrophied and lost all of their spermatogenic cells (2). Note the eosinophilic Leydig cells present between the atrophic tubules (3).File:IPLab2Atrophy6.jpg|In this slide, the atrophy of the tubules is extending to include the Rete testes (arrow) as well.File:IPLab2Atrophy7.jpg|In this gross photograph of kidneys and the abdominal aorta, there is narrowing of the left renal artery at its ostium from the aorta. This atherosclerotic narrowing of the renal artery causes reduced blood pressure in the kidney whose artery is affected. The result is a characteristic Goldblatt’s hypertension syndrome. Note that the kidney with the narrowed renal artery is atrophied compared to the kidney with the normal vessel on the right. What is the cause of the atrophy in this kidney?File:IPLab2Atrophy8.jpg|These kidneys were removed from a patient who had blockage of one ureter leading to increased pressure in the renal pelvis. The increased pressure produced hydronephrosis (arrow) in one kidney. What is the cause of atrophy in this case?File:IPLab2Atrophy9.jpg|The two kidneys in this slide are from the same patient. One kidney (1) is relatively normal, although increased in size due to compensatory hypertrophy. The other kidney (2) is very small with only rudimentary nodules of renal parenchyma. This kidney had never developed and therefore this process represents hypoplasia. How does one differentiate between atrophy and hypoplasia?File:IPLab2Atrophy10.jpg|This gross photograph shows a normal brain (left) and a brain from a geriatric patient (right). Note the decreased size, the narrowed gyri, and the widened sulci of the brain from this octogenarian. What is the cause of atrophy in this case?</gallery> == Virtual Microscopy ===== Testis: Atrophy ===<peir-vm>IPLab2Atrophy</peir-vm> ===Normal Testis ===<peir-vm>UAB-Histology-00045</peir-vm> == Study Questions ==* <spoiler text="What is PSA and how useful is it as a marker of prostatic cancer?">Prostatic Specific Antigen. PSA can be a useful marker for prostatic cancer; however, PSA levels may be elevated for a number of reasons other than cancer.</spoiler>* <spoiler text="What is the cause of testicular atrophy in this case?">The cause was HORMONAL.

Prostatic growth is dependent upon testicular androgens. Estrogen therapy leads to inhibition of pituitary gonadotropin and/or ACTH production which causes androgen deprivation. Newer drugs use specific testosterone receptor blocking mechanisms to regress prostate hyperplasia and prostate cancer.</spoiler>* <spoiler text="There appears to be an increase in the number of interstitial cells. Is there such a thing as Leydig cell hyperplasia?">No. The Leydig cells appear more prominent due to the paucity of germ cells.</galleryspoiler> == Additional Resources ===== Reference ===* [http://www.cancer.gov/cancertopics/pdq/treatment/prostate/HealthProfessional/page3 National Cancer Institute: Prostate Cancer Treatment]* [http://emedicine.medscape.com/article/457394-overview eMedicine Medical Library: Prostate-Specific Antigen]* [http://emedicine.medscape.com/article/1967731-overview eMedicine Medical Library: Prostate Cancer]* [http://www.merckmanuals.com/professional/genitourinary_disorders/genitourinary_cancer/prostate_cancer.html Merck Manual: Prostate Cancer] === Journal Articles ===* van Leenders GJ, Schalken JA. [http://www.ncbi.nlm.nih.gov/pubmed/11589668 Stem cell differentiation within the human prostate epithelium: implications for prostate carcinogenesis]. ''BJU Int'' 2001 Sep;88 Suppl 2:35-42; discussion 49-50. === Images ===* [{{SERVER}}/library/index.php?/tags/146-prostate/219-adenocarcinoma PEIR Digital Library: Prostatic Adenocarcinoma Images]* [http://library.med.utah.edu/WebPath/MALEHTML/MALEIDX.html WebPath: Male Genital Pathology Images]