IPLab:Lab 2:Atrophy: Difference between revisions

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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: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?
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?
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== 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=" ">  </spoiler>
* <spoiler text=" ">  </spoiler>


{{IPLab 2}}
{{IPLab 2}}


[[Category: IPLab:Lab 2]]
[[Category: IPLab:Lab 2]]

Revision as of 15:01, 21 August 2013

Clinical Summary

This 74-year-old man was found to have carcinoma of the prostate six years prior to his death. The serum prostate-specific antigen (PSA) level was 9.7 ng/ml. His plasma acid phosphatase level on repeated tests ranged from 2 to 4 IU/L. X-rays revealed metastatic lesions in the patient's pelvis and vertebral column. He refused to have an orchiectomy and was placed on estrogen therapy (diethylstilbestrol).

The patient's terminal admission was for renal failure. The tumor had grown into the floor of the urinary bladder causing obstruction of the ureters at their entrance to the bladder. The patient developed acute hydronephrosis which was drained by nephrostomies. Eventually, infection developed in the kidneys resulting in Gram-negative sepsis and death.

Images

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=" "> </spoiler>
  • <spoiler text=" "> </spoiler>