Testicular dysgenesis syndrome, cryptorchidism, testicular neoplasm, histogenesis of malignant germ cell tumors, CIS, prostate enlargement, metastatic routes of prostate carcinoma, hypothalamic-pituitary-ovarian axis, menstrual cycle

6 Pages
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Department
Biomedical Science
Course Code
BMS 460
Professor
D.Rao Veeramachaneni

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Description
9 December Testicular Dysgenesis Syndrome A collection of disorders of the male reproductive system that may be related to one another and have a common cause – abnormal development of the testes during fetal development Environmental and lifestyle factors, intrauterine growth disorders, genetic defects and polymorphisms → testicular dysgenesis Decreased Leydig cell function Cryptorchidism Hypospadias Disturbed Sertoli cell function CIS → testicular cancer Impaired spermatogenesis → infertility Cryptorchidism: Undescended/Ectopic Testes Risk of cancer High scrotal 60% Inguinal canal 25% Abdominal 15% Testicular Neoplasia Germ cell tumors Precursor Carcinoma in situ, CIS Occurs during development Seminoma Classical Occurs in young men Spermatocytic Occurs in older men Non-seminomas Non-germ cell tumors or sex cord cell tumors Leydig cell tumors Sertoli cell tumors Histogenesis of Malignant Germ Cell Tumors The tumors originate from intratubular germ cells that form carcinoma in situ, CIS, also called intratubular germ cell Neoplasia, ITGCN. Tumors derived from ITGCN are divided into 2 major groups: seminomas and non- seminomatous germ cell tumors. NSGCT include several subtypes; embryonal carcinoma cells are the stem cells of most NSGCT. Embryonal carcinoma Teratocarcinoma mixed NSGCT Choriocarcinoma Yolk sac carcinoma Testicular tumors have a peak incidence in men 25 to 45 years old. Tumor markers Seminoma Embryonal Teratocarcinom Choriocarcino Yolk sac carcinoma a mixed ma carcinoma NSGCT AFP (alpha- - - + - + fetoprotein) hCG (human - - + + - chorionic gonadotropin ) CIS gives rise to classical type of seminoma and non-seminoma Tumors derived from germ cells, mostly in the testis and ovary, contain embryonic cells (embryonal carcinoma cells) that differentiate into embryonic germ layers – ectoderm, mesoderm, and endoderm. Benign (teratoma) when ECs differentiate into somatic tissues or malignant (teratocarcinomas) when ECs differentiate into somatic as well as extra-embryonic tissues. Histopathology and immunohistochemistry discern types and origins of germ cell tumors E.g., diagnostic markers: PLAP for CIS, KIT for classical seminoma, DMRT1 for spermatocytic seminoma, hCG for choriocarcinoma Enlargement of prostate may occur as a result of benign hyperplasia or carcinoma Origins of prostate hyperplasia and carcinoma differ BPH (benign prostatic hyperplasia) originate in the central (periurethral) part of the gland and often involves the median lobe In contrast, carcinoma of the prostate originates preferentially in the peripheral portion of the gland and often in the posterior lobe, which is readily accessible to digital palpation through the rectum. Diagnostic procedures Digital palpation per rectum Prostate-specific antigen, PSA Biopsy Prostate intraepithelial Neoplasia, PIN Serum alkaline phosphatase in bone metastases Metastatic Routes of Prostate Carcinoma Carcinoma of the prostate invades locally into the rectum and the urinary bladder Perineural invasion is also common Distant metastases occur via the lymphatics or blood Vertebral bones, lungs and liver
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