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THE GONADS. Dr. Nimir Dr. Safaa. OBJECTIVES Describe development of the testis. Describe development of the ovary. Discuss their congenital anomalies of the testis. Discuss their congenital anomalies of the ovary. The Genital System
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THE GONADS • Dr. Nimir • Dr. Safaa
OBJECTIVES • Describe development of the testis. • Describe development of the ovary. • Discuss their congenital anomalies of the testis. • Discuss their congenital anomalies of the ovary.
The Genital System • Develops from the genital ridge(coelomic epithelium covering the mesenchyme). • During the 5th week, the epithelium invades the mesenchyme and produces primitive sex cords. • During the 6th week, the area is invaded by the primordial germ cells which migrate in from the yolk sac.
The primordial germ cells invade the primitive sex cords. • Epithelium from the surface of the gonad is incorporated into the gonad as follicular cells(female) and Sertolicells(male). • The indifferent stage is that time during which one cannot tell whether the gonad is a testis or a ovary; the gonads begin to acquire adult charactristics and can be distinguished as testis or ovary during the 7th week.
The testis: • The short arm of the Y chromosome contains SRY gene (sex-determining region on Y). • The primitive sex cords proliferate and grow deep into the substance of the gonad to produce testis (medullary) cords. • If there is no Y chromosome , then the gonad develops into an ovary.
The primordial germ cells--spermatogonia-- along with some surface epithelial cells invade the testis cords. • The surface epithelial cells in the cords become Sertoli cells. • The testis cords acquire a lumen at puberty and are then properly termed seminiferous tubules.
The cells of Leydig, the testosterone secreting cells, are derived from mesenchyme (splanchnic mesoderm) of the gonadal ridge. • Testosterone production begins by the 8th week, is stimulated by the presence of human chorionic gonadotropin and is necessary for the production of the duct system.
The ovary: • The primitive sex cords break up and disappear. • The surface epithelium proliferates and produces another set of cords called the cortical cords.
The primordial germ cells -- oogonia--invade the cortical cords; the cords give rise to the follicular cells that surround the developing oocyte. • The oogonia undergo mitosis during fetal life and differentiate into millions of primary oocytes.
Two waves of atresia sweep over the fetal ovary; these waves of destruction kill all the oogonia and many primary oocytes; about 2 million primary oocytes are present at birth.At birth, the ovary contains NO oogonia. During late childhood, another wave of atresia sweeps over the ovary and reduces the number of primary oocytes to 200,000.
Congenital malformations Agenesis of gonads: Externally, these individuals have the appearance of a female due to maternal estrogens.
Testicular feminization (androgen insensitivity syndrome): 46, XY, but are externally FEMALE; these individuals have testes but they are undescended. During embryonic life, the testis produced testosterone and paramesonephric duct inhibiting substance, so the paramesonephric duct failed to develop; thus, even though these individuals appear to be female, they have no uterus, no oviducts, and a blind ending vagina.
True hermaphrodite: • Has both testicular and ovarian tissue; usually the tissue is nonfunctional; can appear either as male or female; usually genetically female.
Pseudohermaphrodites have a normal chromosome pattern: 1. 46, XY: have variable internal and external genitalia; either an inadequate amount of testosterone and/or duct inhibiting hormone were produced or the tissues failed to respond to it.
2. 46, XX: Usually a result of increased production of testosterone by the fetal adrenal gland, a condition termed congenital adrenal hyperplasia (due to an autosomal recessive gene); the excess testosterone causes masculinization of the external genitalia, such as clitorial hypertrophy and partial fusion of the labia majora; other causes of this condition include maternal ingestion/injection of testosterone or a testostrone secreting tumor.
