Block 7 Male Femal Embryo BRS W Xpl

The embryo during weeks 1-6 remains in an indifferent or undifferentiated stage. The
embryo begins phenotypic sexual differentiation during week 7.

The round ligament of the uterus and the ovarian ligament both form from the gubernaculum.

In the female, the urogenital folds remain unfused and form the labia minora.

The cranial portion of the paramesonephric ducts form the uterine tubes.

Failure of the urethral folds to fuse completely results in the external urethral orifice opening onto the ventral surface of the penis, a condition known as hypospadias.

The gene product that is coded on the short arm of the Y chromosome is called the testesdetermining factor (TDF).

Sterility is a common result of bilateral cryptorchidism. When both testes fail to descend
into the scrotum, the increased temperature they are exposed to in the abdominal cavity inhibits
spermatogenesis.

The most common cause of testicular feminization syndrome is the lack of androgen receptors in the urogenital folds and labioscrotal swellings. Because these tissues lack androgen receptors, they are blind or unresponsive to androgens. Consequently, these tissues develop into
female external genitalia even though the fetus has a 46,XY genotype.

The sinovaginal bulbs proliferate, fuse, and form the vaginal plate under the inductive
influence of the paramesonephric ducts. The vaginal plate then canalizes to form the inferior two
thirds of the vagina.

Female pseudointersex individuals have a 46,XX genotype. This condition is most commonly caused by congenital adrenal hyperplasia, in which the fetus produces excessive amounts of androgens. The high androgen level masculinizes the female genitalia.

Male pseudointersex individuals have a 46,XY genotype. This condition is most commonly
caused by inadequate production of testosterone and MIF by the fetal testes. The low testosterone and MIF levels stunt the development of the male genitalia.

This is a classic case of testicular feminization syndrome. A karyotype analysis would reveal that this normal-appearing 17-year-old girl actually has a 46,XY genotype. The mobile masses within the right and left labia majora are the testes and should be surgically removed because this tissue has a propensity toward malignant tumor formation. The most common cause of this syndrome is a lack of androgen receptors in the phallus, urogenital folds, and labioscrotal swellings.

By week 12, female and male characteristics can be recognized. By week 20, phenotypic sexual differentiation is complete.

Reduced levels of androgens during fetal development of a XY male fetus cause feminization of the male external genitalia such that the baby can be phenotypically mistaken for female. Parents raise the XY male baby as a girl until puberty or other medical problems bring the child to medical attention.