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    EMBRYOLOGY - The External Genitalia in The Two Sexes Develop From Common Anlagen (Genital Tubercle

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    Leni Lukman
    The external genitalia of male and female embryos are initially indistinguishable, but begin differentiating around the 9th week of gestation. In males, androgenic stimulation causes the genital tubercle to grow into a phallus and the genital folds to fuse, forming the penile urethra. Failure of the urethral folds to fully fuse results in hypospadias, where the urinary opening is on the underside of the penis. Hypospadias severity depends on the location of the opening and degree of penile curvature. The cause is often unknown but disrupted androgenic stimulation during development is implicated based on genetic defects affecting androgen metabolism and response.

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    EMBRYOLOGY - The External Genitalia in The Two Sexes Develop From Common Anlagen (Genital Tubercle

    Uploaded by

    Leni Lukman
    23 views2 pages
    The external genitalia of male and female embryos are initially indistinguishable, but begin differentiating around the 9th week of gestation. In males, androgenic stimulation causes the genital tubercle to grow into a phallus and the genital folds to fuse, forming the penile urethra. Failure of the urethral folds to fully fuse results in hypospadias, where the urinary opening is on the underside of the penis. Hypospadias severity depends on the location of the opening and degree of penile curvature. The cause is often unknown but disrupted androgenic stimulation during development is implicated based on genetic defects affecting androgen metabolism and response.

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    The external genitalia of male and female embryos are initially indistinguishable, but begin differentiating around the 9th week of gestation. In males, androgenic stimulation causes the genital tubercle to grow into a phallus and the genital folds to fuse, forming the penile urethra. Failure of the urethral folds to fully fuse results in hypospadias, where the urinary opening is on the underside of the penis. Hypospadias severity depends on the location of the opening and degree of penile curvature. The cause is often unknown but disrupted androgenic stimulation during development is implicated based on genetic defects affecting androgen metabolism and response.

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    © All Rights Reserved
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    23 views2 pages

    EMBRYOLOGY - The External Genitalia in The Two Sexes Develop From Common Anlagen (Genital Tubercle

    Uploaded by

    Leni Lukman
    The external genitalia of male and female embryos are initially indistinguishable, but begin differentiating around the 9th week of gestation. In males, androgenic stimulation causes the genital tubercle to grow into a phallus and the genital folds to fuse, forming the penile urethra. Failure of the urethral folds to fully fuse results in hypospadias, where the urinary opening is on the underside of the penis. Hypospadias severity depends on the location of the opening and degree of penile curvature. The cause is often unknown but disrupted androgenic stimulation during development is implicated based on genetic defects affecting androgen metabolism and response.

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    EMBRYOLOGY The external genitalia in the two sexes develop from common anlagen (genital tubercle,

    swellings, and fold) and are indistinguishable up until seven to eight weeks gestation (figure 1).
    At the ninth week of gestation, the external genitalia begin to differentiate between the two sexes.
    In the male fetus, genetic programming results
    in androgenic stimulation that induces posterior
    fusion of the genital folds and growth of the
    genital tubercle into a phallic structure (picture
    2). The penile urethra forms as a result of
    remolding and fusion of the medial edges of the
    endodermal urethral folds [1]. By 12 weeks
    gestation, the coronal sulcus separates the glans
    from the shaft of the penis. By 16 to 18 weeks,
    urethral formation is complete, and the foreskin
    covers the glans.
    In patients with hypospadias, the urethral folds
    fail to completely or partial close. The extent of
    the failure determines the position of the
    urethral opening. In most cases, it remains
    unknown what causes the disruption of normal
    penile development.
    Penile curvature occurs normally during
    development and resolves by the end of urethral
    formation (picture 2). In patients with
    hypospadias, abnormal penile curvature (also
    referred to as chordee) is often an associated
    physical finding suggesting an accompanying
    disruption in the development of the penile
    shaft.
    The lack of androgenic stimulation results in
    the female external genital phenotype, although
    additional data suggest that female development
    is not a completely passive process.
    ANATOMY Surgical correction of hypospadias requires understanding of the anatomy of both the normal
    and hypospadiac penis [2].
    The penis in the uncircumcised male consists of the penile shaft, glans penis with the coronal sulcus (rim of the
    glans), and the foreskin (figure 2). The structural components include the corpus spongiosum, which contains
    the urethra, and the paired corpora cavernosa. The corpus spongiosum lies ventral in between the two corporal
    bodies. The corpora cavernosa structures are covered by the thick, elastic tunica albuginea. The dorsal penile
    nerve lies within Buck's fascia, which circumferentially envelops the corpus spongiosum and cavernosa.
    Sensation of the penile shaft, glans, and anterior urethra is primarily derived from the dorsal penile nerves. The
    neurovascular bundles lie in the 11 and 1 o'clock position with branches extending longitudinally from 11 to 7
    o'clock and 1 to 5 o'clock along the surface of the tunica albuginea, enclosing the corpora cavernosa, and
    terminating in the glans. No nerve fibers are found at the 12 o'clock position in either the normal or hypospadiac
    penis [3].
    Classification The severity of hypospadias is graded upon the position of the urinary meatus and the extent
    of ventral penile angulation. Severity rises as the distance of the displaced urethral opening increases from the
    normal position at the tip of the glans, and with increasing penile curvature.
    Historically, hypospadias was divided into three classes, as the distance of the displaced urethral opening
    increases from the normal position at the tip of the glans.
    First degree (mild) Urethral opening within
    the glans or subcorona
    Second degree (moderate) Urethral opening
    on the penile shaft
    Third degree (severe) Urethral opening
    within the scrotum or perineum
    However, this classification does not account for the effect of penile curvature (chordee). As an example,
    patients with the abnormal urethral meatus at the glans or distal penile shaft who have severe chordee will
    require extensive surgical correction to correct the curvature resulting in a more proximal hypospadiac urethral
    opening.
    PATHOGENESIS Disruption of the androgenic stimulation that is required for the development of the
    normal male external genitalia is the proposed mechanism resulting in hypospadias [4,5]. Support for this theory
    is based upon reports of patients with defects in genes that affect androgen metabolism, and estrogen and
    androgen response (eg, androgen receptor) [6-14]. Genome-wide association studies using SNP (single
    nucleotide peptide) microarrays have shown an association between variants of the gene DGKK located on the
    X chromosome and hypospadias [15,16]. DGKK is expressed in preputial skin and encodes a human type II
    diacylglycerol kinase, which plays an important role in signal transduction. Changes in the genes activating
    transcription factor 3, CXorf6, and the zinc finger-box gene 1 have also been associated with an increased risk
    of hypospadias [8,9,13].
    Exposure to estrogenic compounds (eg, maternal progestin or diethylstilbestrol) during pregnancy, which may
    affect androgenic stimulation, is also associated with hypospadias [17-19]. In contrast, a study using data from
    the National Birth Defects Prevention study found that maternal high dietary intake of phytoestrogens (plant
    constituents with estrogenic properties) was associated with a decreased risk of hypospadias [20]. The observed
    associations merit investigation in additional populations before firm conclusions can be reached. (See"Outcome
    and follow-up of diethylstilbestrol (DES) exposed individuals", section on 'Genitourinary abnormalities'.)
    In most cases of hypospadias, however, the cause is unknown. Both genetic and environmental factors are
    associated with hypospadias, suggesting that the etiology is multifactorial [17,19,21,22]. These include the
    following:
    Advanced maternal age
    Preexisting maternal diabetes mellitus
    Gestational age before 37 weeks
    History of paternal hypospadias
    Exposure to smoking and pesticides

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