Embryonic development of the urogenital system

Development of the urogenital system in humans and associated disorders

1. Embryology Urogenital System

2. The Urogenital System

3. The Urogenital System The urogenital system develops from the intermediate mesenchyme (mesoderm) – Urogenital Ridge. The part of the urogenital ridge giving rise to the urinary system is the nephrogenic cord and the part giving rise to the genital system is the gonadal ridge

4. Development of Urinary System

5. Development of Kidneys and Ureters Three sets of successive kidneys develop in human embryos .

6. Pronephroi

7. Mesonephroi

8. Metanephroi

9. The ureteric bud is a diverticulum (outgrowth) from the mesonephric duct near its entrance into the cloaca . The metanephrogenic blastema is derived from the caudal part of the nephrogenic cord. As the ureteric bud elongates, it penetrates the metanephrogenic blastema —a metanephric mass of mesenchyme

10. Development of Kidneys and Ureters The stalk of the ureteric bud becomes the ureter . The cranial part of the bud undergoes repetitive branching, forming branches which differentiate into the collecting tubules of the metanephros . The first four generations of tubules enlarge and become confluent to form the major calices, and the second four generations coalesce to form the minor calices. The end of each arched collecting tubule induces clusters of mesenchymal cells in the metanephrogenic blastema to form small metanephric vesicles. These vesicles elongate and become metanephric tubules

11. Development of Kidneys and Ureters The proximal ends of the metanephric tubules are invaginated by glomeruli . The tubules differentiate into proximal and distal convoluted tubules, and the nephron loop ( Henle loop ), together with the glomerulus and its capsule, constitute a nephron . Each distal convoluted tubule contacts an arched collecting tubule , and the tubules become confluent.

12. Between the 10th and 18th weeks, the number of glomeruli increases gradually and then increases rapidly until the 32nd week. The increase in kidney size after birth results mainly from the elongation of the proximal convoluted tubules as well as an increase of interstitial tissue . Nephron formation is complete at birth except in premature infants. Although glomerular filtration begins at approximately the ninth fetal week, functional maturation of the kidneys and increasing rates of filtration occur after birth .

13. Positional Changes of Kidneys

14. Changes in Blood Supply of Kidneys

15. CONGENITAL ANOMALIES OF KIDNEYS AND URETERS

16. Renal Agenesis Renal Agenesis (absence): Can be unilateral or bilateral Renal agenesis results when the ureteric buds do not develop or the primordia (stalks of buds) of the ureters degenerate. Failure of the ureteric buds to penetrate the metanephrogenic blastema results in failure of kidney development

17. Unilateral Renal Agenesis Unilateral renal agenesis (absence) occurs approximately once in every 1000 neonates. Males are affected more often than females and the left kidney is usually the one that is absent. Unilateral renal agenesis often causes no symptoms and is usually not discovered during infancy because the other kidney usually undergoes compensatory hypertrophy and performs the function of the missing kidney . Unilateral renal agenesis should be suspected in infants with a single umbilical artery

18. Bilateral renal agenesis Bilateral renal agenesis is associated with oligohydramnios (small amount of amniotic fluid) because little or no urine is excreted into the amniotic cavity. This condition occurs approximately once in 3000 births, and is incompatible with postnatal life. Infants with bilateral renal agenesis usually die shortly after birth.

19. Malrotated Kidney If a kidney fails to rotate, the hilum faces anteriorly ; that is, the fetal kidney retains its embryonic position Abnormal rotation of the kidneys is often associated with ectopic kidneys.

20. Ectopic Kidneys One or both kidneys may be in an abnormal position. Most ectopic kidneys are located in the pelvis, but some lie in the inferior part of the abdomen. Pelvic kidneys and other forms of ectopia result from failure of the kidneys to ascend.

21. Horseshoe Kidney In 0.2% of the population, the poles of the kidneys are fused ; usually it is the inferior poles that fuse. The large U-shaped kidney usually lies in the pubic region. Normal ascent of the fused kidneys is prevented because they are held down by the root of the inferior mesenteric artery . A horseshoe kidney usually produces no symptoms because its collecting system develops normally and the ureters enter the bladder. Approximately 7% of persons with Turner syndrome have horseshoe kidneys.

22. Duplications of Urinary Tract Duplications of the abdominal part of the ureter and the renal pelvis are common . These defects result from abnormal division of the ureteric bud.

23. A supernumerary kidney with its own ureter , which is rare, probably results from the formation of two ureteric buds.

24. Ectopic Ureter An ectopic ureter does not enter the urinary bladder . In males , the ureter usually opens into the neck of the bladder or the prostatic part of the urethra. They may also enter the ductus deferens, prostatic utricle, or seminal gland . In females , the ureter opens into the neck of the bladder, or the urethra, vagina, or vestibule of vagina. Incontinence is the common complaint resulting from an ectopic ureter because the urine flowing from the orifice does not enter the bladder; instead it continually dribbles from the urethra in males and the urethra and/or vagina in females .

25. Cystic Kidney Diseases In autosomal recessive polycystic kidney disease both kidneys contain many small which result in renal insufficiency. Death of the infant usually occurs shortly after birth. Multicystic dysplastic kidney disease results from dysmorphology during development of the renal system. In this kidney disease, fewer cysts are seen than in autosomal recessive polycystic kidney disease and they range in size from a few millimeters to many centimeters in the same kidney . T he cystic structures are wide dilations of parts of the otherwise continuous nephrons, particularly the nephron loops (of Henle ).

26. Development of Urinary Bladder The urogenital sinus is divided into three parts (imaginary):

27. Development of Urinary Bladder The bladder develops mainly from the vesical part of the urogenital sinus but its trigone (triangular area at the base of the bladder between the openings of the ureters ) is derived from the caudal ends of the mesonephric ducts. The entire epithelium of the bladder is derived from the endoderm of the vesical part of the urogenital sinus. The other layers of its wall develop from adjacent splanchnic mesenchyme .

28. Development of Urinary Bladder In infants and children, the urinary bladder, even when empty , is in the abdomen . It begins to enter the greater pelvis at approximately 6 years of age, but it does not enter the lesser pelvis and become a pelvic organ until after puberty.

29. Initially the bladder is continuous with the allantois . The allantois soon constricts and becomes a thick fibrous cord, the urachus .

30. Abnormalities with the development of the urinary bladder

31. URACHAL ANOMALIES In infants, a remnant of the urachal lumen may persist in the inferior part of the urachus . In approximately 50% of cases, the lumen is continuous with the cavity of the bladder. Remnants of the epithelial lining of the urachus may give rise to urachal cysts. The inferior end of the urachus may dilate to form a urachal sinus that opens into the bladder. The lumen in the superior part of the urachus may also remain patent and form a urachal sinus that opens at the umbilicus . Very rarely the entire urachus remains patent and forms a urachal fistula that allows urine to escape from its umbilical orifice

32. CONGENITAL MEGACYSTIS A pathologically large urinary bladder— megacystis or megalocystis —may result from a congenital disorder of the ureteric bud, which may be associated with dilation of the renal pelvis. Many infants die from this disorder or suffer from renal failure in early childhood .

33. EXSTROPHY OF BLADDER A deficiency of the anterior abdominal wall, is caused by incomplete median closure of the inferior part of the wall. The defect involves both the abdominal wall and the anterior wall of the urinary bladder; it results from failure of mesoderm to migrate between the ectoderm and endoderm of the abdominal wall. As a result, the inferior parts of the rectus muscles are absent and the external and internal oblique and the transversus abdominus muscles are deficient.

34. EXSTROPHY OF BLADDER This rare birth defect occurs approximately once in every 10,000 to 40,000 births . Exstrophy ( eversion ) of the bladder usually occurs in males. Exposure and protrusion of the mucosal surface of the anterior wall of the bladder characterize this defect. The trigone of the bladder and the ureteric orifices are exposed, and urine dribbles from the everted bladder . Epispadias (urethra opens on dorsum of penis) and wide separation of the pubic bones are associated with complete exstrophy of the bladder.

35. Development of Urethra The epithelium of most of the male urethra and the entire female urethra is derived from endoderm of the urogenital sinus. In males, the distal part of the urethra in the glans of the penis is derived from ectodermal cells that grows inward from the tip of the glans and joins the rest of the spongy urethra . Consequently, the epithelium of the terminal part of the urethra is derived from the surface ectoderm. The connective tissue and smooth muscle of the urethra in both sexes are derived from splanchnic mesenchyme.

36. DEVELOPMENT OF SUPRARENAL GLANDS The cortex and medulla of the suprarenal glands (adrenal glands) have different origins. The cortex develops from mesenchyme and the medulla from neural crest cells.

37. CONGENITAL ADRENAL HYPERPLASIA AND ADRENOGENITAL SYNDROME An abnormal increase in the cells of the suprarenal cortex results in excessive androgen production during the fetal period. In females, this usually causes masculinization of the external genitalia. Affected male infants have normal external genitalia, and the syndrome may go undetected in early infancy. Later in childhood in both sexes, androgen excess leads to rapid growth and accelerated skeletal maturation.

38. Urogenital System Development of the Genital System

39. DEVELOPMENT OF GENITAL SYSTEM Chromosomal sex of an embryo is determined at fertilization by the kind of sperm (X or Y) that fertilizes the oocyte. Male and female morphologic characteristics do not begin to develop until the seventh week.

40. Development of Gonads The gonads (testes and ovaries) are derived from three sources:

41. Indifferent Gonads The initial stages of gonadal development occur during the fifth week when a thickened area of mesothelium develops on the medial side of the mesonephros . Proliferation of this epithelium and the underlying mesenchyme produces a bulge on the medial side of the mesonephros —the gonadal ridge . Fingerlike epithelial cords— gonadal cords—soon grow into the underlying mesenchyme . The indifferent gonad now consists of an external cortex and an internal medulla. In embryos with an XX sex chromosome complex, the cortex of the indifferent gonad differentiates into an ovary , and the medulla regresses. In embryos with an XY sex chromosome complex, the medulla differentiates into a testis, and the cortex regresses.

42. Primordial Germ Cells Large , spherical sex cells are first recognizable at 24 days after fertilization among the endodermal cells of the umbilical vesicle near the origin of the allantois . During the sixth week, the primordial germ cells enter the underlying mesenchyme and are incorporated in the gonadal cords

43. Development of Testes TDF (testis determining factor) induces the seminiferous cords to condense and extend into the medulla of the indifferent gonad, where they branch and anastomose to form the rete testis. Gradually the enlarging testis separates from the degenerating mesonephros and is suspended by its own mesentery, the mesorchium . The seminiferous cords develop into the seminiferous tubules, tubuli recti , and rete testis . The seminiferous tubules are separated by mesenchyme that gives rise to the interstitial cells ( Leydig cells ). By the eighth week, these cells begin to secrete androgenic hormones—testosterone and androstenedione

44. In addition to testosterone ( Steroli cells), the fetal testes produce a glycoprotein, antimüllerian hormone (AMH) or müllerian -inhibiting substance ( MIS). AMH suppresses development of the paramesonephric ducts, which form the uterus and uterine tubes . The walls of the seminiferous tubules are composed of two types of cells: Sertoli cells, supporting cells derived from the surface epithelium of the testis Spermatogonia , primordial sperm cells derived from the primordial germ cells

45. Development of Ovaries Gonadal development occurs slowly in female embryos. The ovary is not identifiable histologically until approximately the 10 th week. Cortical cords extend from the surface epithelium of the developing ovary into the underlying mesenchyme during the early fetal period. As the cortical cords increase in size, primordial germ cells are incorporated in them. At approximately 16 weeks, these cords begin to break up into isolated cell clusters—primordial follicles—each of which contains an oogonium , derived from a primordial germ cell

46. Development of Genital Ducts During the fifth and sixth weeks, the genital system is an indifferent state, and two pairs of genital ducts are present: The mesonephric ducts ( Wolffian ducts) play an important part in the development of the male reproductive system and The paramesonephric ducts ( müllerian ducts) have a leading role in the development of the female reproductive system .

47. Development of Male Genital Ducts and Glands Testosterone stimulates the mesonephric ducts to form male genital ducts, whereas MIS causes the paramesonephric ducts to regress . Under the influence of testosterone, each mesonephric duct becomes the epididymis (proximal), Efferent ductules and a muscular ductus deference (Distal).

48. Development of Female Genital Ducts and Glands The mesonephric ducts of female embryos regress because of the absence of testosterone. The paramesonephric ducts develop because of the absence of MIS . Female sexual development during the fetal period does not depend on the presence of ovaries or hormones . Later, estrogens produced by the maternal ovaries and the placenta stimulate development of the uterine tube , uterus, and the superior part of the vagina .

49. Development of Female Genital Ducts and Glands The paramesonephric ducts form most of the female genital tract . The uterine tubes develop from the unfused cranial parts of these ducts . The caudal fused portions form the uterovaginal primordium , which gives rise to the uterus and the superior part of the vagina. The endometrial stroma and myometrium are derived from splanchnic mesenchyme . Auxiliary Genital Glands in Females: Outgrowths from the urethra into the surrounding mesenchyme form the urethral glands and paraurethral glands

50. Development of Vagina

51. DEVELOPMENT OF EXTERNAL GENITALIA Up to the seventh week, the external genitalia are similar in both sexes. Distinguishing sexual characteristics begin to appear during the 9th week, but the external genitalia are not fully differentiated until the 12th week. Early in the fourth week, proliferating mesenchyme produces a genital tubercle ( primordium of penis or clitoris) in both sexes at the cranial end of the cloacal membrane. Labioscrotal swellings and urogenital folds soon develop on each side of the cloacal membrane.

52. Development of Male External Genitalia Masculinization of the indifferent external genitalia is induced by testosterone . The urethral folds fuse with each other along the ventral surface of the penis to form the spongy urethra. The surface ectoderm fuses in the median plane of the penis, forming the penile raphe and enclosing the spongy urethra within the penis . During the 12th week, a circular ingrowth of ectoderm occurs at the periphery of the glans penis. When this ingrowth breaks down, it forms the prepuce (foreskin). The corpora cavernosa and corpus spongiosum of the penis develop from mesenchyme in the phallus (forms penis). The labioscrotal swellings grow toward each other and fuse to form the scrotum. The line of fusion of these folds is clearly visible as the scrotal raphe .

53. Development of Female External Genitalia The primordial phallus in the female fetus gradually becomes the clitoris. The clitoris is still relatively large at 18 weeks. The urethral folds do not fuse, except posteriorly , where they join to form the frenulum of the labia minora . The unfused parts of the urogenital folds form the labia minora . The labioscrotal folds fuse posteriorly to form the posterior labial commissure and anteriorly to form the anterior labial commissure and mons pubis. Most parts of the labioscrotal folds remain unfused , but develop into two large folds of skin, the labia majora .

54. DEVELOPMENT OF INGUINAL CANALS The inguinal canals form pathways for the testes to descend from the abdominal wall into the scrotum. Inguinal canals develop in both sexes. As the mesonephros degenerates, a ligament—the gubernaculum —develops on each side of the abdomen from the caudal pole of the gonad. The gubernaculum attaches caudally to the internal surface of the labioscrotal swellings (future halves of the scrotum or labia majora ).

55. RELOCATION OF TESTES AND OVARIES: Testicular Descent Testicular descent is associated with : Enlargement of the testes and atrophy of the mesonephroi allowing movement of the testes caudally along the posterior abdominal wall Atrophy of the paramesonephric ducts induced by the müllerian -inhibiting substance (MIS), enabling the testes to move transabdominally to the deep inguinal rings. Enlargement of the processus vaginalis guiding the testis through the inguinal canal into the scrotum

56. Ovarian Descent The ovaries also descend from the lumbar region of the posterior abdominal wall and relocate to the lateral wall of the pelvis. The gubernaculum is attached to the uterus near the attachment of the uterine tube . The cranial part of the gubernaculum becomes the ovarian ligament, and the caudal part forms the round ligament of the uterus. The relatively small processus vaginalis in the female usually obliterates and disappears long before birth

57. Genital System Abnormalities

58. MESONEPHRIC DUCT REMNANTS IN MALES The cranial end of the mesonephric duct may persist as an appendix of the epididymis , which is usually attached to the head of the epididymis . Caudal to the efferent ductules , some mesonephric tubules may persist as a small body, the paradidymis

59. MESONEPHRIC DUCT REMNANTS IN FEMALES The cranial end of the mesonephric duct may persist as an appendix vesiculosa . A few blind tubules and a duct, the epoophoron may persist in the mesovarium between the ovary and uterine tube. Closer to the uterus, some rudimentary tubules may persist as the paroophoron . Parts of the mesonephric duct, corresponding to the ductus deferens and ejaculatory duct, may persist as Gartner duct cysts between the layers of the broad ligament along the lateral wall of the uterus and in the wall of the vagina.

60. PARAMESONEPHRIC DUCT REMNANTS IN MALES The cranial end of the paramesonephric duct may persist as a vesicular appendix of the testis, which is attached to the superior pole of the testis. The prostatic utricle, a small saclike structure arising from the paramesonephric duct, opens into the prostatic urethra.

61. ANDROGEN INSENSITIVITY SYNDROME Persons with androgen insensitivity syndrome (AIS)— previously called testicular feminization syndrome—(1 in 20,000 live births) are normal-appearing females, despite the presence of testes and a 46, XY chromosome constitution. The external genitalia are female, but the vagina usually ends in a blind pouch and the uterus and uterine tubes are absent or rudimentary. At puberty there is normal development of breasts and female characteristics, but menstruation does not occur. The testes are usually in the abdomen or the inguinal canals, but they may be within the labia majora . The failure of masculinization to occur in these individuals results from a resistance to the action of testosterone at the cellular level in the genital tubercle and labioscrotal and urethral folds.

62. ANDROGEN INSENSITIVITY SYNDROME Persons with partial AIS exhibit some masculinization at birth, such as ambiguous external genitalia, and may have an enlarged clitoris. The vagina ends blindly and the uterus is absent. Testes are in the inguinal canals or the labia majora . There are usually point mutations in the sequence that codes for the androgen receptor. AIS follows X-linked recessive inheritance.

63. MIXED GONADAL DYSGENESIS Persons with this rare condition usually have a 46, XY chromosomal complement, with a testis on one side, and an undifferentiated gonad on the other side. The internal genitalia are female, but male derivatives of the mesonephric ducts are sometimes present. The external genitalia range from normal female through intermediate states to normal male. At puberty, neither breast development nor menstruation occurs.

64. Disorders of Sex Development (DSD). DSD implies a discrepancy between the morphology of the gonads (testes/ovaries) and the appearance of the external genitalia – ambiguous genitalia. Intersexual conditions are classified according to the histological appearance of the gonads: Ovotesticular DSD (true hermaphroditism )—ovarian and testicular tissue is found either in the same or in opposite gonads. 46 XX, DSD (female pseudohermaphroditism )—ovaries are present 46 XY, DSD (male pseudohermaphroditism )—testicular tissue is present

65. Ovotesticular DSD Approximately 70% of them have a 46, XX chromosome constitution; approximately 20% have 46, XX/46, XY mosaicism and approximately 10% have a 46, XY chromosome constitution. Most persons have both testicular and ovarian tissue or an ovotestis . These tissues are not usually functional. An ovotestis (containing both testicular and ovarian tissue) forms if both the medulla and cortex of the indifferent gonads develop. The phenotype may be male or female but the external genitalia are always ambiguous.

66. 46 XX, DSD This anomaly results from exposure of the female fetus to excessive androgens, causing virilization of the external genitalia (clitoral enlargement and labial. A common cause of 46 XX, DSD (female pseudohermaphroditism ) is CAH (congenital adrenal hyperplasia). There is no ovarian abnormality, but the excessive production of androgens by the fetal suprarenal glands causes varying degrees of masculinization of the external genitalia. Commonly there is clitoral hypertrophy and partial fusion of the labia majora

67. 46 XY, DSD The external genitalia are developmentally variable as is the development of the internal genitalia due to varying degrees of development of the paramesonephric ducts. These anomalies are caused by inadequate production of testosterone and MIS by the fetal testes. Genetic defects in the enzymatic synthesis of testosterone by the fetal testes and in interstitial cells produce 46 XY, DSD (male pseudohermaphroditism ) through inadequate virilization of the male fetus.

68. HYPOSPADIAS Hypospadias is the most common birth defect of the penis. There are four main types:

69. HYPOSPADIAS In 1 of every 125 male infants, the external urethral orifice is on the ventral surface of the glans of the penis ( glanular hypospadias ), or on the ventral surface of the body of the penis (penile hypospadias ). Glanular hypospadias and penile hypospadias constitute approximately 80% of cases . In penoscrotal hypospadias , the urethral orifice is at the junction of the penis and scrotum. In perineal hypospadias , the labioscrotal folds fail to fuse and the external urethral orifice is located between the unfused halves of the scrotum.

70. HYPOSPADIAS Hypospadias results from inadequate production of androgens by the fetal testes and/or inadequate receptor sites for the hormones. It has been suggested that the expression of testosterone-related genes is affected. These defects result in failure of canalization of the ectodermal cord in the glans of the penis and/or failure of fusion of the urethral folds; as a consequence, there is incomplete formation of the spongy urethra.

71. EPISPADIAS In one of every 30,000 male infants, the urethra opens on the dorsal surface of the penis. Although epispadias may occur as a separate entity, it is often associated with exstrophy of the bladder. Epispadias may result from inadequate ectodermal-mesenchymal interactions during development of the genital tubercle. As a consequence, the genital tubercle develops more dorsally than in normal embryos. Urine is expelled at the root of the malformed penis.

72. AGENESIS OF EXTERNAL GENITALIA Congenital absence of the penis or clitoris is an extremely rare condition. Failure of the genital tubercle to develop may result from inadequate ectodermal mesenchymal interactions during the seventh week. The urethra usually opens into the perineum near the anus.

73. BIFID PENIS AND DOUBLE PENIS These defects are rare. Bifid penis is usually associated with exstrophy of the bladder. It may also be associated with urinary tract abnormalities and imperforate anus. Double penis results when two genital tubercles develop.

74. MICROPENIS In this condition, the penis is so small that it is almost hidden by the suprapubic pad of fat. Micropenis results from fetal testicular failure and is commonly associated with hypopituitarism .

75. ANOMALIES OF UTERINE TUBES, UTERUS, AND VAGINA Defects of the uterine tubes are rare; only a few types have been reported. These include hydatid cysts, accessory ostia (openings), complete and segmental absence, duplication of a uterine tube, lack of the muscular layer, and failure of the tube to canalize. Various types of uterine duplication and vaginal anomalies result from arrests of development of the uterovaginal primordium during the eighth week by: Incomplete development of a paramesonephric duct Failure of parts of one or both paramesonephric ducts to develop Incomplete fusion of the paramesonephric ducts Incomplete canalization of the vaginal plate to form the vagina

76. Double uterus Double uterus (uterus didelphys ) results from failure of fusion of the inferior parts of the paramesonephric ducts. It may be associated with a double or a single vagina. In some cases, the uterus appears normal externally but is divided internally by a thin septum. If the duplication involves only the superior part of the body of the uterus, the condition is called bicornuate uterus

77. If growth of one paramesonephric duct is retarded and does not fuse with the other one, a bicornuate uterus with a rudimentary horn ( cornu ) develops . The rudimentary horn may not communicate with the cavity of the uterus. A unicornuate uterus develops when one paramesonephric duct fails to develop; this results in a uterus with one uterine tube. In many cases, the individuals are fertile but may have an increased incidence of preterm delivery or recurrent pregnancy loss.

78. Absence of Vagina and Uterus Once in approximately every 5000 births, absence of the vagina occurs. This results from failure of the sinovaginal bulbs to develop and form the vaginal plate. When the vagina is absent, the uterus is usually absent because the developing uterus ( uterovaginal primordium ) induces the formation of sinovaginal bulbs, which fuse to form the vaginal plate.

79. Vaginal Atresia Failure of canalization of the vaginal plate results in atresia (blockage) of the vagina. A transverse vaginal septum occurs in approximately one in 80,000 women. Usually the septum is located at the junction of the middle and superior thirds of the vagina. Failure of the inferior end of the vaginal plate to perforate results in an imperforate hymen. Variations in the appearance of the hymen are common. The vaginal orifice varies in diameter from very small to large, and there may be more than one orifice.

80. CRYPTORCHIDISM Cryptorchidism (hidden testes) is the most common anomaly in neonates and occurs in about 30% of premature males and in 3% to 5% of full-term males. Cryptorchidism may be unilateral or bilateral. In most cases, undescended testes descend into the scrotum by the end of the first year. If both testes remain within or just outside the abdominal cavity, they fail to mature and sterility is common. Cryptorchid testes may be in the abdominal cavity or anywhere along the usual path of descent of the testis, but they are usually in the inguinal canal.

81. ECTOPIC TESTES After traversing the inguinal canal, the testes may deviate from its usual path of descent and lodge in various abnormal locations : Interstitial (external to aponeurosis of external oblique muscle) In the proximal part of the medial thigh Dorsal to the penis On the opposite side (crossed ectopia ) All types of ectopic testes are rare. An ectopic testis occurs when a part of the gubernaculum passes to an abnormal location and the testis follows it.

82. CONGENITAL INGUINAL HERNIA If the communication between the tunica vaginalis and the peritoneal cavity fails to close, a persistent processus vaginalis exists. A loop of intestine may herniate through it into the scrotum or labium majus . Embryonic remnants resembling the ductus deferens or epididymis are often found in inguinal hernial sacs. Congenital inguinal hernia is much more common in males, especially when there are undescended testes. Congenital inguinal hernias are also common with ectopic testes and in females with androgen insensitivity syndrome

83. HYDROCELE Occasionally the abdominal end of the processus vaginalis remains open but is too small to permit herniation of intestine. Peritoneal fluid passes into the patent processus vaginalis and forms a scrotal hydrocele . If the middle part of the processus vaginalis remains open, fluid may accumulate and give rise to a hydrocele of the spermatic cord

84. References The Developing Human, Clinically Oriented Embryology - Moore, Keith L Langman's Medical Embryology 12th ed. - T. Sadler (Lippincott, 2012) BBS Netter's Atlas of Human Embryology, Updated Edition- Larry R Cochard