Timothy C. Nichols, MD

The ureteric nerves consist of relatively large bundles of axons that form an irregular plexus in the adventitia of the ureter bacteria wanted poster discount 300 mg cefdinir amex. The plexus receives branches from the renal and aortic plexuses (in its upper part); from the superior hypogastric plexus and hypogastric nerve (in its intermediate part); and from the hypogastric nerve and inferior hypogastric plexus (in its lower part) spironolactone versus antibiotics for acne order cefdinir 300 mg otc. Numerous small branches penetrate the ureteric muscle coat; some of the adventitial nerves accompany the blood vessels and branch with them as they extend into the muscle layer; others are unrelated to the vascular supply and lie free in the adventitial connective tissue around the circumference of the ureter virus ti 2 discount 300 mg cefdinir free shipping. The density of innervation increases gradually from the renal pelvis and upper ureter (where autonomic nerves are sparse) to a maximum density in the juxtavesical segment infection in finger discount 300 mg cefdinir overnight delivery. At least three different neurotransmitter phenotypes ­ cholinergic antibiotics for uti guidelines order cefdinir 300 mg online, noradrenergic and peptidergic (substance P) ­ are well known and others have been reported. The functional significance of these different types of autonomic nerve fibres in relation to ureteric smooth muscle activity is not fully understood; although they are thought to influence the inherent motility of the ureter, they are not essential for the initiation and propagation of ureteric contraction waves. A branching plexus of fine cholinergic, noradrenergic and peptidergic axons occurs throughout the lamina propria and extends from the inner aspect of the muscle coat towards the base of the urothelium. Some of these axons form perivascular plexuses, while others lie in isolation from the vascular supply and may be sensory in function. There is a good longitudinal anastomosis between these branches on the wall of the ureter, which means that the ureter can be safely transected at any level intraoperatively, and a uretero-ureterostomy performed, without compromising its viability. The branches from the inferior vesical artery are constant in their occurrence and supply the lower part of the ureter, as well as a large part of the trigone of the bladder. The branch from the renal artery is also constant and is preserved whenever possible in renal transplantation to ensure good vascularity of the ureter. SeCtiOn 8 1252 Veins the venous drainage of the ureters generally follows the arterial supply. Lymphatic drainage Lymph vessels draining the ureter begin in submucosal, intramuscular and adventitial plexuses, which all communicate. The proximal part takes its blood supply medially, and the distal part is supplied laterally. Contraction waves are propagated away from the kidney, and so undesirable pressure rises are not directed against the renal parenchyma. Since several potential pacemaker sites exist, the initiation of contraction waves is unimpaired by partial nephrectomy; the minor calyces spared by the resection remain in situ to continue their pacemaking function. Experimental evidence indicates that autonomic nerves do not play a major part in the propagation of peristalsis. It seems more likely that they play a modulatory role on the contractile events occurring in the musculature of the upper urinary tract. Ureteric peristalsis Under normal conditions, contraction waves originate in the proximal part of the upper urinary tract and are propagated in an anterograde direction towards the bladder. Atypical smooth muscle cells in the wall of the minor calyces act individually or collectively as pacemaker sites. The pain is spasmodic and agonizing, particularly if the obstruction is gradually forced down the ureter by the muscle spasm. It is referred to cutaneous areas innervated from spinal segments that supply the ureter, mainly T11­L2, and shoots down and forwards from the loin to the groin and scrotum or labium majus; it may extend into the proximal anterior aspect of the thigh by projection to the genitofemoral nerve (L1, 2). Stones in the lower pole of the kidney clear less well if the angle between the infundibulum of the calyx containing the stone and the ureter is acute, or if there is a particularly long and narrow infundibulum. Percutaneous stone extraction is most frequently achieved by puncturing a posterior calyx with a needle. Ureteric calculi tend to be arrested in their descent in either the pelviureteric region, or the point where the ureter passes over the pelvic brim as it crosses the common iliac artery, or the vesico-ureteric junction, because these are the three areas where the ureter is narrowest. The vesico-ureteric junction is the narrowest of these areas and can be responsible for arresting the passage of stones of as little as 2­3 mm. The kidney and upper ureter move with respiration within the perirenal fascia, and this can affect the visualization and tracking of a stone, both at the time of extracorporeal shock wave lithotripsy and at retrograde endoscopy. Throughout its length, the muscle coat of the ureter is fairly uniform in thickness and, in crosssection, measures 750­800 µm in width. The muscle bundles that constitute this coat are frequently separated from one another by relatively large amounts of connective tissue. However, branches that interconnect muscle bundles are common and there is frequent interchange of muscle fibres between adjacent bundles. As a consequence of this extensive branching, individual muscle bundles do not spiral around the ureter, but form a complex meshwork of interweaving bundles. In the upper part of the ureter, the inner muscle bundles tend to lie longitudinally while those on the outer aspect have a circular or oblique orientation. In the middle and lower parts, there are additional outer longitudinally orientated fibres, and as the ureterovesical junction is approached, the muscle coat consists predominantly of longitudinally orientated muscle bundles. The mucosa of the ureter consists of an epithelium, the urothelium, lying on a layer of subepithelial fibroelastic connective tissue lamina propria. The latter varies in thickness from 350 to 700 µm and is a conduit for small blood vessels and bundles of unmyelinated nerve fibres. Occasional lymphocytes may be present in the lamina propria but their aggregation into definitive lymph nodules is rare. The urothelium is usually extensively folded, giving the ureteric lumen a stellate outline. In the male, the ureter can insert at the bladder neck or posterior urethra, or, rarely, into the seminal vesicle, but it always inserts cranial to the external urethral sphincter. In the female, ectopic insertion can be distal to the external urethral sphincter in the urethra, or into the vagina, resulting in persistent childhood incontinence. Ureteroceles A ureterocele is a cystic dilation of the lower end of the ureter; the ureteric orifice is covered by a membrane that expands as it is filled with urine and then deflates as it empties. Ureteroceles can vary in size and usually have no influence on ureteric drainage; however, they can be a cause of obstruction in the ureter and pelvicalyceal system more proximally. Prolapsing ureteroceles, though small, prolapse from their position around the ureterovesical junction region into the urethra, causing intermittent bladder outflow obstruction. In adults, ureteroceles tend to be bilateral and small, and are often found incidentally when the urinary tract is being imaged in the investigation of a coincidental pathology. Retrocaval ureter A persistence of the posterior cardinal vein, associated with high confluence of the right and left common iliac veins or a double inferior vena cava, may result in a retrocaval (or circumcaval) ureter that passes behind the inferior vena cava, usually at the level of the inferior edge of the third part of the duodenum, before it emerges anterior to it to pass from medial to lateral. Duplex ureters are the product of two ureteric buds arising from the mesonephric duct; they share a single fascial sheath and may either fuse at any point along their course, or remain separate until they insert through separate ureteric orifices into the bladder. Care must be taken not to compromise the blood supply of the second ureter when excising or reimplanting a single ureter of a duplex. The ureter from the upper pole of the kidney (the longer ureter) inserts more medially and caudally in the bladder than the ureter from the lower pole (Weigert­Meyer rule). This reflects the embryological development of the ureter: the ureteric bud that is initially more proximal on the mesonephric duct has a shorter time to be pulled cranially in the bladder and so it inserts more distally in the mature bladder. The ureter from the lower pole has a shorter intramural course than the longer ureter and is prone to reflux. A review of the imaging literature describing the contentious anatomy of the perirenal fascia. An account that demonstrates that the perirenal fascia is a multilaminar structure rather than a single fused fascia. The ureter passes cranially, medially and then caudally, and can be followed into the pelvis. Key: 1, contrast within dilated collecting system of right kidney and upper ureter; 2, contrast within ureter turning behind inferior vena cava; 3, contrast within normal calibre ureter seen below the obstruction; 4, contrast within normal collecting system of left kidney and upper ureter. The original description of a relatively avascular longitudinal zone within the kidney, proposed as a site for surgical incision. An early paper describing the identification of pacemaker cells in various species. Manalich R, Reyes L, Herrera M et al 2000 Relationship between weight at birth and the number and size of renal glomeruli in humans: a histomorphometric study. Veyrac C, Baud C, Lopez C et al 2003 the value of colour Doppler ultrasonography for identification of crossing vessels in children with pelviureteric junction obstruction. Its size, shape, position and relations all vary, according to its content and the state of the neighbouring viscera. When the bladder is empty, it lies entirely in the lesser pelvis, but as it distends, it expands anterosuperiorly into the abdominal cavity (Video 75. An empty bladder is somewhat tetrahedral and has a base (fundus), neck, apex, and a superior (dome) and two inferolateral surfaces. The neck, which is most fixed, lies most inferiorly, 3­4 cm behind the lower part of the pubic symphysis and just above the plane of the inferior aperture of the lesser pelvis. The bladder neck is, essentially, the internal urethral orifice, which lies in a constant position that is independent of the varying positions of the bladder and rectum. In males, the neck rests on, and is in direct continuity with, the base of the prostate; in females, it is related to the pelvic fascia that surrounds the upper urethra. In both sexes, the apex of the bladder faces towards the upper part of the pubic symphysis. This is more adherent to the bladder than to the anterior surface of the prostate, which aids reliable identification of the region of the bladder neck surgically. In males, each inferolateral surface is related anteriorly to the pubis and puboprostatic ligaments. In females, the relations are similar, except that the pubovesical ligaments replace the puboprostatic ligaments. The triangular superior surface is bounded by lateral borders from the apex to the ureteric entrances, and by a posterior border that joins them. In females, the superior surface is largely covered by peritoneum, which is reflected posteriorly on to the uterus at the level of the internal os (the junction of the uterine body and cervix), to form the vesicouterine pouch. The posterior part of the superior surface, devoid of peritoneum, is separated from the supravaginal cervix by fibroareolar tissue. Extraperitoneal injuries can often be managed conservatively because urine is contained, whereas intraperitoneal injuries usually require surgical repair. The relationship of the bladder to the peritoneum and anterior abdominal wall on filling allows suprapubic cystostomy without intraperitoneal urinary leak. Anteriorly, it displaces the parietal peritoneum from the suprapubic region of the abdominal wall. Its inferolateral surfaces become anterior and rest against the abdominal wall without intervening peritoneum for a distance above the pubic symphysis that varies with the degree of distension, but is commonly 5­7 cm. The summit of the full bladder points up and forwards above the attachment of the median umbilical ligament, so that the peritoneum forms a supravesical recess of varying depth between the summit and the anterior abdominal wall; this recess often contains coils of small intestine. At birth, the bladder is higher than in the adult because the true pelvis is shallow, and the internal urethral orifice is level with the upper symphysial border. The bladder is then abdominal rather than pelvic, and extends about two-thirds of the distance towards the umbilicus. The bladder progressively descends with growth, and reaches the adult position shortly after puberty. In both sexes, stout bands of fibromuscular tissue, the pubovesical ligaments, extend from the bladder neck to the inferior aspect of the pubic bones; they lie on each side of the median plane, leaving a midline hiatus through which numerous small veins pass. In the female, they constitute the superior extensions of the pubourethral ligaments. In the male, the detrusor apron is described as an extension of detrusor that extends over the anterior surface of the prostate, and condenses distally and anteriorly to form the puboprostatic ligaments. Other ligaments that have been described in relation to the base of the urinary bladder are the lateral, sacrogenital/uterosacral and cardinal ligaments. The lateral ligament was described by Miles in 1908; although never described in anatomical cadaveric dissection studies, it is recognized clinically as an important structure in the pararectal space at operation. It is a broad band of dense connective tissue, varying in depth from 5 to 7 cm, and passing between the lateral wall of the pelvis and the base of the bladder at the point where the ureter terminates. It contains the middle rectal artery and lymphatic vessels that pass from the lower rectum to the iliac lymph nodes (Takahashi et al 2000). Composed of longitudinal muscle fibres derived from the detrusor, it becomes more fibrous towards the umbilicus. It usually maintains a lumen lined with epithelium that persists into adult life but is only rarely complicated by a urachal cyst, sinus, fistula or adenocarcinoma. B, A view of the left side of the anterior abdominal wall and ligaments during laparoscopy. Over the trigone, immediately above and behind the internal urethral orifice, it is adherent to the subjacent muscle layer and is always smooth. The anteroinferior angle of the trigone is formed by the internal urethral orifice, its posterolateral angles by the ureteric orifices. The superior trigonal boundary is a slightly curved inter-ureteric bar, which connects the two ureteric orifices and is produced by the continuation into the vesical wall of the ureteric internal longitudinal muscle. Laterally, this ridge extends beyond the ureteric openings as ureteric folds, produced by the terminal parts of the ureters, which run obliquely through the bladder wall. Trigone the smooth muscle of the trigone consists of two distinct layers, sometimes termed the superficial trigonal muscle and deep trigonal detrusor muscle. The latter is composed of muscle cells, indistinguishable from those of the detrusor, and is simply the posteroinferior portion of the detrusor muscle proper. The superficial trigonal muscle represents a morphologically distinct component of the trigone, which, unlike the detrusor, is composed of relatively small-diameter muscle bundles that 1257 Chapter 75 Bladder, prostate and urethra the urachus may play a critical role in maintaining fetal life when atresia of the urethra results in complete obstruction to the flow of amniotic fluid. The bladder is released from the anterior abdominal wall, the space of Retzius is developed and the endopelvic fascia opened. In males, the detrusor extends over the anterosuperior aspect of the prostate and inserts into the pubic bone. The arrangement of smooth muscle in this region is quite different in males and females, and therefore will be described separately. The superficial trigonal muscle is relatively thin but is generally described as becoming thickened along its superior border to form the interureteric ridge (bar). In both sexes, the superficial trigone muscle becomes continuous with the smooth muscle of the proximal urethra, and extends in the male along the urethral crest as far as the openings of the ejaculatory ducts.

A range of molecular markers associated with the migration and proliferation of primordial germ cells has been described (SotoSuazo and Zorn 2005 infection you get in hospital order cheap cefdinir, Runyan et al 2006 antibiotics for sinus infection and alcohol 300 mg cefdinir buy amex, De Felici 2013) virus bulletin rap test generic 300 mg cefdinir. Primordial germ cells proliferate both during and after migration to the mesonephric ridges antibiotic for mrsa cefdinir 300 mg sale. Cells that do not complete this migration mainly degenerate antimicrobial mouthwash brands buy discount cefdinir 300 mg on-line, but if they survive, they can give rise to germ cell tumours, usually in the midline (Runyan et al 2006). After segregation, when they are often termed primary gonocytes, they divide to form secondary gonocytes. The morphological events that occur in each type of gonadal development are presented first. The cords lengthen, partly by addition from the coelomic epithelium, and encroach on the medulla, where they unite with a network of cells derived from the mesonephric mesenchyme destined to become the rete testis. Primor dial germ cells are incorporated into the cords, which later become enlarged and canalized to form the seminiferous tubules. The cells derived from the surface of the early gonad form the supporting Sertoli cells. The latter proliferate throughout fetal and early postnatal life (less than 6 months) and perhaps again at puberty initiation (Sharpe et al 2003); when they stop dividing, they mature and cannot be reactivated. Each Sertoli cell can only support a fixed number of germ cells during their development into spermatozoa, i. Because the germ cells make up the bulk of the adult testis, the number of Sertoli cells is a major determinant of the size to which the testes will grow (factors that impair the process of spermatogenesis, resulting in the loss of germ cells, will also affect testicular size). Variation in Sertoli cell number is probably the most important factor in accounting for the enormous variation in sperm counts between individual men, whether fertile or infertile. Indeed, the available data for adult men indicate that Sertoli cell numbers vary across a fiftyfold range (Sharpe et al 2003). Although some of this variation may result from attrition of Sertoli cell numbers because of ageing, the major differences in Sertoli cell numbers will have been determined by events in fetal and/or childhood life. The interstitial cells of the testis are derived from mesenchyme and, possibly, also from coelomic epithelial cells that do not become incor porated into the tubules. Among other cell lines, they form the embry onic and fetal cells of Leydig, which secrete testosterone and insulinlike factor 3 (Insl3). A later migration of mesenchyme beneath the coelomic epithelium forms the tunica albuginea of the testis. The cords of the rete testis become connected to the glomerular capsules in the persisting part of the mesonephros. Ultimately, they become connected to the mesonephric duct by the 5­12 most cranial persisting mesonephric tubules. These become exceedingly convoluted and form the lobules of the head of the epididymis. The seminifer ous tubules do not acquire lumina until the seventh month; the tubules of the testicular rete become canalized somewhat earlier. Disorders of development of the testis and reproductive tract in the male fetus seem to be increasing in incidence. Testicular maldescent (cryptorchidism) and hypospadias appear to have doubled or trebled in incidence in the last 30­50 years, while testicular cancer has increased by an even greater margin and is now the most common cancer of young men. However, the most dramatic change that appears to have occurred in the relatively recent past is a fall in sperm counts of around 40­50% (1% per year over the last 50 years). Although this dramatic decrease is obviously manifest only in adult hood, as is the case with testicular cancer there is growing evidence that it may reflect impaired testicular development during fetal or childhood life (Dean and Sharpe 2013). The majority remain in the cortex, where they may be joined by a second proliferation from the coelomic epithelium overlying the gonad. In histological sections of ovaries from the third and subsequent months, the epithelial cords appear as clusters of cells, which may contain primitive germ cells, separated by fine septa of undifferentiated mesenchyme. An ovarian rete condenses in the medullary mesenchyme and some of its cords may join mesonephric glomeruli. The medulla subsequently regresses, and connective tissue and blood vessels from this region invade the cortex to form the ovarian stroma. During this invasion, the clusters of epithelial cortical cells break into individual groups of supporting cells (now identified as granulosa cells), which surround the primordial germ cells (now identified as primary oocytes) that have entered the prophase of the first meiotic division. Primary oocytes are derived from a mitotic division of the primordial germ cells (naked oogonia). Their epithelial capsules consist of flattened pregranu losa cells derived from proliferations of coelomic epithelium. The majority undergo atresia, a hormonally controlled apoptotic process, but the remainder resume development after puberty, when they complete the first meiotic division shortly before ovulation. The granulosa cells at this time enlarge and multiply to form the stratum granulosum; as they do so, they become surrounded by thecal cells, which differentiate from the stroma. Neu rotropins and their receptors have been shown to be expressed within the fetal ovary between 13 and 21 weeks. Expression of p450c17, a steroidogenic enzyme involved in the pro duction of androgens, has been shown in the human fetal ovary during the second and third trimesters (Cole et al 2006). Its temporospatial expression showed a movement from the cortex to the medulla, with its presence in primary interstitial cells in the cortex from 14 weeks to 23 weeks, but not in hilus interstitial cells; between 27 and 33 weeks, few cells stained for p450c17, but there was an increase after 33 weeks in theca interstitial cells associated with preantral follicles. The temporospatial expression was similar in anencephalic fetuses of the same age, indicating that anterior pituitary function is not regulating this maturation. The authors suggest a possible role for insulin in regu lating fetal ovary androgen production. It is noted that overexpression of interstitial androgen production is a component in the pathophysiol ogy of polycystic ovary syndrome (Cole et al 2006). The cranial part of the gonadal ridge becomes the suspensory ligament of the ovary (infundibulopelvic fold of peritoneum), and its caudal region is incorporated into the ovarian ligament. It is now clear that the germ cells may be essentially irrelevant to testis determination; embryos in which the genital ridges are devoid of germ cells may still undergo otherwise normal testis development. The processes of sex determination and differentiation involve inter acting pathways of gene activity, which lead to the total patterning of the embryo as either male or female. These cells can potentially differentiate into either Sertoli or granulosa cells (the sup porting cells for the germ cells in the testis and ovary, respectively). Gene expression is seen first in cells designated as preSertoli, located cen trally in the developing gonad, and then later in the cranial and caudal poles. Once the developmental pathway of Sertoli cells is directed, this influences the differentiation of the other cell types in the testicular pathway, so that Leydig cells appear later, and the connective tissue becomes organized into a male pattern. When they arrive, they become enclosed within the Sertoli cells and do not enter meiosis; they continue to proliferate (which is characteristic of spermatogenesis), instead of ceasing prolif eration and entering meiosis and meiotic arrest, as occurs in the ovary. Therefore, development of either a testis or an ovary results from a reinforcing programme of gene expression changes, and inacti vating mutations in any one of these genes, or their aberrant expression in the wrong sex fetus, has the potential to interfere, partially or com pletely, with normal gonad formation and, thus, with downstream sexual development (BiasonLauber 2010, Munger et al 2013). Of these, testosterone is the most important, as it has bodywide effects, both on the developing repro ductive system/genitalia and on numerous other organs/tissues, includ ing the brain. Also important is the development of the appropriate cytoplasmic testosteronebinding receptor protein (the androgen recep tor). As it enlarges, its cranial end degenerates and the remaining organ therefore occupies a more caudal position. It is attached to the mesonephric fold by the mesorchium (the mesogenitale of the undifferentiated gonad), a peri toneal fold that contains the testicular vessels and nerves, and a quantity of undifferentiated mesenchyme. It also acquires a secondary attach ment to the ventral abdominal wall, which has a considerable influence on its subsequent movements. It has been suggested that this line corresponds to the original lateral edge of the embryo, which expresses the apical ectodermal ridges and mesenchymal progress zones of the upper and lower limbs (Hutson 2013, Hutson et al 2014). This serves to anchor the fetal testis near the future inguinal canal as the abdominal cavity enlarges between 10 and 15 weeks. By comparison, the gubernaculum in females remains thin and subsequently develops into the round ligament (see below). The cranial attachment of the urogenital ridge, known as the cranial suspen sory ligament, regresses in males under the action of androgens. After the midgut loop returns to the abdomen, the anterior abdomi nal wall inferior to the umbilical cord lengthens. As each umbilical artery runs ventrally from the dorsal to the ventral wall, it pulls up a falciform peritoneal fold, which forms the medial boundary of a peri toneal fossa, the saccus vaginalis of lateral inguinal fossa, into which each testis projects. Inguinoscrotal phase the caudal end of the gubernaculum is initially associated with a spe cific portion of the milk line of the abdominal wall around which the future inguinal canal is formed by differentiating abdominal wall muscles. An interaction with the mammary line ectoderm and underly ing mesenchyme may trigger gubenacular meristematic growth similar to that seen in the progress zone of the limb bud. An outpocketing of peritoneum, the processus vaginalis, extends into the gubernaculum, hollowing it out so that the proximal part is divided into a crescentic parietal layer within which the cremaster muscle develops, and a central column attached to the epididymis. Elongation of the soft, gelatinous end of the gubernaculum, which, in the early stage, is formed mainly of hyaluronic acid, is controlled by androgens. In rodent models, there is good evidence that androgens cause sexual dimorphism of the sensory branches of the genitofemoral nerve, which supplies the gubernaculum, the developing cremaster muscle within it, and part of the scrotum. The testis remains in apposition with the deep inguinal ring, held by the gubernaculum during the fourth to sixth months (Barteczko and Jacob 2000). From 35 weeks the extracellular matrix of the gubernacu lum is resorbed and it forms a fibrous attachment to the inside of the scrotum. Testis descent during the inguinoscrotal phase occurs relatively rapidly about the seventh month, the left testis usually descending ahead of the right. It is thought that intraabdominal pressure acting through the patent processus vaginalis contributes to this migration (Hutson 2012). In fullterm male neonates, over 95% have descended testes, although, in premature babies, descent may not be complete. This region receives a rich blood supply, which is directed to the gonads as the mesonephros involutes. Both gonads descend, the testis to lie outside the abdominal cavity, and the ovary to the pelvis; however, they both retain their early blood supply from the dorsal aorta. Descent of the testis the mechanism of testicular descent is not completely understood and, to some extent, remains controversial. A, the gubernaculum attached to the lower part of the testis has an abdominal part covered with developing peritoneum, an interstitial part and a distal end embedded in the anterior abdominal wall at the site of the future inguinal canal. The distal-most portion of the gubernaculum bulges into abdominal wall muscles and grows 3­5 cm over the superior pubic ramus and into the scrotum. A crescentic column of peritoneum, the processus vaginalis, develops in the expanding gubernaculum. C, the testis gains a crescentic covering of visceral and parietal peritoneum (which forms the tunica vaginalis) and muscle and connective tissue layers as it passes through the deep and superficial inguinal rings. The coverings remain around the ductus deferens, whereas the proximal processus vaginalis normally becomes obliterated by 3 weeks after birth. At birth, the processus vaginalis is narrowed and collapsed, but not necessarily completely obliterated. It remains patent for 2 weeks in nearly 70% of male infants but, by 3 weeks after birth, it is at least partially obliterated in 80% of male infants, the left side before the right. Persistent patency of the processus vaginalis leads to indirect inguinal hernia (widely patent and allowing prolapse of bowel), or hydrocele (narrow patency permitting only intraperitoneal fluid to trickle down into the tunica vaginalis). During obliteration, fluid may trickle only part of the way down the processus vaginalis to produce an encysted hydrocele of the cord. This is a relatively common but transient state and usually resolves completely within a few weeks by further oblitera tion. Because of perinatal androgen exposure, the spermatic cord and scrotum are relatively large in the neonate, as are the seminal vesicles and adjacent ampullae of the vas deferens. In aberrant testicular descent, the testis may remain in the abdomen, although this is thought to be uncommon because the hormonal and morphological features of the transabdominal phase are relatively simple. By contrast, the indirect endocrine regulation and complex migratory process of the gubernaculum during the inguinoscrotal phase is frequently abnormal, leading to the testis lying in the inguinal or pubic region in 2­5% of neonates. Rarely, the testis may lie in the perineum, in the upper part of the thigh or at the root of the penis. The cause for these aberrant locations is unknown but is most likely to be secondary to aberrant migration of the gubernaculum, perhaps caused by a mislocated genitofemoral nerve. Testes that have descended may not remain within the scrotum if the spermatic cord does not double its length between birth and puberty (Hutson 2013). It is thought that the aetiology of such acquired unde scended testes is also linked to that of hydrocele and hernia. Cryptorchidism is common in infants with abdominal wall defects such as bladder exstrophy, exomphalos (30% affected) and gastroschisis (15% affected). It is also seen in myelomeningocoele affecting the upper lumbar spinal cord (>30% affected), although in these latter cases it is not clear whether low abdominal pressure or genitofemoral nucleus dysplasia is the cause (Hutson 2012). Cryptorchidism used to be con sidered a relatively minor birth defect that was corrected surgically sometime during childhood. It is now considered to be a symptom of testicular dysgenesis syndrome, a spectrum that includes hypospadias, impaired semen quality and testicular germ cell cancer (Toppari et al 2014). Since germ cell numbers decrease rapidly in undescended testes, orchipexy is now undertaken between 6­9 months of postnatal life. Further delay results in impaired testicular catchup growth in boys: even with early orchipexy, men with bilateral undescended testes are six times more likely to be infertile (Lee and Shortliffe 2014). Descent of the ovary the relative movements of the ovary are less extensive than those of the testis and are not hormonally regulated. Like the testis, the ovary ulti mately reaches a lower level than it occupies in the early months of fetal life, but it does not leave the pelvis to enter the inguinal canal, except in certain anomalies. A mesenchymatous gubernaculum develops in this fold but, as it traverses the mesonephric fold, it acquires an addi tional attachment to the lateral margin of the uterus near the entrance of the uterine tube. Its lower part, caudal to this uterine attachment, becomes the round ligament of the uterus, and the part cranial to this becomes the ovarian ligament. This new uterine attachment may be correlated with the restricted ovarian descent.

Along with the increasing size of myofibrils interpol virus 300 mg cefdinir purchase, the enzyme systems that provide energy also increase antibiotic list drugs purchase cheap cefdinir on line. This increase is especially true of the enzymes for glycolysis antibiotics for uti planned parenthood discount cefdinir 300 mg online, allowing rapid supply of energy during short-term forceful muscle contraction antibiotics used uti order cefdinir no prescription. When a muscle remains unused for many weeks virus 8 month old baby 300 mg cefdinir for sale, the rate of degradation of the contractile proteins is more rapid than the rate of replacement. Proteasomes are large protein complexes that degrade damaged or unneeded proteins by proteolysis, a chemical reaction that breaks peptide bonds. Ubiquitin is a regulatory protein that basically labels which cells will be targeted for proteosomal degradation. Another type of hyper- added as rapidly as several per minute in newly developing muscle, illustrating the rapidity of this type of hypertrophy. Conversely, when a muscle continually remains shortened to less than its normal length, sarcomeres at the ends of the muscle fibers can actually disappear. It is by these processes that muscles are continually remodeled to have the appropriate length for proper muscle contraction. When it does occur, the mechanism is linear splitting of previously enlarged fibers. When a muscle loses its nerve supply, it no longer receives the contractile signals that are required to maintain normal muscle size. After about 2 months, degenerative changes also begin to appear in the muscle fibers. If the nerve supply to the muscle grows back rapidly, full return of function can occur in as little as 3 months, but from that time onward, the capability of functional return becomes less and less, with no further return of function after 1 to 2 years. In the final stage of denervation atrophy, most of the muscle fibers are destroyed and replaced by fibrous and fatty tissue. The fibers that do remain are composed of a long cell membrane with a lineup of muscle cell nuclei but with few or no contractile properties and little or no capability of regenerating myofibrils if a nerve does regrow. The fibrous tissue that replaces the muscle fibers during denervation atrophy also has a tendency to continue shortening for many months, which is called contracture. Therefore, one of the most important problems in the practice of physical therapy is to keep atrophying muscles from developing debilitating and disfiguring contractures. This goal is achieved by daily stretching of the muscles or use of appliances that keep the muscles stretched during the atrophying process. When some but not trophy occurs when muscles are stretched to greater than normal length. This stretching causes new sarcomeres to be added at the ends of the muscle fibers, where they attach to the tendons. In fact, new sarcomeres can be all nerve fibers to a muscle are destroyed, as commonly occurs in poliomyelitis, the remaining nerve fibers branch off to form new axons that then innervate many of the paralyzed muscle fibers. This process results in large motor units called macromotor units, which can contain as many as five times the normal number of muscle fibers for each motoneuron coming from the spinal cord. The formation of large motor units decreases the fineness of control one has over the muscles but does allow the muscles to regain varying degrees of strength. Several hours after death, all the muscles of the body go into a state of contracture called "rigor mortis"; that is, the muscles contract and become rigid, even without action potentials. The muscles remain in rigor until the muscle proteins deteriorate about 15 to 25 hours later, which presumably results from autolysis caused by enzymes released from lysosomes. The muscular dystrophies include several inherited disorders that cause progressive weakness and degeneration of muscle fibers, which are replaced by fatty tissue and collagen. This disease affects only males because it is transmitted as an X-linked recessive trait and is caused by a mutation of the gene that encodes for a protein called dystrophin, which links actins to proteins in the muscle cell membrane. Dystrophin and associated proteins form an interface between the intracellular contractile apparatus and the extracellular connective matrix. Although the precise functions of dystrophin are not completely understood, lack of dystrophin or mutated forms of the protein cause muscle cell membrane destabilization, activation of multiple pathophysiological processes, including altered intracellular calcium handling, and impaired membrane repair after injury. One important effect of abnormal dystrophin is an increase in membrane permeability to calcium, thus allowing extracellular calcium ions to enter the muscle fiber and to initiate changes in intracellular enzymes that ultimately lead to proteolysis and muscle fiber breakdown. As discussed in Chapter 6, each nerve fiber, after entering the muscle belly, normally branches and stimulates from three to several hundred skeletal muscle fibers. Each nerve ending makes a junction, called the neuromuscular junction, with the muscle fiber near its midpoint. The action potential initiated in the muscle fiber by the nerve signal travels in both directions toward the muscle fiber ends. With the exception of about 2 percent of the muscle fibers, there is only one such junction per muscle fiber. In the synaptic space are large quantities of the enzyme acetylcholinesterase, which destroys acetylcholine a few milliseconds after it has been released from the synaptic vesicles. To each side of each dense bar are protein particles that penetrate the neural membrane; these are voltage-gated calcium channels. When an action potential spreads over the terminal, these channels open and allow calcium ions to diffuse from the synaptic space to the interior of the nerve terminal. The calcium ions, in turn, are believed to activate Ca2+-calmodulin dependent protein kinase, which, in turn, phosphorylates synapsin proteins that anchor the acetylcholine vesicles to the cytoskeleton of the presynaptic terminal. This process frees the acetylcholine vesicles from the cytoskeleton and allows them to move to the active zone of the presynaptic neural membrane adjacent to the dense bars. The vesicles then dock at the release sites, fuse with the neural membrane, and empty their acetylcholine into the synaptic space by the process of exocytosis. Although some of the aforementioned details are speculative, it is known that the effective stimulus for causing acetylcholine release from the vesicles is entry of calcium ions and that acetylcholine from the vesicles is then emptied through the neural membrane adjacent to the dense bars. The nerve fiber forms a complex of branching nerve terminals that invaginate into the surface of the muscle fiber but lie outside the muscle fiber plasma membrane. It is covered by one or more Schwann cells that insulate it from the surrounding fluids. The invaginated membrane is called the synaptic gutter or synaptic trough, and the space between the terminal and the fiber membrane is called the synaptic space or synaptic cleft. At the bottom of the gutter are numerous smaller folds of the muscle membrane called subneural clefts, which greatly increase the surface area at which the synaptic transmitter can act. Notetheproximity of the release sites in the neural membrane to the acetylcholine receptorsinthemusclemembrane,atthemouthsofthesubneural clefts. Each receptor is a protein complex that has a total molecular weight of approximately 275,000. The fetal acetylcholine receptor complex is composed of five subunit proteins, two alpha proteins and one each of beta, delta, and gamma proteins. In the adult, an epsilon protein substitutes for the gamma protein in this receptor complex. The channel remains constricted, as shown in part A of the figure, until two acetylcholine molecules attach respectively to the two alpha subunit proteins. This attachment causes a conformational change that opens the channel, as shown in part B of the figure. Patch clamp studies have shown that one of these channels, when opened by acetylcholine, can transmit 15,000 to 30,000 sodium ions in a millisecond. A, Weakened end plate potential recorded in a curarized muscle that is too weak to elicit an action potential. A Na+ Ach ­ ­ ­ ­ ­ ­ In turn, this end plate potential initiates an action potential that spreads along the muscle membrane and thus causes muscle contraction. B, After acetylcholine (Ach) has become attached and a conformational changehasopenedthechannel,allowingsodiumionstoenterthe muscle fiber and excite contraction. Note the negative charges at the channel mouth that prevent passage of negative ions such as chlorideions. In practice, far more sodium ions flow through the acetylcholine-gated channels than any other ions, for two reasons. First, there are only two positive ions in large concentration: sodium ions in the extracellular fluid and potassium ions in the intracellular fluid. Second, the negative potential on the inside of the muscle membrane, -80 to -90 millivolts, pulls the positively charged sodium ions to the inside of the fiber, while simultaneously preventing efflux of the positively charged potassium ions when they attempt to pass outward. This action creates a local positive potential change inside the muscle fiber membrane, called the end plate potential. However, it is removed rapidly by two means: (1) Most of the acetylcholine is destroyed by the enzyme acetylcholinesterase, which is attached mainly to the spongy layer of fine connective tissue that fills the synaptic space between the presynaptic nerve terminal and the postsynaptic muscle membrane, and (2) a small amount of acetylcholine diffuses out of the synaptic space and is then no longer available to act on the muscle fiber membrane. The short time that the acetylcholine remains in the synaptic space-a few milliseconds at most-normally is sufficient to excite the muscle fiber. Then the rapid removal of the acetylcholine prevents continued muscle re-excitation after the muscle fiber has recovered from its initial action potential. The sudden insurgence of sodium ions into the muscle fiber when the acetylcholine-gated channels open causes the electrical potential inside the fiber at the local area of the end plate to increase in the positive direction as much as 50 to 75 millivolts, creating a local potential called the end plate potential. Recall from Chapter 5 that a sudden increase in nerve membrane potential of more than 20 to 30 millivolts is normally sufficient to initiate more and more sodium channel opening, thus initiating an action potential at the muscle fiber membrane. By contrast, end plate potential B is much stronger and causes enough sodium channels to open so that the self-regenerative effect of more and more sodium ions flowing to the interior of the fiber initiates an action potential. The weakness of the end plate potential at point A was caused by poisoning of the muscle fiber with curare, a drug that blocks the gating action of acetylcholine on the acetylcholine channels by competing for the acetylcholine receptor sites. The weakness of the end plate potential at point C resulted from the effect of botulinum toxin, a bacterial poison that decreases the quantity of acetylcholine release by the nerve terminals. Safety Factor for Transmission at the Neuromuscular Junction; Fatigue of the Junction. Ordinarily, each impulse that arrives at the neuromuscular junction causes about three times as much end plate potential as that required to stimulate the muscle fiber. Therefore, the normal neuromuscular junction is said to have a high safety factor. However, stimulation of the nerve fiber at rates greater than 100 times per second for several minutes often diminishes the number of acetylcholine vesicles so much that impulses fail to pass into the muscle fiber. This situation is called fatigue of the neuromuscular junction, and it is the same effect that causes fatigue of synapses in the central nervous system when the synapses are overexcited. Under normal functioning conditions, measurable fatigue of the neuromuscular junction occurs rarely, and even then only at the most exhausting levels of muscle activity. Molecular Biology of Acetylcholine Formation and Release Formation and release of acetylcholine at the neuromuscular junction occur in the following stages: 1. Small vesicles, about 40 nanometers in size, are formed by the Golgi apparatus in the cell body of the motoneuron in the spinal cord. These vesicles are then transported by axoplasm that "streams" through the core of the axon from the central cell body in the spinal cord all the way to the neuromuscular junction at the tips of the peripheral nerve fibers. About 300,000 of these small vesicles collect in the nerve terminals of a single skeletal muscle end plate. Acetylcholine is synthesized in the cytosol of the nerve fiber terminal but is immediately transported through the membranes of the vesicles to their interior, where it is stored in highly concentrated form- about 10,000 molecules of acetylcholine in each vesicle. When an action potential arrives at the nerve terminal, it opens many calcium channels in the membrane of the nerve terminal because this terminal has an abundance of voltage-gated calcium channels. As a result, the calcium ion concentration inside the terminal membrane increases about 100-fold, which in turn increases the rate of fusion of the acetylcholine vesicles with the terminal membrane about 10,000-fold. This fusion makes many of the vesicles rupture, allowing exocytosis of acetylcholine into the synaptic space. Then, after a few milliseconds, the acetylcholine is split by acetylcholinesterase into acetate ion and choline, and the choline is reabsorbed actively into the neural terminal to be reused to form new acetylcholine. The number of vesicles available in the nerve ending is sufficient to allow transmission of only a few thousand nerve-to-muscle impulses. Therefore, for continued function of the neuromuscular junction, new vesicles need to be re-formed rapidly. Within a few seconds after each action potential is over, "coated pits" appear in the terminal nerve membrane, caused by contractile proteins in the nerve ending, especially the protein clathrin, which is attached to the membrane in the areas of the original vesicles. Within about 20 seconds, the proteins contract and cause the pits to break away to the interior of the membrane, thus forming new vesicles. Within another few seconds, acetylcholine is transported to the interior of these vesicles, and they are then ready for a new cycle of acetylcholine release. Drugs That Enhance or Block Transmission at the Neuromuscular Junction Drugs That Stimulate the Muscle Fiber by AcetylcholineLike Action. Several compounds, including methacholine, carbachol, and nicotine, have nearly the same effect on the muscle fiber as does acetylcholine. The difference between these drugs and acetylcholine is that the drugs are not destroyed by cholinesterase or are destroyed so slowly that their action often persists for many minutes to several hours. The drugs work by causing localized areas of depolarization of the muscle fiber membrane at the motor end plate where the acetylcholine receptors are located. Then, every time the muscle fiber recovers from a previous contraction, these depolarized areas, by virtue of leaking ions, initiate a new action potential, thereby causing a state of muscle spasm. Drugs That Stimulate the Neuromuscular Junction by Inactivating Acetylcholinesterase. Three particularly well- known drugs, neostigmine, physostigmine, and diisopropyl fluorophosphate, inactivate acetylcholinesterase in the synapses so that it no longer hydrolyzes acetylcholine. Therefore, with each successive nerve impulse, additional acetylcholine accumulates and stimulates the muscle fiber repetitively. This activity causes muscle spasm when even a few nerve impulses reach the muscle. Unfortunately, it can also cause death as a result of laryngeal spasm, which smothers the person. Conversely, diisopropyl fluorophosphate, which is a powerful "nerve" gas poison, inactivates acetylcholinesterase for weeks, which makes this poison particularly lethal. For instance, D-tubocurarine blocks the action of acetylcholine on the muscle fiber acetylcholine receptors, thus preventing sufficient increase in permeability of the muscle membrane channels to initiate an action potential. Myasthenia Gravis Causes Muscle Weakness Myasthenia gravis, which occurs in about 1 in every 20,000 persons, causes muscle weakness because of the inability of the neuromuscular junctions to transmit enough signals from the nerve fibers to the muscle fibers. Pathologically, antibodies that attack the acetylcholine receptors have been demonstrated in the blood of most patients with myasthenia gravis. Therefore, myasthenia gravis is believed to be an autoimmune disease in which the patients have developed antibodies that block or destroy their own acetylcholine receptors at the postsynaptic neuromuscular junction.

Elonga tion of the genital folds and urogenital membrane produces a primitive phallus bacterial infection symptoms order cheap cefdinir online. As this structure grows antimicrobial list 300 mg cefdinir purchase otc, it is described as having a cranial surface analogous to the dorsum of the penis infection while pregnant cefdinir 300 mg purchase with visa, and a caudal surface analogous to the perineal surface of both sexes bacteria in mouth 300 mg cefdinir amex. The urogenital sinus bacteria on scalp generic cefdinir 300 mg with visa, contiguous with the internal aspect of the urogenital membrane, becomes attenu ated within the elongating phallus, forming the primitive urethra. The urogenital membrane breaks down at about stage 19, allowing com munication of ectoderm and endoderm at the edges of the disrupted membrane and continuity of the urogenital sinus with the amniotic cavity. The endodermal layer of the attenuated distal portion of the urogenital sinus, which is now displayed on the caudal aspect of the phallus, is termed the urethral plate. As mesenchyme proliferates within the genital folds, the urethral plate sinks into the body of the phallus, forming a primary urethral groove. The genital folds meet proximally in a trans verse ridge immediately ventral to the anal membrane. As a general rule, epithelium, which can be touched easily and has a somatic innervation, is derived from ectoderm. In the buccal cavity and pharynx, the ectoderm/endoderm zone is towards the posterior third of the tongue; touch here usually elicits the gag reflex. In the anal canal, the outer portion, distal to the anal valves, is derived from ecto derm and has a somatic innervation, whereas the epithelium proximal to the valves is derived from endoderm and has an autonomic innervation. As the urethral folds meet to form the terminal part of the urethra, the ventral horns of the ridge fuse to form the frenulum. The epithelial lamella breaks down over the dorsum and sides of the glans to form the preputial sac, and thus free the prepuce from the surface of the glans. Thereafter, the prepuce grows as a free fold of skin, which covers the terminal part of the glans. Although the prepuce and glans begin to separate from the fifth month in utero, they may still be joined at birth. The preputial sac may not be complete until 6­12 months or more after birth and, even then, the presence of some connecting strands may still interfere with the retractability of the prepuce. The mesenchymal core of the phallus is comparatively undifferenti ated in the first 2 months, but the blastemata of the corpora cavernosa become defined during the third month. Despite containing less smooth muscle and elastic tissue than the adult, the neonatal penis is capable of erection. The gelatinous matrix of the gubernaculum is then resorbed and the tunica vaginalis becomes adherent to the connective tissue of the scrotum. Female genitalia the female phallus, which exceeds the male in length in the early stages, becomes the clitoris. The perineal orifice of the urogenital sinus is retained as the cleft between the labia minora, above which the urethra and vagina open. By the fourth month, the female external geni talia can no longer be masculinized by androgens. At birth, neonatal females have relatively enlarged labia minora, clitoris and labia majora. The distal end of the round ligament of the uterus, the gubernaculum ovarii, ends just outside the external inguinal ring. Such individuals are often raised as girls; however, at puberty the external genitalia become responsive to testosterone, which causes masculinization at this time. Male genitalia the growth of male external characteristics is stimulated by androgens regardless of the genetic sex. The genital folds fuse with each other from behind forwards, enclosing the phallic part of the urogenital sinus behind to form the bulb of the urethra, and closing the definitive urethral groove in front to form the greater part of the spongiose urethra. Fusion of the folds results in the formation of a median raphe and occurs in such a way that the lining of the postglan dular urethra is mainly, perhaps wholly, endodermal in origin, formed by canalization of the urethral plate. Thus, as the phallus lengthens, the urogenital orifice is carried onwards until it reaches the base of the glans at the apex of the penis. From the tip of the phallus, an ingrowth of surface ectoderm occurs within the glans to meet and fuse with the penile urethra. Subsequent canalization of the ectoderm permits a con tinuation of the urethra within the glans. The prepuce also begins to develop in the third month, when the primary external orifice of the urethra is still at the base of the glans. A ridge consisting of a mesenchymal core covered by epithelium appears proximal to the neck of the penis and extends forwards over the glans. A solid lamella of epithelium deep to this ridge extends backwards to the base of the glans. The ventral extremities of the ridge curve back Disorders of sex development the acquisition of appropriate gonads, reproductive ducts, external genital structures and matching gender identity occurs through a myriad of complex processes, both local and systemic. Anomalous develop mental processes, leading to differences in sex chromosomes, gonadal structure and position, retention of ductal homologues, androgen 1219 ChaPter 72 DeveloPment of the urogenital system insensitivity, androgen excess, and ambivalent external genitalia requir ing gender assignment, were previously described as intersexual condi tions or hermaphrodism. Such terminology is nonspecific, confusing and perceived as potentially pejorative by affected individuals. The range of anomalous development and its management by multidisciplinary teams, as well as by the affected family, are comprehensively covered by Arboleda and Vilain (2014). The sequence of these events is much less variable than the age at which they take place. Menarche occurs after the peak of the height spurt; onset is more closely related to radiological than to chronological age. It has been suggested that the menarche occurs as a critical weight of 50 kg is attained, and certainly sports and excessive restriction of diet, which may reduce weight below this level, can cause amenorrhoea in women who were previously menstruating normally. Tall girls reach sexual maturity earlier than short ones, but girls with a late adolescent growth spurt and later puberty are ultimately taller on the average than those who pass through the menarche early, for they have longer to grow. Menarche marks a definitive stage of uterine development but does not mean attainment of full reproductive function. The volume of the testes may be estimated: the average adult volume is 20 ml, and a volume of 6 ml indicates that puberty has started. Increased testosterone levels produced by the Leydig cells of the testes promote changes in the larynx, skin and distribution of bodily hair. The figures beneath the bars indicate the range of ages within which each event may begin and end. The velocity of the strength spurt peaks later than the height spurt in boys, associated with testosterone and growth hormone levels. It is appreciated that the assessment and interpretation of the strength spurt during puberty is complex (De Ste Croix 2007). Origin, devel opment and fate of the gubernaculum Hunteri, processus vaginalis peritonei and gonadal ligaments. This paper presents excellent images of early human testis and its descent into the scrotum. This paper examines the molecular processes behind some of the epithelial:mesenchymal interactions occurring in the developing kidney. This paper considers the relationships between testicular development and final testis maturity. This paper considers the importance of Sertoli cell development and the future sperm count of adult males. This paper presents the molecular evidence for the origin of the bladder trigone mucosa. Allard S, Adin P, Gouédard L et al 2000 Molecular mechanisms of hormone mediated Müllerian duct regression: involvement of catenin. This chapter considers the complexities of disorders of sex development and their management. Batourina E, Tsai S, Lambert S et al 2005 Apoptosis induced by vitamin A signalling is crucial for connecting the ureters to the bladder. De Felici M 2013 Origin, migration, and proliferation of human primordial germ cells. De Ste Croix M 2007 Advances in paediatric strength assessment: changing our perspective on strength development. Dias T, Sairam S, Kumarasiri S 2014 Ultrasound diagnosis of fetal renal abnormalities. Faa G, Gerosa C, Fanni D et al 2012 Morphogenesis and molecular mecha nisms involved in human kidney development. Kojima K, Kohri K, Hayashi Y 2010 Genetic pathway of external genitalia formation and molecular etiology of hypospadias. Kurita T 2011 Normal and abnormal epithelial differentiation in the female reproductive tract. Kuroki S, Matoba S, Akiyoshi M et al 2013 Epigenetic regulation of mouse sex determination by the histone demethylase Jmjd1a. Mendelsohn C 2009 Using mouse models to understand normal and abnor mal urogenital tract development. RajpertDe Meyts E 2006 Developmental model for the pathogenesis of testicular carcinoma in situ: genetic and environmental aspects. Runyan C, Schaible K, Molyneaux K et al 2006 Steel factor controls midline cell death of primordial germ cells and is essential for their normal proliferation and migration. Suzuki K, Economides A, Yanagita M et al 2009 New horizons at the cau dal embryo: coordinated urogenital/reproductive organ formation by growth factor signalling. Viana R, Batourina E, Huang H et al 2007 the development of the bladder trigone, the center of the antireflux mechanism. Wang C, Gargollo P, Guo C et al 2011 Six1 and Eya1 are critical regulators of pericloacal mesenchymal progenitors during genitourinary tract development. This paper considers the development of the cloacal region and its separation into enteric and urogenital parts. This paper considers the evidence that impaired nephrogenesis caused by low birth weight may give rise to chronic kidney disease. The true pelvis is considered to start at the level of the plane passing through the promontory of the sacrum, the arcuate line on the ilium, the iliopectineal line and the posterior surface of the pubic crest. In children, the width of the pelvic inlet is an age-independent predictor of chest width and thoracic dimensions (Emans et al 2005). The bones surround a central pelvic canal that forms a ventrally concave curve (the curve of Carus); in the female, it constitutes the birth canal. The details of the topography of the bony and ligamentous pelvis are considered fully in Chapter 80. The fasciae investing the muscles are continuous with visceral pelvic fascia above, perineal fascia below, and obturator fascia laterally. Piriformis Piriformis forms part of the posterolateral wall of the true pelvis and is attached to the anterior surface of the sacrum, the gluteal surface of the ilium near the posterior inferior iliac spine, the capsule of the adjacent sacroiliac joint and, sometimes, to the upper part of the pelvic surface of the sacrotuberous ligament. It passes out of the pelvis through the greater sciatic foramen above the sacrospinous ligament. Within the pelvis, the posterior surface of the muscle lies against the sacrum, and the anterior surface is related to the rectum (especially on the left), the sacral plexus of nerves and branches of the internal iliac vessels. Levator ani and Greater sciatic foramen Obturator internus and the fascia over its upper, inner (pelvic), surface form part of the anterolateral wall of the true pelvis. It is attached to the structures surrounding the obturator foramen, ischio-pubic ramus, the pelvic surface of the hip bone below and behind the pelvic brim, and the upper part of the greater sciatic foramen. It is also attached to the medial part of the pelvic surface of the obturator membrane. The muscle is covered by a fascial layer, and the muscle fibres can be seen through this semi-transparent membrane from within the pelvis. Those muscles relating only to the pelvis or perineum have been omitted for clarity. The superior gluteal and obturator vessels and nerves, as well as the pelvic viscera, have been omitted for clarity. The anorectal junction, vagina and urethra have been divided at the level of the pelvic floor. Pubococcygeus Iliococcygeus Rectum Ischium Ischiococcygeus Piriformis Anococcygeal ligament Sacrum Third and fourth sacral foramina Iliac wing portion of obturator internus can be seen from above. In the male, the upper portion lies lateral to the bladder, the obturator and vesical vessels, and the obturator nerve. In the female, the attachments of the broad ligament of the uterus, the ovarian end of the uterine tubes and the uterine vessels also lie medial to obturator internus and its fascia. Levator ani (pubococcygeus, iliococcygeus and puborectalis) Levator ani is a broad muscular sheet of variable thickness attached to the internal surface of the pelvis. The muscle is subdivided into named portions according to their attachments and the pelvic viscera to which they are related (pubococcygeus, iliococcygeus and puborectalis). These parts are often referred to as separate muscles but the boundaries between each part cannot be easily distinguished and, moreover, they perform many similar physiological functions. Ischiococcygeus (coccygeus) lies immediately cranial to levator ani and is contiguous with it. Pubococcygeus is often subdivided into separate parts according to the pelvic viscera to which each part relates (puboperinealis, puboprostaticus or pubovaginalis, puboanalis, puborectalis). Levator ani arises from each side of the walls of the pelvis along the condensation of the obturator fascia (the tendinous arch of levator ani). Fibres from ischiococcygeus attach to the sacrum and coccyx but the remaining parts of the muscle converge in the midline. Fibres from iliococcygeus join by a partly fibrous intersection and form the iliococcygeal raphe posterior to the anorectal junction. Closer to the anorectal junction, and elsewhere in the pelvic floor, the fibres are more nearly continuous with those of the opposite side, such that the muscle forms a sling (iliococcygeus, puborectalis).

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