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Smith & Tanagho’s

General Urology
NINETEENTH EDITION
Edited by
Jack W. McAninch, MD, FACS, FRCS(E)(Hon)

Professor of Urology
University of California School of Medicine
Chief, Department of Urology
San Francisco General Hospital
San Francisco, California
Tom F. Lue, MD, FACS, ScD (Hon)

Department of Urology
University of California School of Medicine
New York Chicago San Francisco Athens London Madrid Mexico City
Milan New Delhi Singapore Sydney Toronto
McAninch_FM_pi-xii.indd 1 11/02/20 11:21 AM

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Contents
Contributors vii 10 Laparoscopic Surgery 149
Preface xi
David B. Bayne, MD, MPH;
J. Stuart Wolf, Jr., MD, FACS;
1 Anatomy of the Genitourinary Tract 1
Marshall L. Stoller, MD; & Thomas Chi, MD
Emil A. Tanagho, MD; &
Tom F. Lue, MD, ScD (Hon), FACS 11 Robotic Surgery in Urology 167
Maxwell V. Meng, MD, MPH
2 Embryology of the Genitourinary System 17
Emil A. Tanagho, MD; Hiep T. Nguyen, MD; 12 Urinary Obstruction & Stasis 177
& Michael DiSandro, MD
Marshall L. Stoller, MD; &
3 Symptoms of Disorders of the
Genitourinary Tract 31
13 Vesicoureteral Reflux 191
Benjamin N. Breyer, MD, MAS, FACS
Thomas W. Gaither, MD, MAS; &
Hillary L. Copp, MD, MS
4 Physical Examination of the
Genitourinary Tract 41
14 Bacterial Infections of the
Maxwell V. Meng, MD, MPH; & Genitourinary Tract 201
Emil A. Tanagho, MD
Mary K. Wang, MD; &
Hillary L. Copp, MD, MS
5 Urologic Laboratory Examination 49
Anobel Y. Odisho, MD, MPH; 15 Specific Infections of the
Sima P. Porten, MD, MPH; & Genitourinary Tract 229
Kirsten L. Greene, MD, MS
Emil A. Tanagho, MD; &
Christopher J. Kane, MD, FACS
6 Radiology of the
Urinary Tract 63
16 Sexually Transmitted Infections 243
Daniela Franz, MD; Scott Gerst, MD; &
Hedvig Hricak, MD, PhD Kristin Madden, PharmD;
Amanda B. Reed-Maldonado, MD, FACS;
& John N. Krieger, MD
7 Vascular Interventional Radiology 107
Ryan Kohlbrenner, MD; & Roy L. Gordon, MD 17 Urinary Stone Disease 259
Marshall L. Stoller, MD
8 Retrograde Instrumentation of
the Urinary Tract 117
18 Injuries to the Genitourinary Tract 291
9 Percutaneous Endourology and
Ureterorenoscopy 129 19 Urothelial Carcinoma: Cancers of the
Bladder, Ureter, and Renal Pelvis 309
David B. Bayne, MD, MPH;
Joachim W. Thüroff, MD; Badrinath R. Konety, MD, MBA; &
Rolf Gillitzer, MD; & Thomas Chi, MD Peter R. Carroll, MD, MPH
iii

iv Contents
20 Renal Parenchymal Neoplasms 329 31 Disorders of the Adrenal Glands 509

Anobel Y. Odisho, MD, MPH; & Michelle L. McDonald, MD; &
Kirsten L. Greene, MD, MS Christopher J. Kane, MD, FACS
21 Cancer of the Prostate Gland 351 32 Disorders of the Kidneys 521

Matthew R. Cooperberg, MD, MPH; David B. Bayne, MD, MPH;
Samuel L. Washington III, MD; & Jack W. McAninch, MD, FACS, FRCS(E)(Hon); &
Peter R. Carroll, MD, MPH Thomas Chi, MD
22 Genital Tumors 377 33 Diagnosis of Medical Renal Diseases 539

Sima P. Porten, MD, MPH; & Brian K. Lee, MD; & Flavio G. Vincenti, MD
Joseph C. Presti, Jr., MD
34 Acute Kidney Injury and Oliguria 551
23 Urinary Diversion and
Brian K. Lee, MD; & Flavio G. Vincenti, MD
Bladder Substitutions 391
Maxwell V. Meng, MD, MPH; 35 Chronic Kidney Disease and
Susan Barbour, RN, MS, WOCN; & Renal Replacement Therapy 557
Peter R. Carroll, MD, MPH
Brian K. Lee, MD; &
Flavio G. Vincenti, MD
24 Systemic Therapy of Urologic Tumors 407
Vadim S. Koshkin, MD; & Eric J. Small, MD 36 Renal Transplantation 563
John M. Barry, MD
25 Immunotherapy in
Urologic Malignancies 415
37 Disorders of the Ureter and
Arpita Desai, MD; & Eric J. Small, MD Ureteropelvic Junction 571
Barry A. Kogan, MD
26 Radiotherapy of
Urologic Tumors 421
38 Disorders of the Bladder, Prostate,
Yun Rose Li, MD, PhD; and Seminal Vesicles 585
Alexander R. Gottschalk, MD, PhD; &
Mack Roach III, MD Samuel L. Washington III, MD; &
Katsuto Shinohara, MD
27 Neurophysiology and Pharmacology
of the Lower Urinary Tract 453 39 Male Sexual Dysfunction 605
Karl-Erik Andersson, MD, PhD Amanda B. Reed-Maldonado, MD, FACS; &
Tom F. Lue, MD
28 Neurogenic Bladder 473
40 Women’s Sexual Health 631
Anne M. Suskind, MD, MS, FACS
Alan W. Shindel, MD, MAS; &
Tami S. Rowen, MD, MS
29 Urodynamics 485
Anne M. Suskind, MD, MS, FACS 41 Disorders of the Penis and
Male Urethra 645
30 Urinary Incontinence 499
Benjamin N. Breyer, MD, MAS, FACS; &
Tom F. Lue, MD, FACS, ScD (Hon); & Jack W. McAninch, MD, FACS, FRCS(E)(Hon)
Emil A. Tanagho, MD

Contents v
42 Disorders of the Female Urethra 659 46 Genital Gender-Affirming Surgery:

Patient Care, Decision Making, and
Donna Y. Deng, MD, MS
Surgery Options 747
43 Disorders of Sex Development 671 Maurice M. Garcia, MD, MAS
Laurence S. Baskin, MD
47 History and Physical Examination in
Pediatric Urology 769
44 Male Infertility 703
Michael DiSandro, MD
Thomas J. Walsh, MD, MS; &
James F. Smith, MD, MS
48 Introduction to Clinical
Research Design 781
45 The Aging Male 735
June M. Chan, ScD; David Tat, DO; &
James F. Smith, MD, MS; Stacey Kenfield, ScD
Bogdana Schmidt, MD, MPH; &
Thomas J. Walsh, MD, MS Index 793

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Contributors
Karl-Erik Andersson, MD, PhD June M. Chan, ScD
Institute for Regenerative Medicine Program Director, Genitourinary Cancer Epidemiology and
Wake Forest University School of Medicine Population Sciences
Winston Salem, North Carolina Department of Urology
UCSF School of Medicine
Susan Barbour, RN, MS, WOCN San Francisco, California
Palliative Care Services
UCSF School of Medicine Thomas Chi, MD
San Francisco, California Associate Professor and Katzman Endowed Professor in
Clinical Urology
John M. Barry, MD Department of Urology
Professor of Urology and Professor of Surgery UCSF School of Medicine
Division of Abdominal Organ Transplantation San Francisco, California
Organ Health and Science University
Portland, Oregon Matthew R. Cooperberg, MD, MPH
Associate Professor
Laurence S. Baskin, MD Department of Urology
Chief of Pediatric Urology Helen Diller Family Comprehensive Cancer Center
University of California Children’s Medical Center UCSF School of Medicine
UCSF School of Medicine San Francisco, California
Attending Urologist Hillary L. Copp, MD, MS
Children’s Hospital Oakland Associate Professor of Urology and Pediatric Urology
Oakland, California Fellowship Director
Benioff Children’s Hospital
David B. Bayne, MD, MPH UCSF School of Medicine
Endourology Fellow San Francisco, California
UCSF School of Medicine Donna Y. Deng, MD, MS
San Francisco, California Neurourology Lead, Kaiser Permanente Northern
California
Benjamin N. Breyer, MD, MAS, FACS Medical Director, Kaiser NorCal Regional Spina Bifida
Associate Professor and Vice Chair Program
Department of Urology Associate Fellowship Director, Female Pelvic Medicine
UCSF School of Medicine Reconstructive Surgery, Kaiser East Bay/UCSF
San Francisco, California Oakland, California
Peter R. Carroll, MD, MPH Arpita Desai, MD

Professor Clinical Instructor
Ken and Donna Derr-Chevron Endowed Chair in Department of Genitourinary Medical Oncology
Prostate Cancer Helen Diller Family Comprehensive Cancer Center
Department of Urology UCSF School of Medicine
UCSF School of Medicine San Francisco, California
vii

viii Contributors
Michael DiSandro, MD Kirsten L. Greene, MD, MS

Professor of Urology Professor and Chair
Department of Urology Department of Urology
UCSF School of Medicine University of Virginia
San Francisco, California Charlottesville, Virginia
Daniela Franz, MD Hedvig Hricak, MD, PhD

Department of Diagnostic and Interventional Radiology Chair
Klinikum rechts der Isar Department of Radiology
Munich Technical University Memorial Sloan-Kettering Cancer Center
Munich, Germany Professor of Radiology
Cornell University
Thomas W. Gaither, MD, MAS New York, New York
Urology resident
University of California Christopher J. Kane, MD, FACS
Los Angeles, California Dean of Clinical Affairs
UC San Diego School of Medicine
Maurice M. Garcia, MD, MAS CEO, UC San Diego Health Physician Group
Associate Professor of Urology and Anatomy (Adjunct) La Jolla, California
Departments of Urology and Anatomy
UCSF Medical Center Stacey A. Kenfield, ScD
San Francisco, California Associate Professor
Director, Cedars-Sinai Transgender Surgery and Department of Urology
Health Program UCSF School of Medicine
Division of Urology San Francisco, California
Cedars-Sinai Medical Center
Los Angeles, California Barry A. Kogan, MD
Professor, Surgery and Pediatrics
Scott Gerst, MD Falk Chair in Urology
Associate Attending Physician Albany Medical College
Department of Radiology Albany, New York
Memorial Hospital, Memorial Sloane-Kettering
Cancer Center Ryan Kohlbrenner, MD
New York, New York Assistant Professor of Interventional Radiology
Departments of Radiology and Biomedical Imaging
Rolf Gillitzer, MD UCSF School of Medicine
Clinical Director San Francisco, California
Johannes Gutenberg University Medical Center Mainz Badrinath R. Konety, MD, MBA
Mainz, Germany Associate Dean for Innovation
Roy L. Gordon, MD Director of the Institute for Prostate and Urologic Cancers
Professor of Interventional Radiology University of Iowa
Department of Radiology Iowa City, Iowa
San Francisco, California Vadim S. Koshkin, MD
Assistant Clinical Professor
Alexander R. Gottschalk, MD, PhD Genitourinary Medical Oncologist
Professor of Radiation Oncology Departments of Hematology and Oncology
Director of CyberKnife UCSF School of Medicine
Departments of Radiation and Oncology San Francisco, California

Contributors ix
John N. Krieger, MD Anobel Y. Odisho, MD, MPH

Professor of Urology Assistant Professor
University of Washington School of Medicine Department of Urologic Oncology
Seattle, Washington UCSF School of Medicine
Brian K. Lee, MD
Professor of Medicine Sima P. Porten, MD, MPH
The Connie Frank Kidney Transplant Center Assistant professor
UCSF School of Medicine Department of Urology
San Francisco, California UCSF School of Medicine
Yun Rose Li, MD, PhD
Resident Physician Joseph C. Presti, Jr., MD
Departments of Radiation and Oncology Lead for Urologic Oncology
UCSF School of Medicine Kaiser Permanente Northern California
San Francisco, California Oakland, California
Tom F. Lue, MD, FACS, ScD (Hon) Amanda B. Reed-Maldonado, MD, FACS
Professor of Urology Chief, Male Reproductive Urology
Emil Tanagho Endowed Chair in Clinical Urology Department of Urology
Department of Urology Tripler Army Medical Center
UCSF School of Medicine Honolulu, Hawaii
Mack Roach III, MD
Kristin Madden, PharmD Professor of Radiation Oncology and Urology
Pharmacist Department of Urology
Department of Veterans Affairs UCSF School of Medicine
San Antonio, Texas San Francisco Comprehensive Cancer Center
Jack W. McAninch, MD, FACS, FRCS(E)(Hon)
Professor of Urology Tami S. Rowen, MD, MS
UCSF School of Medicine Assistant Professor
San Francisco, California Departments of Obstetrics, Gynecology, and
Reproductive Sciences
Michelle L. McDonald, MD UCSF School of Medicine
Urologist San Francisco, California
San Diego, California
Bogdana Schmidt, MD, MPH
Maxwell V. Meng, MD, MPH Urologic Oncology Fellow
Professor Stanford University Medical Center
Department of Urology Stanford, California
San Francisco, California Alan W. Shindel, MD, MAS
Associate Professor
Hiep T. Nguyen, MD Department of Urology
Associate Professor University of California
Surgery and Urology Davis, California
Harvard Medical School and Children’s Hospital
Boston, Massachusetts

x Contributors
Katsuto Shinohara, MD David Tat, DO

Professor Infectious Disease Specialist
Helen Diller Family Chair in Clinical Urology Moses H. Cone Memorial Hospital
Department of Urology Greensboro, North Carolina
San Francisco, California Joachim W. Thüroff, MD
Professor
Eric J. Small, MD Department of Urology
Professor of Medicine and Urology University Medical Center
Urologic Oncology Program and Program Member, Mannheim, Germany
Comprehensive Cancer Center
UCSF School of Medicine Flavio G. Vincenti, MD
San Francisco, California Professor of Medicine
The Connie Frank Kidney Transplant Center
James F. Smith, MD, MS UCSF School of Medicine
Associate Professor San Francisco, California
Director, Male Reproductive Health
Departments of Urology, Obstetrics, Gynecology, and Thomas J. Walsh, MD, MS
Reproductive Sciences Associate Professor
UCSF School of Medicine Department of Urology
San Francisco, California University of Washington School of Medicine
Seattle, Washington
Professor of Urology Mary K. Wang, MD
Department of Urology Childrens’ Urology
UCSF School of Medicine Austin, Texas
Samuel L. Washington, III, MD
Anne M. Suskind, MD, MS, FACS Urologic Oncology Clinical Fellow
Associate Professor of Urology, Obstetrics, Gynecology, and Department of Urology
Reproductive Sciences UCSF School of Medicine
Director, Neurourology, Female Pelvic Medicine & San Francisco, California
Reconstructive Surgery
UCSF School of Medicine J. Stuart Wolf, Jr., MD, FACS
San Francisco, California Professor, Department of Surgery and Perioperative Care
Dell Medical School
Emil A. Tanagho, MD The University of Texas at Austin
Professor of Urology Austin, Texas

Preface
Smith & Tanagho’s General Urology, nineteenth edition, provides the updated information for the understanding, diagnosis,
and treatment of urological diseases in a concise and well-organized format. The book is up-to-date, to the point, and readable.
Medical students will find this book useful because of its concise, easy-to-follow format, and its breadth of information on
common urological diseases. Residents, as well as practicing physicians in urology, family practice, or general medicine, will find
it an efficient and current reference, particularly because of its emphasis on diagnosis and treatment.
This nineteenth edition has been thoroughly updated with clinical information and current references. The reader will find
that this edition is written in an uncomplicated, straightforward manner that provides relevant clinical information and guide-
lines for diagnosis and management of urologic conditions. Chapters on immunotherapy in urologic malignancies, radiotherapy
of urologic tumors, urinary incontinence, and vascular interventional radiology have all undergone extensive revision. For
this current edition, we have added two chapters on the timely topic of gender dysphoria and introduction to clinical research
design.
Many illustrations and figures have been modernized and improved with added color. The classic fine anatomic drawings
demonstrate well the important clinical findings.
This book has been one of the leading sources of information for students, trainees, and urologists around the world. In addi-
tion to English, this book has been published in many other foreign languages, like Chinese, French, Greek, Italian, Japanese,
Korean, Portuguese, Russian, Spanish, and Turkish.
We greatly appreciate the patience and efforts of our McGraw-Hill staff, the expertise of our contributors, and the support
of our readers.
Jack W. McAninch, MD, FACS, FRCS(E) (Hon)

San Francisco, California, January 2020
xi

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1
1
Anatomy of the
Genitourinary Tract
Emil A. Tanagho, MD; & Tom F. Lue, MD, ScD (Hon), FACS
Urology deals with diseases and disorders of the adrenal ▶▶Blood Supply
gland, the male genitourinary tract, and the female
urinary tract. These systems are illustrated in Figures 1–1 A. Arterial
and 1–2. Each adrenal gland receives three arteries: one from the infe-
rior phrenic artery, one from the aorta, and one from the
ADRENALS renal artery.
B. Venous
▶▶Gross Appearance
A. Anatomy Blood from the right adrenal gland is drained by a very short
vein into the vena cava; the left adrenal vein terminates in the
Each kidney is capped by an adrenal gland, and both left renal vein.
organs are enclosed within Gerota’s (perirenal) fascia.
Each adrenal gland weighs 4–5 g. The right adrenal is tri- ▶▶Lymphatics
angular in shape; the left is more rounded and crescentic.
The average dimensions are 3 cm width, 5 cm length, and The lymphatic vessels accompany the suprarenal vein and
1 cm thickness. Each gland is composed of a cortex, chiefly drain into the lumbar lymph nodes.
influenced by the pituitary gland, and a medulla derived
from chromaffin tissue (Avisse et al, 2000; O’Donoghue KIDNEYS
et al, 2010).
B. Relations A. Anatomy
Figure 1–2 shows the relationships between the adrenals and The kidneys lie along the borders of the psoas muscles and
other organs. The right adrenal lies between the liver and are therefore obliquely placed. The position of the liver
the vena cava. The left adrenal lies close to the aorta and is causes the right kidney to be lower than the left (Figures 1–2
covered on its lower surface by the pancreas. The spleen lies and 1–3). The adult kidney weighs between 125 and 170 g in
superior and lateral to it. men and 115 and 155 g in women. It is about 10–12 cm long,
5–7 cm wide, and 3–5 cm thick.
The kidneys are supported by the perirenal fat (which is
▶▶Histology enclosed in the perirenal fascia), the renal vascular pedicle,
The adrenal cortex, which makes up 85% of the mass, is com- abdominal muscle tone, and the general bulk of the abdomi-
posed of three distinct layers: the outer zona glomerulosa, the nal viscera (Rusinek et al, 2004). Variations in these factors
middle zona fasciculata, and the inner zona reticularis. The permit variations in the degree of renal mobility. The aver-
medulla lies centrally and is made up of polyhedral cells with age descent on inspiration or on assuming the upright posi-
hormone-containing granular cytoplasm. These chromaf- tion is 4–5 cm. Lack of mobility suggests abnormal fixation
fin cells are accompanied by a small number of sympathetic (eg, perinephritis), but extreme mobility is not necessarily
ganglion cells. pathologic.
McAninch_CH01_p001-p016.indd 1 07/02/20 9:58 AM

2 SMITH & TANAGHO’S GENERAL UROLOGY
▲▲Figure 1–1. Anatomy of the male genitourinary tract. The upper tract and midtract have urologic function only.
The lower tract has both genital and urinary functions.

ANATOMY OF THE GENITOURINARY TRACT CHAPTER 1 3
▲▲Figure 1–2. Relations between the kidneys, ureters, and bladder (anterior aspect).
On longitudinal section (Figure 1–4), the kidney is seen gastrointestinal symptoms that accompany kidney diseases
to be made up of an outer cortex, a central medulla, and the (Glassberg, 2002).
internal calices and pelvis. The cortex is homogeneous in
appearance. Portions of it project toward the pelvis between ▶▶Histology
the papillae and fornices and are called the columns of A. Nephron
Bertin. The medulla consists of numerous pyramids formed
by the converging collecting renal tubules, which drain into The functioning unit of the kidney is the nephron, which is
the minor calices at the tip of the papillae. composed of a tubule that has both secretory and excretory
functions (Figure 1–4). The secretory portion is contained
largely within the cortex and consists of a renal corpuscle and
B. Relations
the secretory part of the renal tubule. The excretory portion of
Figures 1–2 and 1–3 show the relationships between the this duct lies in the medulla. The renal corpuscle is composed
kidneys and adjacent organs and structures. Their intimacy of the vascular glomerulus, which projects into Bowman’s cap-
with intraperitoneal organs and the autonomic innervation sule, which, in turn, is continuous with the epithelium of the
that they share with these organs explain, in part, some of the proximal convoluted tubule. The secretory portion of the renal

▲▲Figure 1–3. Relations between the kidneys (posterior aspect). The dashed lines represent the outline of the kidneys,
where they are obscured by overlying structures.
tubule is made up of the proximal convoluted tubule, the loop of the posterior surface. The anterior branch supplies both
of Henle, and the distal convoluted tubule. upper and lower poles as well as the entire anterior surface.
The excretory portion of the nephron is the collecting The renal arteries are all end arteries.
tubule, which is continuous with the distal end of the ascend- The renal artery branches further divide into interlobar
ing limb of the convoluted tubule. It empties its contents arteries, which travel in the columns of Bertin (between the
through the tip (papilla) of a pyramid into a minor calyx. pyramids) and then arch along the base of the pyramids
(arcuate arteries). These arteries then divide as interlobular
B. Supporting Tissue arteries. From these vessels, smaller (afferent) branches pass
to the glomeruli. From the glomerular tuft, efferent arterioles
The renal stroma is composed of loose connective tissue and
pass to the tubules in the stroma.
contains blood vessels, capillaries, nerves, and lymphatics.
B. Venous
▶▶Blood Supply (Figures 1–2, 1–4, and 1–5)
The renal veins are paired with the arteries, but any of them
A. Arterial
will drain the entire kidney if the others are tied off.
Usually there is one renal artery, a branch of the aorta that Although the renal artery and vein are usually the sole blood
enters the hilum of the kidney between the pelvis, which vessels of the kidney, accessory renal vessels are common and
normally lies posteriorly, and the renal vein. It may branch may be of clinical importance if they are so placed so as to com-
before it reaches the kidney, and two or more separate arter- press the ureter, in which case hydronephrosis may result.
ies may be noted (Budhiraja et al, 2010). In duplication of the
pelvis and ureter, it is common for each renal segment to have
its own arterial supply. ▶▶Nerve Supply
The renal artery divides into anterior and posterior The renal nerves derived from the renal plexus accompany
branches. The posterior branch supplies the midsegment the renal vessels throughout the renal parenchyma.

▲▲Figure 1–4. Anatomy and histology of the kidney and ureter. Upper left: Diagram of the nephron and its blood supply.
(Courtesy of Merck, Sharp, Dohme: Seminar. 1947; 9[3].) Upper right: Cast of the pelvic caliceal system and the arterial
supply of the kidney. Middle: Renal calices, pelvis, and ureter (posterior aspect). Lower left: Histology of the ureter. The
smooth-muscle bundles are arranged in both spirally and longitudinally. Lower right: Longitudinal section of kidney
showing calices, pelvis, ureter, and renal blood supply (posterior aspect).

▲▲Figure 1–5. (A) The posterior branch of the renal artery and its distribution to the central segment of the posterior
surface of the kidney. (B) Branches of the anterior division of the renal artery supplying the entire anterior surface of the
kidney as well as the upper and lower poles at both surfaces. The segmental branches lead to interlobar, arcuate, and
interlobular arteries. (C) The lateral convex margin of the kidney. Brödel’s line, which is 1 cm from the convex margin, is
the bloodless plane demarcated by the distribution of the posterior branch of the renal artery.

▶▶Lymphatics
The lymphatics of the kidney drain into the lumbar lymph
nodes.
CALICES, RENAL PELVIS, AND URETER
A. Anatomy
1. Calices—The tips of the minor calices (8–12 in number)

are indented by the projecting pyramids (Figure 1–4). These
calices unite to form two or three major calices that join to
form the renal pelvis (Sozen et al, 2008).
2. Renal pelvis—The pelvis may be entirely intrarenal or
partly intrarenal and partly extrarenal. Inferomedially, it
tapers to join the ureter.
▲▲Figure 1–6. Anatomy and relations between the
3. Ureter—The adult ureter is about 30 cm long, varying ureters, bladder, prostate, seminal vesicles, and vasa
in direct relation to the height of the individual. It follows a deferentia (anterior view).
rather smooth S curve. Areas that stones are often impacted
are (a) at the ureteropelvic junction, (b) where the ureter
crosses over the iliac vessels, and (c) where it courses through helical and longitudinal smooth-muscle fibers. They are not
the bladder wall. arranged in discrete layers. The outermost adventitial coat is
composed of fibrous connective tissue.
B. Relations
▶▶Blood Supply
1. Calices—The calices are intrarenal and are intimately A. Arterial
related to the renal parenchyma.
The renal calices, pelvis, and upper ureters derive their blood
2. Renal pelvis—If the pelvis is partly extrarenal, it lies along supply from the renal arteries; the midureter is fed by the
the lateral border of the psoas muscle and on the quadratus internal spermatic (or ovarian) arteries. The lowermost por-
lumborum muscle; the renal vascular pedicle is just anterior tion of the ureter is served by branches from the common
to it. The left renal pelvis lies at the level of the first or second iliac, internal iliac (hypogastric), and vesical arteries.
lumbar vertebra; the right pelvis is a little lower.
3. Ureter—On their course downward, the ureters lie on the B. Venous
psoas muscles, pass medially to the sacroiliac joints, and then The veins of the renal calices, pelvis, and ureters are paired
swing laterally near the ischial spines before passing medi- with the arteries.
ally to enter the base of the bladder (Figure 1–2). In females,
the uterine arteries are closely related to the juxtavesical por-
tion of the ureters. The ureters are covered by the posterior
▶▶Lymphatics
peritoneum; their lowermost portions are closely attached to The lymphatics of the upper portions of the ureters as well
it, while the juxtavesical portions are embedded in vascular as those from the pelvis and calices enter the lumbar lymph
retroperitoneal fat (Koff, 2008). nodes. The lymphatics of the midureter pass to the internal
The vasa deferentia, as they leave the internal inguinal iliac (hypogastric) and common iliac lymph nodes; the lower
rings, sweep over the lateral pelvic walls anterior to the ureteral lymphatics empty into the vesical and hypogastric
ureters (Figure 1–6). They lie medial to the latter before join- lymph nodes.
ing the seminal vesicle and penetrating the base of the pros-
tate to become the ejaculatory ducts. BLADDER
▶▶Histology (Figure 1–4) ▶▶Gross Appearance

The walls of the calices, pelvis, and ureters are composed of The bladder is a hollow muscular organ that serves as a res-
transitional cell epithelium under which lies loose connec- ervoir for urine. In women, its posterior wall and dome are
tive tissue (lamina propria). External to these are a mixture of invaginated by the uterus. The adult bladder normally has

a capacity of 400–500 mL. The wall of the bladder is about ▶▶Blood Supply
3–5 mm in thickness; it is thinner when it is distended.
A. Arterial
A. Anatomy The bladder is supplied by the superior, middle, and inferior
When empty, the adult bladder lies behind the pubic sym- vesical arteries, which arise from the anterior trunk of the
physis and is largely a pelvic organ. In infants and children, internal iliac (hypogastric) artery, and by smaller branches
it is situated higher (Berrocal et al, 2002). When it is full, it from the obturator and inferior gluteal arteries. In females,
rises well above the symphysis and can readily be palpated the uterine and vaginal arteries also send branches to the
or percussed. When overdistended, as in acute or chronic bladder.
urinary retention, it may cause the lower abdomen to bulge
visibly. B. Venous
Extending from the dome of the bladder to the umbilicus Surrounding the bladder is a rich plexus of veins that ulti-
is a fibrous cord, the median umbilical ligament, which rep- mately empties into the internal iliac (hypogastric) veins.
resents the obliterated urachus. The ureters enter the bladder
posteroinferiorly in an oblique manner and at these points ▶▶Nerve Supply
are about 5 cm apart (Figure 1–6). The orifices, situated at
the extremities of the crescent-shaped interureteric ridge that The bladder receives innervation from sympathetic and
forms the proximal border of the trigone, are about 2.5 cm parasympathetic nervous systems. The sensory afferent of
apart. The trigone occupies the area between the ridge and the bladder originates from both subepithelial nerve endings
the bladder neck. and nerve fibers between detrusor muscle bundles (Andersson,
The internal sphincter, or bladder neck, is not a true cir- 2010; Birder et al, 2010; McCloskey, 2010).
cular sphincter but a thickening formed by interlaced and
converging muscle fibers of the detrusor as they pass distally ▶▶Lymphatics
to become the smooth muscle component of the urethra. The lymphatics of the bladder drain into the vesical, external
iliac, internal iliac (hypogastric), and common iliac lymph
B. Relations nodes.
In males, the bladder is related posteriorly to the seminal
vesicles, vasa deferentia, ureters, and rectum (Figures 1–7 PROSTATE GLAND
and 1–8). In females, the uterus and vagina are interposed
between the bladder and rectum (Figure 1–9). The dome ▶▶Gross Appearance
and posterior surfaces are covered by peritoneum; hence, in
A. Anatomy
this area, the bladder is closely related to the small intestine
and sigmoid colon. In both males and females, the bladder is The prostate is a fibromuscular and glandular organ lying just
related to the posterior surface of the pubic symphysis, and, inferior to the bladder (Figures 1–6 and 1–7). The normal
when distended, it is in contact with the lower abdominal prostate weighs about 20 g and contains the posterior urethra,
wall. which is about 2.5 cm in length. It is supported anteriorly by
the puboprostatic ligaments and inferiorly by the urogenital
diaphragm (Figure 1–6). The prostate is perforated posteri-
▶▶Histology (Figure 1–10) orly by the ejaculatory ducts, which pass obliquely to empty
The mucosa of the bladder is composed of transitional epi- through the verumontanum on the floor of the prostatic ure-
thelium. Beneath it is a well-developed submucosal layer thra just proximal to the striated external urinary sphincter
formed largely of connective and elastic tissues. The mucosa (Figure 1–11).
may be considered as a single functional unit that consists The prostate can be subdivided into two ways: by lobe
of the epithelial layer, basement membrane, and lamina pro- or by zone. The lobe classification is often used in cystoure-
pria. Physical or chemical stress on the bladder elicits releases throscopic examinations and consists of five lobes: anterior,
of multiple factors that modulate afferent and efferent nerve posterior, median, right lateral, and left lateral. The zone clas-
activities (Fry and Vahabi, 2016). External to the submu- sification is often used in pathology. McNeal (1981) divides
cosa is the detrusor muscle that is made up of a mixture of the prostate into four zones: peripheral zone, central zone
smooth-muscle fibers arranged at random in a longitudi- (surrounds the ejaculatory ducts), transitional zone (sur-
nal, circular, and spiral manner without any layer formation rounds the urethra), and anterior fibromuscular zone (Myers
or specific orientation except for proximity to the internal et al, 2010) (Figure 1–12). The segment of urethra that tra-
meatus, where the detrusor muscle assumes three definite verses the prostate gland is the prostatic urethra. It is lined
layers: inner longitudinal, middle circular, and outer longitu- by an inner longitudinal layer of muscle (continuous with
dinal (John et al, 2001). a similar layer of the vesical wall). Incorporated within the

▲▲Figure 1–7. (A) Anatomic relationship between the bladder, prostate, prostatomembranous urethra, and root of
the penis. (B) Histology of the testis. Seminiferous tubules lined by supporting basement membrane for the Sertoli and
spermatogenic cells. The latter are in various stages of development. (C) Cross sections of the testis and epididymis.
(Images [A] and [C] reproduced with permission from Walsh PC, Campbell MF: Campbell’s Urology, 6th ed. Philadelphia, PA:
Saunders; 1992.)

▲▲Figure 1–8. Top: Relations between the bladder, prostate, seminal vesicles, penis, urethra, and scrotal contents.
Lower left: Transverse section through the penis. The paired upper structures are the corpora cavernosa. The single
lower body surrounding the urethra is the corpus spongiosum. Lower right: Fascial planes of the lower genitourinary
tract. (After Wesson.)
prostate gland is an abundant amount of smooth muscula- separated from the rectum by the two layers of Denonvilliers’
ture derived primarily from the external longitudinal bladder fascia, serosal rudiments of the pouch of Douglas, which
musculature. This musculature represents the involuntary once extended to the urogenital diaphragm (Raychaudhuri
smooth muscle sphincter of the posterior urethra in males. and Cahill, 2008) (Figure 1–8).
B. Relations ▶▶Histology (Figure 1–10)

The prostate gland lies behind the pubic symphysis. Located The prostate consists of a thin fibrous capsule under
closely to the posterosuperior surface are the vasa deferentia which lie circularly oriented smooth-muscle fibers and
and seminal vesicles (Figure 1–7). Posteriorly, the prostate is collagenous tissue that surrounds the urethra (involuntary

▲▲Figure 1–9. Anatomy and relations of the bladder, urethra, uterus and ovary, vagina, and rectum.
▲▲Figure 1–10. Left: Histology of the prostate. Epithelial glands embedded in a mixture of connective and elastic tissue
and smooth muscle. Right: Histology of the bladder. The mucosa is transitional cell in type and lies on a well-developed
submucosal layer of connective tissue. The detrusor muscle is composed of interlacing longitudinal, circular, and spiral
smooth-muscle bundles.

▲▲Figure 1–11. Section of the prostate gland shows the

prostatic urethra, verumontanum, and crista urethralis,
in addition to the opening of the prostatic utricle and
the two ejaculatory ducts in the midline. Note that the
prostate is surrounded by the prostatic capsule, which
is covered by another prostatic sheath derived from the
endopelvic fascia. The prostate is resting on the genitouri-
nary diaphragm. (Reproduced with permission from Walsh
PC, Campbell MF: Campbell’s Urology, 6th ed. Philadelphia,
PA: Saunders; 1992.) ▲▲Figure 1–12. Anatomy of the prostate gland. Prostatic
adenoma develops from the periurethral glands at the
site of the median or lateral lobes. The posterior lobe,
however, is prone to cancerous degeneration. (Adapted
sphincter). Deep in this layer lies the prostatic stroma,
with permission from McNeal JE: The zonal anatomy of the
composed of connective tissues and smooth-muscle fibers
prostate. Prostate 1981;2(1):35–49.)
in which are embedded the epithelial glands. These glands
drain into the major excretory ducts (about 25 in number),
which open chiefly on the floor of the urethra between
the verumontanum and the vesical neck. Just beneath ▶▶Lymphatics
the transitional epithelium of the prostatic urethra lie the The lymphatics from the prostate drain into the internal iliac
periurethral glands. (hypogastric), sacral, vesical, and external iliac lymph nodes
(Saokar et al, 2010).
▶▶Blood Supply
A. Arterial SEMINAL VESICLES
The arterial supply to the prostate is derived from the inferior
vesical, internal pudendal, and middle rectal (hemorrhoidal) ▶▶Gross Appearance
arteries. The seminal vesicles lie just cephalic to the prostate under
the base of the bladder (Figures 1–6 and 1–7). They are about
B. Venous 6 cm long and quite soft. Each vesicle joins its corresponding
vas deferens to form the ejaculatory duct (Kim et al, 2009).
The veins from the prostate drain into the periprostatic The ureters lie medial to each, and the rectum is contiguous
plexus, which has connections with the deep dorsal vein of with their posterior surfaces.
the penis and the internal iliac (hypogastric) veins.
▶▶Histology
▶▶Nerve Supply The mucous membrane is pseudostratified. The submu-
The prostate gland receives a rich innervation from the sym- cosa consists of dense connective tissue covered by a thin
pathetic and parasympathetic nerves of the inferior hypogas- layer of muscle that, in turn, is encapsulated by connective
tric plexus. tissue.

▶▶Blood Supply EPIDIDYMIS

The blood supply of the seminal vesicles is similar to that of
the prostate gland. ▶▶Gross Appearance
A. Anatomy
▶▶Nerve Supply The upper portion of the epididymis (globus major) is con-
The nerve supply is mainly from the sympathetic nerve nected to the testis by numerous efferent ducts from the testis
plexus. (Figure 1–7). The epididymis consists of a markedly coiled
duct that, at its lower pole (globus minor), is continuous with
▶▶Lymphatics the vas deferens. An appendix of the epididymis is often seen
on its upper pole; this is a cystic body that in some cases is
The lymphatics of the seminal vesicles are those that serve
pedunculated, but in others, it is sessile.
the prostate.
B. Relations
SPERMATIC CORD
The epididymis lies posterolateral to the testis and is nearest
▶▶Gross Appearance to the testis at its upper pole. Its lower pole is connected to
the testis by fibrous tissue. The vas lies posteromedial to the
The two spermatic cords extend from the internal ingui- epididymis.
nal rings through the inguinal canals to the testicles
(Figure 1–7). Each cord contains the vas deferens, the
internal and external spermatic arteries, the artery of
▶▶Histology
the vas, the venous pampiniform plexus (which forms The epididymis is covered by serosa. The ductus epididy-
the spermatic vein superiorly), lymph vessels, and nerves midis is lined by pseudostratified columnar epithelium
(Jen et al, 1999). The entire cord contents are enclosed in throughout its length.
investing layers of thin fascia. A few fibers of the cremaster
muscle insert on the cords in the inguinal canal (Bhosale ▶▶Blood Supply
et al, 2008; Kim et al, 2009). A. Arterial
▶▶Histology The arterial supply to the epididymis comes from the internal
spermatic artery and the artery of the vas (deferential artery).
The fascia covering the cord is formed of loose connective
tissue that supports arteries, veins, nerve, and lymphatics. B. Venous
The vas deferens is a small, thick-walled tube consisting of an
internal mucosa and submucosa surrounded by three well- The venous blood drains into the pampiniform plexus, which
defined layers of smooth muscle encased in a covering of becomes the spermatic vein.
fibrous tissue. Above the testes, this tube is straight. Its proxi-
mal 4 cm tends to be convoluted. ▶▶Lymphatics
The lymphatics drain into the external iliac and internal iliac
▶▶Blood Supply (hypogastric) lymph nodes.
A. Arterial
TESTIS
The external spermatic artery, a branch of the inferior epigas-
tric, supplies the fascial coverings of the cord. The internal ▶▶Gross Appearance
spermatic artery passes through the cord on its way to the
testis. The deferential artery is close to the vas. A. Anatomy
The average testicle measures about 4 × 3 × 2.5 cm
B. Venous (Figure 1–7). The volume can be measured by an orchidom-
The veins from the testis and the coverings of the spermatic eter or by a formula with ultrasonic measurement (length ×
cord form the pampiniform plexus, which, at the internal width × height × 0.71). The average volume is 18 mL (rang-
inguinal ring, unites to form the spermatic vein. ing from 12 to 30 mL). The testicle has a dense fascial cov-
ering called the tunica albuginea testis, which, posteriorly,
is invaginated somewhat into the body of the testis to form
▶▶Lymphatics the mediastinum testis. This fibrous mediastinum sends
The lymphatics from the spermatic cord empty into the fibrous septa into the testis, thus separating it into about
external iliac lymph nodes. 250 lobules.

The testis is covered anteriorly and laterally by the visceral SCROTUM

layer of the serous tunica vaginalis, which is continuous with
the parietal layer that separates the testis from the scrotal ▶▶Gross Appearance
wall (Bidarkar and Hutson, 2005). A small amount of fluid
normally exists within the tunica vaginalis sac. At the upper Beneath the corrugated skin of the scrotum lies the dartos
pole of the testis is the appendix testis, a small pedunculated muscle. Deep to this are the three fascial layers derived from
or sessile body similar in appearance to the appendix of the the abdominal wall at the time of testicular descent. Beneath
epididymis. these is the parietal layer of the tunica vaginalis (Kim et al,
2007).
B. Relations The scrotum is divided into two sacs by a septum of con-
nective tissue. The scrotum not only supports the testes but
The testis is closely attached posterolaterally to the epididy- also, by relaxation or contraction of its muscular layer, helps
mis, particularly at its upper and lower poles (Klonisch et al, to regulate their temperature.
2004).
▶▶Histology
▶▶Histology (Figure 1–7) The dartos muscle, under the skin of the scrotum, is nonstri-
Each lobule contains one to four markedly convoluted ated. The deeper layer is made up of connective tissue.
seminiferous tubules, each of which is about 60 cm long.
These ducts converge at the mediastinum testis, where ▶▶Blood Supply
they connect with the efferent ducts that drain into the A. Arterial
epididymis.
The seminiferous tubule has a basement membrane con- The arteries to the scrotum arise from the femoral, internal
taining connective and elastic tissue. This supports the semi- pudendal, and inferior epigastric arteries.
niferous cells that are of two types: (1) Sertoli (supporting)
cells and (2) spermatogenic cells. The stroma between the B. Venous
seminiferous tubules contains connective tissue in which the The veins are paired with the arteries.
interstitial Leydig cells are located.
▶▶Lymphatics
▶▶Blood Supply The lymphatics drain into the superficial inguinal and subin-
The blood supply to the testes is closely associated with that guinal lymph nodes.
to the kidneys because of the common embryologic origin of
the two organs. PENIS AND MALE URETHRA
A. Arterial
The arteries to the testes (internal spermatics) arise from the The penis is composed of two corpora cavernosa and the
aorta just below the renal arteries and course through the corpus spongiosum, which contains the urethra. The corpus
spermatic cords to the testes, where they anastomose with spongiosum enlarges distally and forms the glans penis. Each
the arteries of the vasa deferentia that branch off from the corpus is enclosed in a fascial sheath (tunica albuginea), and
internal iliac (hypogastric) artery. all three corpora are surrounded by a thick fibrous envelope
known as Buck’s fascia. A covering of skin, devoid of fat, is
B. Venous loosely wrapped these bodies. The prepuce forms a hood
The blood from the testis returns in the pampiniform plexus over the glans.
of the spermatic cord. At the internal inguinal ring, the Beneath the skin of the penis (and scrotum) and extend-
pampiniform plexus forms the spermatic vein. ing from the base of the glans to the urogenital diaphragm is
The right spermatic vein enters the vena cava just below Colles’ fascia, which is continuous with Scarpa’s fascia of the
the right renal vein; the left spermatic vein empties into the lower abdominal wall (Figure 1–8).
left renal vein. The proximal ends of the corpora cavernosa are attached
to the pelvic bones just anterior to the ischial tuberosities.
The ischiocavernosus muscles insert into the lateral surface
▶▶Lymphatics of the tunica albuginea at the proximal corpora cavernosa.
The lymphatic vessels from the testes pass to the lumbar Occupying a depression of their ventral surface in the midline
lymph nodes, which, in turn, are connected to the medias- is the corpus spongiosum, which is connected proximally to
tinal nodes. the undersurface of the urogenital diaphragm, below which

lies the urethral bulb. This portion of the corpus spongiosum FEMALE URETHRA
is surrounded by the bulbospongiosus muscle.
The suspensory ligament of the penis arises from the linea ▶▶Gross Appearance
alba and pubic symphysis and inserts into the fascial covering
of the corpora cavernosa. The adult female urethra is about 4 cm long and 8 mm in
diameter. It is slightly curved and lies beneath the pubic sym-
physis just anterior to the vagina.
▶▶Histology
A. Corpora and Glans Penis ▶▶Histology
The corpora cavernosa, the corpus spongiosum, and the The epithelial lining of the female urethra is squamous in
glans penis are composed of smooth muscles, intracaverno- its distal portion and pseudostratified or transitional in the
sal struts (corpus cavernosum only), and endothelium-lined remainder. The submucosa is made up of connective and
sinusoids. The sympathetic and parasympathetic (as well as elastic tissues and spongy venous spaces. Embedded in it are
the nonadrenergic, noncholinergic [NANC]) nerve termi- many periurethral glands, which are most numerous distally;
nals are often seen around the vessels and near the smooth the largest of these are the periurethral glands of Skene that
muscles. open on the floor of the urethra just inside the meatus.
External to the submucosa is a longitudinal layer of
B. Urethra smooth muscle continuous with the inner longitudinal
layer of the bladder wall. Surrounding this is a heavy layer
The urethral mucosa that traverses the glans penis is formed
of circular smooth-muscle fibers extending from the exter-
of squamous epithelium. Proximal to this, the mucosa is tran-
nal vesical muscular layer. This constitutes the involuntary
sitional in type. Underneath the mucosa is the submucosa that
internal urethral sphincter. Distal to this is the external stri-
contains connective and elastic tissue and smooth muscle. In
ated (voluntary) sphincter surrounding the middle third of
the submucosa are the numerous glands of Littre, whose ducts
the urethra composed of smooth and striated muscles within
connect with the urethral lumen. The urethra is surrounded by
the midurethra (Ashton-Miller and Delancey, 2009; Morgan
the vascular corpus spongiosum and the glans penis.
et al 2009; Thor and de Groat, 2010).
▶▶Blood Supply ▶▶Blood Supply

A. Arterial The arterial supply to the female urethra is derived from the
The penis and urethra are supplied by the internal pudendal inferior vesical, vaginal, and internal pudendal arteries. Blood
arteries. Each artery divides into a cavernous artery of the from the urethra drains into the internal pudendal veins.
penis (which supplies the corpora cavernosa), a dorsal artery
of the penis, and the bulbourethral artery. These branches ▶▶Lymphatics
supply the corpus spongiosum, the glans penis, and the ure- Lymphatic drainage from the external portion of the urethra
thra. Accessory pudendal arteries originate from inferior is to the inguinal and subinguinal lymph nodes. Drainage
vesical, obturator, or other arteries may also supply the penis from the deep urethra is into the internal iliac (hypogastric)
(Henry et al, 2017). lymph nodes.
B. Venous BIBLIOGRAPHY
The superficial dorsal vein lies external to Buck’s fascia and
drains to the saphenous vein. The deep dorsal vein is placed Adrenals
beneath Buck’s fascia and lies between the dorsal arteries. The Avisse C et al: Surgical anatomy and embryology of the adrenal
cavernous veins drain the hilum and crura of the penis. These glands. Surg Clin North Am 2000;80:403–415.
veins connect with the pudendal plexus that drains into the O’Donoghue PM et al: Genitourinary imaging: Current and emerg-
internal pudendal vein and periprostatic plexus. ing applications. J Postgrad Med 2010;56:131–139.
Kidneys
▶▶Lymphatics
Budhiraja V et al: Renal artery variations: Embryological basis and
Lymphatic drainage from the skin of the penis is to the super- surgical correlation. Rom J Morphol Embryol 2010;51:533–536.
ficial inguinal and subinguinal lymph nodes. The lymphat- Glassberg KI: Normal and abnormal development of the kidney:
ics from the glans penis pass to the subinguinal and external A clinician’s interpretation of current knowledge. J Urol 2002;
iliac nodes. The lymphatics from the proximal urethra drain 167:2339.
into the internal iliac (hypogastric) and common iliac lymph Rusinek H et al: Renal magnetic resonance imaging. Curr Opin
nodes (Wood and Angermeier, 2010). Nephrol Hypertens 2004;13:667–673.

Calices, Renal Pelvis, and Ureter Spermatic Cord and Seminal Vesicles
Koff SA: Requirements for accurately diagnosing chronic partial Bhosale PR et al: The inguinal canal: Anatomy and imaging fea-
upper urinary tract obstruction in children with hydronephrosis. tures of common and uncommon masses. Radiographics 2008;
Pediatr Radiol 2008;38(Suppl 1):S41–S48. 28(3):819–835.
Sozen S et al: Significance of lower-pole pelvicaliceal anatomy on Jen PY et al: Colocalisation of neuropeptides, nitric oxide synthase
stone clearance after shockwave lithotripsy in nonobstructive iso- and immunomarkers for catecholamines in nerve fibres of the
lated renal pelvic stones. J Endourol 2008;22(5):877–881. adult human vas deferens. J Anat 1999;195(Pt 4):481–489.
Kim B et al: Imaging of the seminal vesicle and vas deferens. Radio-
graphics 2009;29(4):1105–1121.
Bladder
Andersson KE: Detrusor myocyte activity and afferent signaling.
Neurourol Urodyn 2010;29(1):97–106. Testis, Scrotum, and Penis
Berrocal T et al: Anomalies of the distal ureter, bladder, and urethra Bidarkar SS, Hutson JM: Evaluation and management of the
in children: Embryologic, radiologic, and pathologic features. abnormal gonad. Semin Pediatr Surg 2005;14:118.
Radiographics 2002;22:1139. Henry BM et al: Variations in the arterial blood supply to the
Birder L et al: Neural control of the lower urinary tract: Peripheral penis and the accessory pudendal artery: A meta-analysis
and spinal mechanisms. Neurourol Urodyn 2010;29(1):128–139. and review of implications in radical prostatectomy. J Urol
Fry CH, Vahabi B: The role of the mucosa in normal and abnormal 2017;198(2):345–353.
bladder function. Basic Clin Pharmacol Toxicol 2016;119(Suppl 3): Kim W et al: US MR imaging correlation in pathologic conditions of
57–62. the scrotum. Radiographics 2007;27(5):1239–1253.
John H et al: Ultrastructure of the trigone and its functional implica- Klonisch T et al: Molecular and genetic regulation of testis descent
tions. Urol Int 2001;67(4):264–271. and external genitalia development. Dev Biol 2004;270:1.
McCloskey KD: Interstitial cells in the urinary bladder—localization Wood HM, Angermeier KW: Anatomic considerations of the penis,
and function. Neurourol Urodyn 2010;29(1):82–87. lymphatic drainage, and biopsy of the sentinel node. Urol Clin
North Am 2010;37(3):327–334.
Prostate Gland
McNeal JE: The zonal anatomy of the prostate. Prostate 1981;2:
Female Urethra
35–49. Ashton-Miller JA, Delancey JO: On the biomechanics of vaginal birth
Myers RP et al: Making anatomic terminology of the prostate and and common sequelae. Annu Rev Biomed Eng 2009;11:163–176.
contiguous structures clinically useful: Historical review and sug- Delancey JO: Why do women have stress urinary incontinence?
gestions for revision in the 21st century. Clin Anat 2010;23:18–29. Neurourol Urodyn 2010;29(Suppl 1):S13–S17.
Raychaudhuri B, Cahill D: Pelvic fasciae in urology. Ann Roy Coll Morgan et al: Urethral sphincter morphology and function with and
Surg Engl 2008;90:633–637. without stress incontinence. J Urol 2009;182(1):203–209.
Saokar A et al: Detection of lymph nodes in pelvic malignancies with Thor KB, de Groat WC: Neural control of the female urethral and
computed tomography and magnetic resonance imaging. Clin anal rhabdosphincters and pelvic floor muscles. Am J Physiol
Imaging 2010;34:361–366. Regul Integr Compar Physiol 2010;299:R416–R438.

17
2
Embryology of the
Genitourinary System
Emil A. Tanagho, MD; Hiep T. Nguyen, MD;

& Michael DiSandro, MD
At birth, the genital and urinary systems are related only in nearby primary nephric duct as it grows caudally to join
the sense that they share certain common passages. Embryo- the cloaca (Figure 2–1). This primary nephric duct is now
logically, however, they are intimately related. Because of the called the mesonephric duct. After establishing their con-
complex interrelationships of the embryonic phases of the nection with the nephric duct, the primordial tubules elon-
two systems, they are discussed here as five subdivisions: gate and become S-shaped. As the tubules elongate, a series
the nephric system, the vesicourethral unit, the gonads, the of secondary branches increase their surface exposure,
genital duct system, and the external genitalia. thereby enhancing their capacity for interchanging material
with the blood in adjacent capillaries. Leaving the glomeru-
NEPHRIC SYSTEM lus, the blood is carried by one or more efferent vessels that
soon break up into a rich capillary plexus closely related to
The nephric system develops progressively as three distinct
the mesonephric tubules. The mesonephros, which forms
entities: pronephros, mesonephros, and metanephros.
early in the 4th week, reaches its maximum size by the end
of the second month.
▶▶Pronephros
The pronephros is the earliest nephric stage in humans, and ▶▶Metanephros
it corresponds to the mature structure of the most primitive
The metanephros, the final phase of development of the
vertebrate. It extends from the 4th to the 14th somites and
nephric system, originate from both the intermediate meso-
consists of 6–10 pairs of tubules. These open into a pair of
derm and the mesonephric duct. Development begins in the
primary ducts that are formed at the same level, extend cau-
5–6-mm embryo with a budlike outgrowth from the meso-
dally, and eventually reach and open into the cloaca. The pro-
nephric duct as it bends to join the cloaca. This ureteral bud
nephros is a vestigial structure that disappears completely by
grows cephalad and collects mesoderm from the nephro-
the 4th week of embryonic life (Figure 2–1).
genic cord of the intermediate mesoderm around its tip. This
mesoderm with the metanephric cap moves, with the grow-
▶▶Mesonephros ing ureteral bud, more and more cephalad from its point of
The mature excretory organ of the larger fish and amphib- origin. During this cephalic migration, the metanephric cap
ians corresponds to the embryonic mesonephros. It is becomes progressively larger, and rapid internal differentia-
the principal excretory organ during early embryonic life tion takes place. Meanwhile, the cephalic end of the ureteral
(4–8 weeks). It, too, gradually degenerates, although parts bud expands within the growing mass of metanephrogenic
of its duct system become associated with the male repro- tissue to form the renal pelvis (Figure 2–1). Numerous out-
ductive organs. The mesonephric tubules develop from the growths from the renal pelvic dilatation push radially into
intermediate mesoderm caudal to the pronephros shortly this growing mass and form hollow ducts that branch and
before pronephric degeneration. The mesonephric tubules rebranch as they push toward the periphery. These form the
differ from those of the pronephros in that they develop a primary collecting ducts of the kidney. Mesodermal cells
cuplike outgrowth into which a knot of capillaries is pushed. become arranged in small vesicular masses that lie close to
This is called Bowman’s capsule, and the tuft of capillaries the blind end of the collecting ducts. Each of these vesicular
is called a glomerulus. In their growth, the mesonephric masses will form a uriniferous tubule draining into the duct
tubules extend toward and establish a connection with the nearest to its point of origin.

▲▲Figure 2–1. Schematic representation of the development of the nephric system. Only a few of the tubules of the
pronephros are seen early in the 4th week, while the mesonephric tissue differentiates into mesonephric tubules that
progressively join the mesonephric duct. During this time, the first sign of the ureteral bud from the mesonephric duct is
seen. At 6 weeks, the pronephros has completely degenerated and the mesonephric tubules start to do so. The ureteral
bud grows dorsocranially and has met the metanephrogenic cap. At the 8th week, there is cranial migration of the differ-
entiating metanephros. The cranial end of the ureteric bud expands and starts to show multiple successive outgrowths.
(Data from several sources.)
As the kidney grows, increasing numbers of tubules are the ends of the anterior pronephric tubules; (4) this pronephric
formed in its peripheral zone. These vesicular masses develop duct serves subsequently as the mesonephric duct and as such
a central cavity and become S-shaped. One end of the S gives rise to the ureter; (5) the nephric duct reaches the cloaca
coalesces with the terminal portion of the collecting tubules, by independent caudal growth; and (6) the embryonic ureter
resulting in a continuous canal. The proximal portion of the is an outgrowth of the nephric duct, yet the kidney tubules dif-
S develops into the distal and proximal convoluted tubules ferentiate from adjacent metanephric blastema.
and into Henle’s loop; the distal end becomes the glomeru-
lus and Bowman’s capsule. At this stage, the undifferentiated
mesoderm and the immature glomeruli are readily visible on ▶▶Molecular Mechanisms of Renal and
microscopic examination (Figure 2–2). The glomeruli are
Ureteral Development
fully developed by the 36th week or when the fetus weighs The kidney and the collecting system originate from the
2500 g (Osathanondh and Potter, 1964a, b). The metaneph- interaction between the mesonephric duct (Wolffian duct)
ros arises opposite the 28th somite (fourth lumbar segment). and the metanephric mesenchyme (MM). The uretic bud
At term, it has ascended to the level of the first lumbar or (UB) forms as an epithelial outpouching from the meso-
even the twelfth thoracic vertebra. This ascent of the kidney nephric duct and invades the surrounding MM. Reciprocal
is due not only to actual cephalic migration but also to differ- induction between the UB and MM results in branching
ential growth in the caudal part of the body. During the early and elongation of the UB from the collecting system and in
period of ascent (7th–9th weeks), the kidney slides above the condensation and epithelial differentiation of MM around
arterial bifurcation and rotates 90°. Its convex border is now the branched tips of the UB. Branching of the UB occurs
directed laterally, not dorsally. Ascent proceeds more slowly approximately 15 times during human renal development,
until the kidney reaches its final position. generating approximately 300,000 and 1 million nephrons
Certain features of these three phases of development must per kidney (Nyengaard and Bendtsen, 1992).
be emphasized: (1) the three successive units of the system This process of reciprocal induction is dependent on the
develop from the intermediate mesoderm; (2) the tubules at all expression of specific factors. Glial cell-derived neurotrophic
levels appear as independent primordia and only secondarily factor (GDNF) is the primary inducer of ureteric budding
unite with the duct system; (3) the nephric duct is laid down (Costantini and Shakya, 2006). GDNF interacts with sev-
as the duct of the pronephros and develops from the union of eral different proteins from the MM (eg, Wt1, Pax2, Eyal,

EMBRYOLOGY OF THE GENITOURINARY SYSTEM CHAPTER 2 19
▲▲Figure 2–2. Progressive stages in the differentiation of the nephrons and their linkage with the branching collecting
tubules. A small lump of metanephric tissue is associated with each terminal collecting tubule. These are then arranged
in vesicular masses that later differentiate into a uriniferous tubule draining into the duct near which it arises. At one
end, Bowman’s capsule and the glomerulus differentiate; the other end establishes communication with the nearby
collecting tubules.
Six1, Sall1) and from the UB itself (Pax2, Lim1, Ret) result- termination and tubule maintenance (hepatocyte growth fac-
ing in outgrowth of the UB (reviewed by Shah et al, 2004). tor, transforming growth factor-α, epidermal growth factor
Proper activation of the Ret/GDNF signaling pathway in receptor) (reviewed by Shah et al, 2004). BMP7, SHH, and
the tip of UB epithelium appears to be essential in the pro- Wnt11 produced from the branching ureteric bud induce the
gression of branching morphogenesis (reviewed by Michos, MM to differentiate. These factors induce the activation of
2009). B-catenin and Gata3 are important regulators of Ret Pax2, α-8-integrin, and Wnt4 in the renal mesenchymal cells,
expression, and correct activity of Ret is regulated by posi- resulting in condensation of the MM and the formation of
tive (Wnt11 from MM) and negative (Sprouty1 from the UB) pretubular aggregate and primitive renal vesicle (reviewed by
feedback signaling. Additional specific factors are required for Burrow, 2000). With the continued induction from the UB
(1) early branching (eg, Wnt4 and Wnt11, fgf 7–10); (2) late and the autocrine activity of Wnt4, the pretubular aggregates
branching and maturation (bmp2, activin); and (3) branching differentiate into comma-shaped bodies. Platelet-derived

growth factor α-β and vascular endothelial growth factor ureter and is most commonly associated with an accessory
expression are required for initiating the migration of endo- ureteral bud in a duplicated system, but it also can be seen in
thelial cells into the cleft of the comma-shaped bodies to a single system. The migration and insertion of the ureteric
form rudimentary glomerular capillary tufts (reviewed by bud into the bladder depend on Ret gene activity and Ret
Burrow, 2000). Wt1 and Pod1 may have important functions gene expression and is mediated by the action of the retinoic
in the regulation of gene transcription necessary for the dif- acid and Gata3 gene (Schultza, 2016).
ferentiation of podocytes (Ballermann, 2005).
Fibroblast growth factors (FGF) are also important for
VESICOURETHRAL UNIT
early metanephric development, especially the receptors
Fgfr1 and Fgfr2. A loss of both these receptors leads to kid- The blind end of the hindgut caudal to the point of origin of
ney agenesis. Other signaling proteins include Six1 and Sall1. the allantois expands to form the cloaca, which is separated
Six1 is a homeobox protein essential for early kidney devel- from the outside by a thin plate of tissue (the cloacal mem-
opment. Sall1 is a transcription factor that is important for brane) lying in an ectodermal depression (the proctodeum)
the development of the metanephros. Lack of Sall1 leads to under the root of the tail. At the 4-mm stage, starting at the
renal agenesis (Krause, 2015). cephalic portion of the cloaca where the allantois and gut
meet, the cloaca progressively divides into two compartments
by the caudal growth of a crescentic fold, the urorectal fold.
ANOMALIES OF THE NEPHRIC SYSTEM
The two limbs of the fold bulge into the lumen of the cloaca
Failure of the metanephros to ascend leads to an ectopic kidney. from either side, eventually meeting and fusing. The division
An ectopic kidney may be on the proper side but low (simple of the cloaca into a ventral portion (urogenital sinus) and a
ectopy) or on the opposite side (crossed ectopy) with or with- dorsal portion (rectum) is completed during the 7th week.
out fusion. Failure to rotate during ascent causes a malrotated During the development of the urorectal septum, the cloacal
kidney. Fusion of the paired metanephric masses leads to vari- membrane undergoes a reverse rotation, so that the ectoder-
ous anomalies—most commonly a “horseshoe” kidney. mal surface is no longer directed toward the developing ante-
The ureteral bud from the mesonephric duct may bifur- rior abdominal wall but gradually is turned to face caudally
cate, causing a bifid ureter at various levels depending on and slightly posteriorly. This change facilitates the subdivision
the time of the bud’s subdivision. An accessory ureteral bud of the cloaca and is brought about mainly by development of
may develop from the mesonephric duct, thereby forming the infraumbilical portion of the anterior abdominal wall and
a duplicated ureter, usually meeting the same metaneph- regression of the tail. The mesoderm that passes around the
ric mass. Rarely, each bud has a separate metanephric mass, cloacal membrane to the caudal attachment of the umbilical
resulting in supernumerary kidneys. cord proliferates and grows, forming a surface elevation, the
If the double ureteral buds are close together on the meso- genital tubercle. Further growth of the infraumbilical part
nephric duct, they open near each other in the bladder. In of the abdominal wall progressively separates the umbilical
this case, the main ureteral bud, which is the first to appear cord from the genital tubercle. The division of the cloaca is
and the most caudal on the mesonephric ducts, reaches the completed before the cloacal membrane ruptures, and its two
bladder first. It then starts to move upward and laterally and parts therefore have separate openings. The ventral part is the
is followed later by the second accessory bud as it reaches the primitive urogenital sinus, which has the shape of an elon-
urogenital sinus. The main ureteral bud (now more cranial gated cylinder and is continuous cranially with the allantois;
on the urogenital sinus) drains the lower portion of the kid- its external opening is the urogenital ostium. The dorsal part
ney. The two ureteral buds reverse their relationship as they is the rectum, and its external opening is the anus.
move from the mesonephric duct to the urogenital sinus. Traditionally, it is believed that the urogenital sinus
This is why duplicated ureters always cross (Weigert–Meyer receives the mesonephric ducts. The caudal end of the meso-
law). If the two ureteral buds are widely separated on the nephric duct distal to the ureteral bud (the common excre-
mesonephric duct, the accessory bud appears more proximal tory duct) is progressively absorbed into the urogenital sinus.
on the mesonephric duct and therefore ends in the bladder By the 7th week, the mesonephric duct and the ureteral bud
more distal than usual, with an ectopic orifice lower than the have independent opening sites. This introduces an island of
normal one. This ectopic orifice could still be in the bladder mesodermal tissue amid the surrounding endoderm of the
close to its outlet, in the urethra, or even in the genital duct urogenital sinus. As development progresses, the opening
system (Figure 2–3). A single ureteral bud that arises more of the mesonephric duct (which will become the ejaculatory
proximal than normal on the mesonephric duct can also end duct) migrates downward and medially. The opening of the
in a similar ectopic location, although this is less common. ureteral bud (which will become the ureteral orifice) migrates
Lack of development of a ureteral bud results in a solitary upward and laterally. The absorbed mesoderm of the meso-
kidney and a hemitrigone. The ureteral bud may also develop nephric duct expands with this migration to occupy the area
or migrate into the bladder, abnormally leading to a uretero- limited by the final position of these tubes (Figure 2–3).
cele. A ureterocele is a cystic dilation of the distal intramural This will later be differentiated as the trigonal structure,

▲▲Figure 2–3. Development of the ureteral bud from the mesonephric duct and the relationship of both to the urogenital
sinus. The ureteral bud appears at the 4th week. The mesonephric duct distal to this ureteral bud is gradually absorbed
into the urogenital sinus, resulting in separate endings for the ureter and the mesonephric duct. The mesonephric tissue
that is incorporated into the urogenital sinus expands and forms the trigonal tissue.
which is the only mesodermal inclusion in the endodermal supported by more recent studies that suggest the trigone is
vesicourethral unit. formed mostly from bladder smooth muscle and less so from
More recent studies suggest an alternative path of devel- the ureters. Condensation of myoblasts in the region between
opment (reviewed by McInnes and Michaud, 2009). The the openings of the ureters and Wolffian ducts at 12 weeks of
right and left common excretory ducts appear to undergo gestation gives rise to the trigone, as a single circular muscu-
gradual programmed cell death; the elimination of the com- lar layer and the muscles from the distal ureters cross midline
mon excretory ducts brings the distal ureters into immediate to form the interureteral fold (Oswald et al, 2006).
contact with the urogenital sinus epithelium. Concurrently, The urogenital sinus can be divided into two main seg-
the ureters undergo a 180° rotation around the axis of the ments. The dividing line, the junction of the combined
mesonephric duct (also known as the Wolffian duct). The Müllerian ducts with the dorsal wall of the urogenital sinus, is
distal segment of the ureters then also undergoes apoptosis. an elevation called Müller’s tubercle, which is the most fixed
As a result, this process generates a new ureteral connection reference point in the whole structure and is discussed in a
point in the urogenital sinus region that will give rise to the subsequent section. The segments are as follows:
bladder, while the Wolffian duct remains in the region giving 1. The ventral and pelvic portion forms the bladder, part of
rise to the urethra. Further growth of the bladder and ure- the urethra in males, and the whole urethra in females.
thra moves the ureteral orifices cranially, while those to the This portion receives the ureter.
Wolffian ducts move caudally. This pattern of development is

2. The urethral, or phallic, portion receives the mesonephric The part of the urogenital sinus caudal to the opening of
and the fused Müllerian ducts. This will be part of the ure- the Müllerian duct forms the vaginal vestibule and contrib-
thra in males and forms the lower fifth of the vagina and utes to the lower fifth of the vagina in females (Figure 2–5).
the vaginal vestibule in females. In males, it forms the inframontanal part of the prostatic
During the 3rd month, the ventral part of the urogenital urethra and the membranous urethra. The penile urethra
sinus starts to expand and forms an epithelial sac whose apex is formed by the fusion of the urethral folds on the ventral
tapers into an elongated, narrowed urachus. The pelvic por- surface of the genital tubercle. In females, the urethral folds
tion remains narrow and tubular; it forms the whole urethra remain separate and form the labia minora. The glandular
in females and the supramontanal portion of the prostatic urethra in males is formed by canalization of the urethral
urethra in males. The splanchnic mesoderm surrounding the plate. The bladder originally extends up to the umbilicus,
ventral and pelvic portion of the urogenital sinus begins to where it is connected to the allantois that extends into the
differentiate into interlacing bands of smooth-muscle fibers umbilical cord. The allantois usually is obliterated at the level
and an outer fibrous connective tissue coat. By the 12th week, of the umbilicus by the 15th week. The bladder then starts to
the layers characteristic of the adult urethra and bladder are descend by the 18th week. As it descends, its apex becomes
recognizable (Figure 2–4). stretched and narrowed, and it pulls on the already obliterated
▲▲Figure 2–4. Differentiation of the urogenital sinus in males. At the 5th week, the progressively growing urorectal
septum separates the urogenital sinus from the rectum. The former receives the mesonephric duct and the ureteral
bud. It retains its tubular structure until the 12th week, when the surrounding mesenchyme starts to differentiate into
the muscle fibers around the whole structure. The prostate gland develops as multiple epithelial outgrowths just above
and below the mesonephric duct. During the 3rd month, the ventral part of the urogenital sinus expands to form the
bladder proper; the pelvic part remains narrow and tubular, forming part of the urethra. (Reproduced with permission
from Tanagho EA, Smith DR: Mechanism of urinary continence. I. Embryologic, anatomic and pathologic considerations, J Urol.
1968 Nov;100(5):640–646.)

▲▲Figure 2–5. Differentiation of the urogenital sinus and the Müllerian ducts in the female embryo. At 9 weeks, the
urogenital sinus receives the fused Müllerian ducts at Müller’s tubercle (sinovaginal node), which is solidly packed with
cells. As the urogenital sinus distal to Müller’s tubercle becomes wider and shallower (15 weeks), the urethra and fused
Müllerian duct will have separate openings. The distal part of the urogenital sinus forms the vaginal vestibule and the
lower fifth of the vagina (shaded area), and that part above Müller’s tubercle forms the urinary bladder and the entire
female urethra. The fused Müllerian ducts form the uterus and the upper four-fifths of the vagina. The hymen is formed at
the junction of the sinovaginal node and the urogenital sinus.
allantois, now called the urachus. By the 20th week, the blad- anterior lobe tubules are large and show multiple branches,
der is well separated from the umbilicus, and the stretched they gradually contract and lose most of the branches. They
urachus becomes the middle umbilical ligament. continue to shrink so that at birth, they show no lumen and
appear as small, solid embryonic epithelial outgrowths. In
contrast, the tubules of the posterior lobe are fewer in num-
PROSTATE ber yet larger, with extensive branching. These tubules, as
The prostate develops as multiple solid outgrowths of the they grow, extend posterior to the developing median and lat-
urethral epithelium both above and below the entrance of the eral lobes and form the posterior aspect of the gland, which
mesonephric duct. These simple tubular outgrowths begin to may be felt rectally.
develop in five distinct groups at the end of the 11th week and Prostate development results from complex interaction
are complete by the 16th week (112-mm stage). They branch between urogenital sinus epithelium and mesenchyme in
and rebranch, ending in a complex duct system that encoun- the presence of androgens (reviewed by Cunha et al, 2004,
ters the differentiating mesenchymal cells around this seg- and Thomson, 2008). Early in development, the androgen
ment of the urogenital sinus. These mesenchymal cells start receptors are solely expressed in the urogenital sinus mesen-
to develop around the tubules by the 16th week and become chyme. Under the influence of androgen, the mesenchyme
denser at the periphery to form the prostatic capsule. By the induces epithelial bud formation, regulates the growth and
22nd week, the muscular stroma is considerably developed, branching of epithelial bud, promotes differentiation of a
and it continues to increase progressively until birth. secretory epithelium, and specifies differential expression
From the five groups of epithelial buds, five lobes are eventu- of prostatic secretory proteins. Genome-wide analyses have
ally formed: anterior, posterior, median, and two lateral lobes. revealed critical molecular events in prostate development.
Initially, these lobes are widely separated, but later they meet, These include Nkx3.1, Sox, and homeobox genes for ductal
with no definite septa dividing them. Tubules of each lobe do morphology development; sonic hedgehog, fibroblast growth
not intermingle with each other but simply lie side by side. factor and the Wnt5a gene for bud development; and bone
The anterior lobe tubules begin to develop simultaneously morphogenic protein and notch genes for branching (Meeks,
with those of the other lobes. In the early stages, although the 2011). Other factors such as activin A serve to inhibit ductal

branching in order to maintain tissue homeostasis and regu- mesonephros is converted into a gonadal mesentery known
lated growth in the prostate. as the mesorchium. The cells of the germinal epithelium
grow into the underlying mesenchyme and form cordlike
ANOMALIES OF THE VESICOURETHRAL UNIT masses. These are radially arranged and converge toward the
mesorchium, where a dense portion of the blastemal mass
Failure of the cloaca to subdivide is rare and results in a
is also emerging as the primordium of the rete testis. A net-
persistent cloaca. Incomplete subdivision is more frequent,
work of strands soon forms that is continuous with the testis
ending with rectovesical, rectourethral, or rectovestibular
cords. The latter also split into three to four daughter cords.
fistulas (usually with imperforate anus or anal atresia).
These eventually become differentiated into the seminifer-
Failure of descent or incomplete descent of the blad-
ous tubules by which the spermatozoa are produced. The rete
der leads to a urinary umbilical fistula (urachal fistula),
testis unites with the mesonephric components that will form
urachal cyst, or urachal diverticulum depending on the
the male genital ducts, as discussed in a subsequent section
stage and degree of maldescent.
(Figure 2–6).
Development of the genital primordia in an area more
If the gonad develops into an ovary, it (like the testis) gains
caudal than normal can result in formation of the corpora
a mesentery (mesovarium) and settles in a more caudal posi-
cavernosa just caudal to the urogenital sinus outlet, with the
tion. During the 9th week the internal blastema differentiates
urethral groove on its dorsal surface. This defect results in
in the into a primary cortex beneath the germinal epithelium
complete or incomplete epispadias depending on its degree.
and a loose primary medulla. A compact cellular mass bulges
A more extensive defect results in bladder exstrophy. Failure
from the medulla into the mesovarium and establishes the
of fusion of urethral folds leads to various grades of hypospa-
primitive rete ovarii. At 3–4 months of age, the internal cell
dias. This defect, because of its mechanism, never extends
mass becomes young ova. A new definitive cortex is formed
proximal to the bulbous urethra. This is in contrast to epi-
from the germinal epithelium as well as from the blastema
spadias, which usually involves the entire urethra up to the
in the form of distinct cellular cords (Pflüger’s tubes), and a
internal meatus.
permanent medulla is formed. The cortex differentiates into
ovarian follicles containing ova.
GONADS
Genetically, in the presence of a Y chromosome, SRY (as
Most of the structures that make up the embryonic genital sys- known as testis determining factor [TDF]) induces the upreg-
tem have been taken over from other systems, and their read- ulation of Sox9 in the undifferentiated gonad (reviewed by
aptation to genital function is a secondary and relatively late Sekido, 2010). This in turn upregulates the expression of FGF9
phase in their development. The early differentiation of such and increases PGD2 synthesis, both helping to maintain Sox9
structures is therefore independent of sexuality. Furthermore, expression. Sox9 directs the differentiation of cells into Sertoli
each embryo is at first morphologically bisexual, possessing all cell by activating several downstream genes such as Amh,
the necessary structures for either sex. The development of one Cbln4, FGF9, and Ptgds. In the absence of a Y chromosome
set of sex primordia and the gradual involution of the other are and SRY, Rspo1 is upregulated in the undifferentiated gonads
determined by the sex of the gonad. (reviewed by Nef and Vassalli, 2009). Rspo1 is required for
The sexually undifferentiated gonad is a composite struc- Wnt4 expression, and together they activate β-catenin, which,
ture. Male and female potentials are represented by specific in turn, suppresses the formation of the testis cords by inhibit-
histologic elements (medulla and cortex) that have alterna- ing Sox9 and FGF9. A second pathway involving the upregu-
tive roles in gonadogenesis. Normal differentiation involves lation of Foxl2 also serves to inhibit Sox 9 and FGF9 activity,
the gradual predominance of one component. contributing to the development of the ovary.
The primitive sex glands appear during the 5th and 6th New genetic data on human sex determination from
weeks within a localized region of the thickening known as modern gene sequencing will create opportunities for the
the urogenital ridge (this contains both the nephric and the development of mechanistic models and should lead to
genital primordia). At the 6th week, the gonad consists of better understanding of this complex process (reviewed by
a superficial germinal epithelium and an internal blastema. Bashamboo, 2017).
The blastemal mass is derived mainly from proliferative
ingrowth from the superficial epithelium, which comes loose ▶▶Descent of the Gonads
from its basement membrane.
A. Testis
During the 7th week, the gonad begins to assume the
characteristics of a testis or ovary. Differentiation of the In addition to its early caudal migration, the testis later leaves
ovary usually occurs somewhat later than differentiation of the abdominal cavity and descends into the scrotum. By the
the testis. 3rd month of fetal life, the testis is located retroperitoneally
If the gonad develops into a testis, the gland increases in in the false pelvis. A fibromuscular band (the gubernacu-
size and shortens into a more compact organ while achiev- lum) extends from the lower pole of the testis through the
ing a more caudal location. Its broad attachment to the developing muscular layers of the anterior abdominal wall

▲▲Figure 2–6. Transformation of the undifferentiated genital system into the definitive male and female systems.

to terminate in the subcutaneous tissue of the scrotal swell- the 4-mm stage) joins the ventral part of the cloaca, which
ing. The gubernaculum also has several other subsidiary will be the urogenital sinus. This duct gives rise to the ureteral
strands that extend to adjacent regions. Just below the bud close to its caudal end. The ureteral bud grows cranially
lower pole of the testis, the peritoneum herniates as a and meets metanephrogenic tissue. The part of each meso-
diverticulum along the anterior aspect of the gubernacu- nephric duct caudal to the origin of the ureteric bud becomes
lum, eventually reaching the scrotal sac through the ante- absorbed into the wall of the primitive urogenital sinus so
rior abdominal muscles (the processus vaginalis). The testis that the mesonephric duct and ureter open independently.
remains at the abdominal end of the inguinal canal until the This is achieved at the 15-mm stage (7th week). During this
7th month. It then passes through the inguinal canal behind period, starting at the 10-mm stage, the Müllerian ducts start
(but invaginating) the processus vaginalis. Normally, it to develop. They reach the urogenital sinus relatively late—at
reaches the scrotal sac by the end of the 8th month. the 30-mm stage (9th week); their partially fused blind ends
producing the elevation called Müller’s tubercle. Müller’s
B. Ovary tubercle is the most constant and reliable point of reference
in the whole system.
In addition to undergoing an early internal descent, the ovary If the gonad starts to develop into a testis (17-mm stage,
becomes attached through the gubernaculum to the tissues 7th week), the Wolffian duct will start to differentiate into
of the genital fold and then attaches itself to the developing the male duct system, forming the epididymis, vas deferens,
uterovaginal canal at its junction with the uterine (fallopian) seminal vesicles, and ejaculatory ducts, when the Müllerian
tubes. This part of the gubernaculum between the ovary and duct proceeds toward its junction with the urogenital sinus
uterus becomes the ovarian ligament; the part between the and immediately starts to degenerate. Only its upper and
uterus and the labia majora becomes the round ligament lower ends persist, the former as the appendix testis and the
of the uterus. These ligaments prevent extra-abdominal latter as part of the prostatic utricle.
descent, and the ovary enters the true pelvis. It eventually lies If the gonad starts to differentiate into an ovary (22-mm
posterior to the uterine tubes on the superior surface of the stage, 8th week), the Müllerian duct system forms the uter-
urogenital mesentery, which has descended with the ovary ine (fallopian) tubes, uterus, and most of the vagina. The
and now forms the broad ligament. A small processus vag- Wolffian ducts, aside from their contribution to the urogeni-
inalis forms and passes toward the labial swelling, but it is tal sinus, remain rudimentary.
usually obliterated at full term.
MALE DUCT SYSTEM
GONADAL ANOMALIES
The gonad may either (1) not develop (agenesis), (2) develop ▶▶Epididymis
incompletely (hypogenesis), (3) develop incorrectly (dysgen- Because of the proximity of the differentiating gonads and the
esis), or (4) develop correctly, but then suffer an embryologic nephric duct, some of the mesonephric tubules are retained
injury (eg, intrauterine torsion). Supernumerary gonads are as the efferent ductules, and their lumens become continu-
rare. The commonest anomaly involves descent of the gonads, ous with those of the rete testis. These tubules, together with
especially the testis. Retention of the testis in the abdomen or the part of the mesonephric duct into which they empty, will
arrest of its descent at any point along its natural pathway form the epididymis. Each coiled ductule makes a conical
is called cryptorchidism, which may be either unilateral or mass known as the lobule of the epididymis. The cranial end
bilateral. If the testis does not follow the main gubernacular of the mesonephric duct becomes highly convoluted, com-
structure but follows one of its subsidiary strands, it will end pleting the formation of the epididymis. This is an example of
in an abnormal position, resulting in an ectopic testis. direct inclusion of a nephric structure into the genital system.
Failure of union between the rete testis and mesonephros Additional mesonephric tubules, both cephalad and caudal
results in a testis separate from the male genital ducts (the to those that were included in the formation of the epididy-
epididymis) and azoospermia. mis, remain as rudimentary structures, that is, the appendix
of the epididymis and the paradidymis.
GENITAL DUCT SYSTEM
Alongside the indifferent gonads, there are, early in embry- ▶▶Vas Deferens, Seminal Vesicles, and
Ejaculatory Ducts
onic life, two different yet closely related ducts. One is pri-
marily a nephric duct (Wolffian duct), yet it also serves as a The mesonephric duct caudal to the portion forming the
genital duct if the embryo develops into a male. The other epididymis forms the vas deferens. Shortly before this duct
(Müllerian duct) is primarily a genital structure from the joins the urethra (urogenital sinus), a localized dilatation
start. (ampulla) develops, and the saccular convoluted structure
Both ducts grow caudally to join the primitive urogenital that will form the seminal vesicle is evaginated from its wall.
sinus. The Wolffian duct (known as the pronephric duct at The mesonephric duct between the origin of the seminal

vesicle and the urethra forms the ejaculatory duct. The whole tubes (fallopian tubes, oviducts) are the cephalic two-thirds
mesonephric duct now achieves its characteristic thick of the Müllerian ducts (Figure 2–6).
investment of smooth muscle, with a narrow lumen along
most of its length. ANOMALIES OF THE GONADAL DUCT SYSTEM
Both above and below the point of entrance of the meso-
Nonunion of the rete testis and the efferent ductules can
nephric duct into the urethra, multiple outgrowths of ure-
occur and, if bilateral, causes azoospermia and sterility.
thral epithelium mark the beginning of the development of
Failure of the Müllerian ducts to approximate or to fuse com-
the prostate. As these epithelial buds grow, they meet the
pletely can lead to various degrees of duplication in the geni-
developing muscular fibers around the urogenital sinus,
tal ducts. Congenital absence of one or both uterine tubes or
and some of these fibers become entangled in the branch-
of the uterus or vagina occurs rarely.
ing tubules of the growing prostate and become incorporated
Arrested development of the infratubercular segment of
into it, forming its muscular stroma (Figure 2–4).
the urogenital sinus leads to its persistence, with the urethra
and vagina having a common duct to the outside (urogenital
FEMALE DUCT SYSTEM sinus).
The Müllerian ducts, which are a paired system, are seen
alongside the mesonephric duct. It is not known whether EXTERNAL GENITALIA
they arise directly from the mesonephric ducts or separately During the 8th week, external sexual differentiation begins
as an invagination of the celomic epithelium into the paren- to occur. Not until 3 months, however, do the progressively
chyma lateral to the cranial extremity of the mesonephric developing external genitalia attain characteristics that can
duct, but the latter theory is favored. The Müllerian duct be recognized as distinctively male or female. During the
develops and runs lateral to the mesonephric duct. Its open- indifferent stage of sexual development, three small protu-
ing into the celomic cavity persists as the peritoneal ostium berances appear on the external aspect of the cloacal mem-
of the uterine tube (later it develops fimbriae). The other brane. In front is the genital tubercle, and on either side of the
end grows caudally as a solid tip and then crosses in front of membrane are the genital swellings.
the mesonephric duct at the caudal extremity of the meso- With the breakdown of the urogenital membrane (17-mm
nephros. It continues its growth in a caudomedial direction stage, 7th week), the primitive urogenital sinus achieves a
until it meets and fuses with the Müllerian duct of the oppo- separate opening on the undersurface of the genital tubercle.
site side. The fusion is partial at first, so there is a tempo-
rary septum between the two lumens. This later disappears,
leaving one cavity that will form the uterovaginal canal. The
MALE EXTERNAL GENITALIA
potential lumen of the vaginal canal is completely packed The urogenital sinus opening extends on the ventral aspect
with cells. The solid tip of this cord pushes the epithelium of the genital tubercle as the urethral groove. The primitive
of the urogenital sinus outward, where it becomes Müller’s urogenital orifice and the urethral groove are bound on either
tubercle (33-mm stage, 9th week). The Müllerian ducts fuse side by the urethral folds. The genital tubercle becomes elon-
at the 63-mm stage (13th week), forming the sinovaginal gated to form the phallus. The corpora cavernosa is indicated
node, which receives a limited contribution from the uro- in the 7th week as paired mesenchymal columns within the
genital sinus (this contribution forms the lower fifth of the shaft of the penis. By the 10th week, the urethral folds start
vagina). to fuse from the urogenital sinus orifice toward the tip of the
The urogenital sinus distal to Müller’s tubercle, originally phallus. At the 14th week, the fusion is complete and results
narrow and deep, shortens, widens, and opens to form the in the formation of the penile urethra. The corpus spongio-
floor of the pudendal or vulval cleft. This results in separate sum results from the differentiation of the mesenchymal
openings for the vagina and urethra and brings the vaginal masses around the formed penile urethra.
orifice to its final position nearer the surface. At the same The glans penis becomes defined by the development of a
time, the vaginal segment increases appreciably in length. circular coronary sulcus around the distal part of the phallus.
The vaginal vestibule is derived from the infratubercular seg- The urethral groove and the fusing folds do not extend
ment of the urogenital sinus (in males, the same segment will beyond the coronary sulcus. The glandular urethra develops
form the inframontanal part of the prostatic urethra and the as a result of canalization of an ectodermal epithelial cord that
membranous urethra). The labia minora are formed from the has grown through the glans. This canalization reaches and
urethral folds (in males they form the pendulous urethra). communicates with the distal end of the previously formed
The hymen is the remnant of the Müllerian tubercle. The penile urethra. During the 3rd month, a fold of skin at the
lower fifth of the vagina is derived from the portion of the base of the glans begins growing distally and, 2 months later,
urogenital sinus that combines with the sinovaginal node. surrounds the glans. This forms the prepuce. Meanwhile, the
The remainder of the vagina and the uterus are formed from genital swellings shift caudally and are recognizable as scrotal
the lower (fused) third of the Müllerian ducts. The uterine swellings. They meet and fuse, resulting in the formation of

the scrotum, with two compartments partially separated by Michos O: Kidney development: From ureteric bud formation
a median septum and a median raphe, indicating their line to branching morphogenesis. Curr Opin Genet Dev 2009;19:
of fusion. 484–490.
Mcinnes RR, Michaud JL: Plumbing in the embryo: Development
defects of the urinary tracts. Clin Genet 2009;75:307–317.
FEMALE EXTERNAL GENITALIA
Nef S, Vassalli JD: Complementary pathways in mammalian female
Until the 8th week, the appearance of the female external geni- sex determination. J Biol 2009;8:74.
talia closely resembles that of the male genitalia except that the Nyengaard JR, Bendtsen TF: Glomerular number and size in relation
urethral groove is shorter. The genital tubercle, which becomes to age, kidney weight, and body surface in normal man. Anat Rec
bent caudally and lags in development, becomes the clitoris. As 1992;232(2):194–201.
in males (albeit on a minor scale), mesenchymal columns differ- Oswald J et al: Reevaluation of the fetal muscle development of the
entiate into corpora cavernosa, and a coronary sulcus identifies vesical trigone. J Urol 2006;176(3):1166–1170.
the glans clitoridis. The most caudal part of the urogenital sinus Reddy PP, Mandell J: Prenatal diagnosis: Therapeutic implications.
Urol Clin North Am 1998;25:171.
shortens and widens, forming the vaginal vestibule. The urethral
folds do not fuse but remain separate as the labia minora. The Sekido R: SRY: A transcriptional activator of mammalian testis deter-
mination. Int J Biochem Cell Biol 2010;42(3):417–420.
genital swellings meet in front of the anus, forming the posterior
Shah MM et al: Branching morphogenesis and kidney disease.
commissure, while the swellings enlarge and remain separated Development 2004;131(7):1449–1462.
on either side of the vestibule and form the labia majora.
Stephens FD: Embryopathy of malformations. J Urol 1982;127:13.
Stephens FD: Congenital Malformations of the Urinary Tract. Prae-
ANOMALIES OF THE EXTERNAL GENITALIA ger, New York, 1983.
Absence or duplication of the penis or clitoris is very rare. Tanagho EA: Embryologic development of the urinary tract. In: Ball
More commonly, the penis remains rudimentary or the cli- TP (ed): AUA Update Series. American Urological Association,
Philadelphia, 1982.
toris shows hypertrophy. These anomalies may be seen alone
Tanagho EA: Developmental anatomy and urogenital abnormalities.
or, more frequently, in association with differences of sex
In: Raz S (ed): Female Urology. 2nd ed. Saunders, Philadelphia,
development (DSD). Concealed penis and transposition of 1986.
penis and scrotum are relatively rare anomalies. Thomson AA: Mesenchymal mechanisms in prostate organogenesis.
Failure or incomplete fusion of the urethral folds results Differentiation 2008;76(6):587–598.
in hypospadias (see preceding discussion). Penile develop- Vaughan ED Jr, Middleton GW: Pertinent genitourinary embryology:
ment is also anomalous in cases of epispadias and exstrophy Review for practicing urologist. Urology 1975;6:139.
(see preceding discussion).
Anomalies of the Nephric System

BIBLIOGRAPHY Avni EF et al: Multicystic dysplastic kidney: Natural history from in
utero diagnosis and postnatal followup. J Urol 1987;138:1420.
General
Bomalaski MD et al: Vesicoureteral reflux and ureteropelvic junction
Arey LB: Developmental Anatomy: A Textbook and Laboratory obstruction: Association, treatment options and outcome. J Urol
Manual of Embryology. 7th ed. Saunders, Philadelphia, 1974. 1997;157:969.
Ballermann BJ: Glomerular endothelial cell differentiation. Kidney Chevalier RL: Effects of ureteral obstruction on renal growth. Pediatr
Int 2005;67(5):1668–1671. Nephrol 1995;9:594.
Burrow CR: Regulatory molecules in kidney development. Pediatr Churchill BM et al: Ureteral duplication, ectopy and ureteroceles.
Nephrol 2000;131(7):240–253. Pediatr Clin North Am 1987;34:1273.
Carlson BM: Patten’s Foundations of Embryology. 6th ed. McGraw- Corrales JG, Elder JS: Segmental multicystic kidney and ipsilateral
Hill, New York, 1996. duplication anomalies. J Urol 1996;155:1398.
Costantini F, Shakya R: GDNF/Ret signaling and the development of Cox R et al: Twenty-year follow-up of primary megaureter. Eur Urol
the kidney. Bioessays 2006;28(2):117–127. 1990;17:43.
Cunha GR et al: Hormonal, cellular, and molecular regulation of Decter RM: Renal duplication and fusion anomalies. Pediatr Clin
normal and neoplastic prostatic development. J Steroid Biochem North Am 1997;44:1323.
Mol Biol 2004;92(4):221–236. El-Galley RE, Keane TE: Embryology, anatomy, and surgical applica-
Fine RN: Diagnosis and treatment of fetal urinary tract abnormalities. tions of the kidney and ureter. Surg Clin North Am 2000;80:381.
J Pediatr 1992;121:333. Glassberg KI: Normal and abnormal development of the kidney:
FitzGerald MJT: Human Embryology: A Regional Approach. Harper A clinician’s interpretation of current knowledge. J Urol 2002;
& Row, London, 1978. 167:2339.
Gilbert SG: Pictorial Human Embryology. University of Washington Keating MA et al: Changing concepts in management of primary
Press, Seattle, 1989. obstructive megaureter. J Urol 1989;142:636.
Marshall FF: Embryology of the lower genitourinary tract. Urol Clin Krause M et al: Signaling during kidney development. Cells 2015;
North Am 1978;5:3. 4(2):112.

MacDermot KD et al: Prenatal diagnosis of autosomal dominant Churchill BM et al: Emergency treatment and long-term follow-up of
polycystic kidney disease (PKD1) presenting in utero and progno- posterior urethral valves. Urol Clin North Am 1990;17:343.
sis for very early onset disease. J Med Genet 1998;35:13. Chwalle R: The process of formation of cystic dilatations of the
Magee MC: Ureteroceles and duplicated systems: Embryologic vesicle end of the ureter and of diverticula at the ureteral ostium.
hypothesis. J Urol 1980;123:605. Urol Cutan Rev 1927;31:499.
Maher ER, Kaelin WG Jr: Von Hippel-Lindau disease. Medicine Connor JP et al: Long-term follow-up of 207 patients with bladder
(Baltimore) 1997;76:381. exstrophy: An evolution in treatment. J Urol 1989;142:793.
Mesrobian HG et al: Unilateral renal agenesis may result from Dinneen MD, Duffy PG: Posterior urethral valves. Br J Urol 1996;
in utero regression of multicystic renal dysplasia. J Urol 1993; 78:275.
150:793. Duckett JW: The current hype in hypospadiology. Br J Urol 1995;
Murcia NS et al: New insights into the molecular pathophysiology of 76(Suppl 3):1.
polycystic kidney disease. Kidney Int 1999;55:1187. Eagle JR Jr, Barrett GS: Congenital deficiency of abdominal muscu-
Nguyen HT, Kogan BA: Upper urinary tract obstruction: Experi- lature with associated genitourinary abnormalities: A syndrome.
mental and clinical aspects. Br J Urol 1998;81(Suppl 2):13. Report of nine cases. Pediatrics 1950;6:721.
Osathanondh V, Potter EL: Pathogenesis of polycystic kidneys: Elmassalme FN et al: Duplication of urethra—case report and review
Survey of results of microdissection. Arch Pathol 1964a;77:510. of literature. Eur J Pediatr Surg 1997;7:313.
Osathanondh V, Potter EL: Pathogenesis of polycystic kidneys: Type 4 Escham W, Holt HA: Complete duplication of bladder and urethra.
due to urethral obstruction. Arch Pathol 1964b;77:502. J Urol 1980;123:773.
Pope JC IV et al: How they begin and how they end: Classic and Goh DW et al: Bladder, urethral, and vaginal duplication. J Pediatr
new theories for the development and deterioration of congenital Surg 1995;30:125.
anomalies of the kidney and urinary tract, CAKUT. J Am Soc Greskovich FJ III, Nyberg LM Jr: The prune belly syndrome: A
Nephrol 1999;10:2018. review of its etiology, defects, treatment and prognosis. J Urol
Prasad PV, Priatna A: Functional imaging of the kidneys with fast 1988;140:707.
MRI techniques. Eur J Radiol 1999;29:133. Hinman F Jr: Surgical disorders of the bladder and umbilicus of
Robson WL et al: Unilateral renal agenesis. Adv Pediatr 1995;42:575. urachal origin. Surg Gynecol Obstet 1961;113:605.
Ross JH, Kay R: Ureteropelvic junction obstruction in anomalous Jaramillo D et al: The cloacal malformation: Radiologic findings and
kidneys. Urol Clin North Am 1998;25:219. imaging recommendations. Radiology 1990;177:441.
Scherz HC et al: Ectopic ureteroceles: Surgical management with pres- Jeffs RD: Exstrophy, epispadias, and cloacal and urogenital sinus
ervation of continence. Review of 60 cases. J Urol 1989;142:538. abnormalities. Pediatr Clin North Am 1987;34:1233.
Soderdahl DW et al: Bilateral ureteral quadruplication. J Urol 1976; Landes RR et al: Vesical exstrophy with epispadias: Twenty-year
116:255. follow-up. Urology 1977;9:53.
Somlo S, Markowitz GS: The pathogenesis of autosomal dominant Mackie GG: Abnormalities of the ureteral bud. Urol Clin North Am
polycystic kidney disease: An update. Curr Opin Nephrol Hyper- 1978;5:161.
tens 2000;9:385. Manzoni GA et al: Cloacal exstrophy and cloacal exstrophy variants:
Tanagho EA: Ureteroceles: Embryogenesis, pathogenesis and A proposed system of classification. J Urol 1987;138:1065.
management. J Cont Educ Urol 1979;18:13. Massad CA et al: Morphology and histochemistry of infant testes in
Tanagho EA: Development of the ureter. In: Bergman H (ed): The the prune belly syndrome. J Urol 1991;146:1598.
Ureter. 2nd ed. Springer-Verlag, New York, 1981. Meeks J et al: Genetic regulation of prostate development. J Andrology
Thomsen HS et al: Renal cystic diseases. Eur Radiol 1997;7:1267. 2011;32(3):210.
Tokunaka S et al: Morphological study of ureterocele: Possible clue Mesrobian HG et al: Long-term followup of 103 patients with bladder
to its embryogenesis as evidenced by locally arrested myogenesis. exstrophy. J Urol 1988;139:719.
J Urol 1981;126:726. Mouriquand PD et al: Hypospadias repair: Current principles and
Zerres K et al: Autosomal recessive polycystic kidney disease. Contrib procedures. Br J Urol 1995;76(Suppl 3):9.
Nephrol 1997;122:10. Nguyen HT, Kogan BA: Fetal bladder physiology. Adv Exp Med Biol
1999;462:121.
Orvis BR et al: Testicular histology in fetuses with the prune belly
Anomalies of the Vesicourethral Unit syndrome and posterior urethral valves. J Urol 1988;139:335.
Asopa HS: Newer concepts in the management of hypospadias and Randall A, Campbell EW: Anomalous relationship of the right ureter
its complications. Ann Roy Coll Surg Engl 1998;80:161. to the vena cava. J Urol 1935;34:565.
Austin PF et al: The prenatal diagnosis of cloacal exstrophy. J Urol Rosenfeld B et al: Type III posterior urethral valves: Presentation and
1998;160(3, Pt 2):1179. management. J Pediatr Surg 1994;29:81.
Baskin LS: Hypospadias and urethral development. J Urol 2000; Schultza K et al: Genetic basis of ureterocele. Curr Genom 2016;
163:951. 17(1):62.
Begg RC: The urachus, its anatomy, histology and development. Shapiro E: Embryologic development of the prostate: Insights into
J Anat 1930;64:170. the etiology and treatment of benign prostatic hyperplasia. Urol
Belman AB: Hypospadias update. Urology 1997;49:166. Clin North Am 1990;17:487.
Burbige KA et al: Prune belly syndrome: 35 years of experience. Silver RI: What is the etiology of hypospadias? A review of recent
J Urol 1987;137:86. research. Delaware Med J 2000;72:343.

Stein R, Thuroff JW: Hypospadias and bladder exstrophy. Curr Opin de Palma L et al: Epididymal and vas deferens immaturity in cryptor-
Urol 2002;12:195. chidism. J Urol 1988;140:1166.
Stephens FD: The female anus, perineum and vestibule: Embryo- Diez Garcia R et al: Peno-scrotal transposition. Eur J Pediatr Surg
genesis and deformities. J Obstet Gynaecol Br Commonw 1968; 1995;5:222.
8:55. Elder JS et al: Androgenic sensitivity of gubernaculum testis: Evi-
Tanagho EA: Embryologic basis for lower ureteral anomalies: A dence for hormonal/mechanical interactions in testicular descent.
hypothesis. Urology 1976;7:451. J Urol 1982;127:170.
Uehling DT: Posterior urethral valves: Functional classification. Gad YZ et al: 5 alpha-reductase deficiency in patients with micrope-
Urology 1980;15:27. nis. J Inherit Metab Dis 1997;20:95.
Van Savage JG et al: An algorithm for the management of anterior Hadziselimovic F et al: The significance of postnatal gonadotropin
urethral valves. J Urol 1997;158(3, Pt 2):1030. surge for testicular development in normal and cryptorchid testes.
Wakhlu AK et al: Congenital megalourethra. J Pediatr Surg 1996; J Urol 1986;136:274.
31:441. Honoré LH: Unilateral anorchism: Report of 11 cases with discussion
Workman SJ, Kogan BA: Fetal bladder histology in posterior urethral of etiology and pathogenesis. Urology 1978;11:251.
valves and the prune belly syndrome. J Urol 1990;144:337. Johnson P et al: Inferior vesical fissure. J Urol 1995;154:1478.
Mollard P et al: Female epispadias. J Urol 1997;158:1543.
Gonadal Anomalies Nef S, Parada LF: Hormones in male sexual development. Genes Dev
2000;14:3075.
Barteczko KJ, Jacob MI: The testicular descent in humans: Origin,
development and fate of the gubernaculum Hunteri, processus Newman K et al: The surgical management of infants and children
vaginalis peritonei, and gonadal ligaments. Adv Anat Embryol with ambiguous genitalia: Lessons learned from 25 years. Ann
Cell Biol 2000;156: III–X, 1. Surg 1992;215:644.
Bashamboo A et al: Anomalies in human sex determination provide Pagon RA: Diagnostic approach to the newborn with ambiguous
unique insights into the complex genetic interactions of early genitalia. Pediatr Clin North Am 1987;34:1019.
gonad development. Clin Genet 2017;91(2):143. Parker KL et al: Gene interactions in gonadal development. Annu
Belville C et al: Persistence of Müllerian derivatives in males. Am J Rev Physiol 1999;61:417.
Med Genet 1999;89:218? Rajfer J, Walsh PC: Testicular descent: Normal and abnormal. Urol
Ben-Chaim J, Gearhart JP: Current management of bladder Clin North Am 1978;5:223.
exstrophy. Scand J Urol Nephrol 1997;31:103. Toppari J, Kaleva M: Maldescendus testis. Horm Res 1999;51:261.
Borzi PA, Thomas DF: Cantwell-Ransley epispadias repair in male Zaontz MR, Packer MG: Abnormalities of the external genitalia.
epispadias and bladder exstrophy. J Urol 1994;151:457. Pediatr Clin North Am 1997;44:1267.
Crankson SJ, Ahmed S: Female bladder exstrophy. Int Urogynecol J
Pelvic Floor Dysfunct 1997;8:98.

31
3
Symptoms of Disorders of
the Genitourinary Tract
In the workup of any patient, the history is of paramount General malaise may be noted with tumors, chronic
importance; this is particularly true in urology. It is neces- pyelonephritis, or renal failure. The presence of many of
sary to discuss here only those urologic symptoms that are these symptoms may be compatible with human immunode-
apt to be brought to the physician’s attention by the patient. ficiency virus (HIV; see Chapter 17).
It is important to know not only whether the disease is acute
or chronic but also whether it is recurrent, since recurring LOCAL AND REFERRED PAIN
symptoms may represent acute exacerbations of chronic
disease. Two types of pain have their origins in the genitourinary
Obtaining the history is an art that depends on the skill organs: local and referred. The latter is especially common.
and methods used to elicit information. The history is only Local pain is felt in or near the involved organ. Thus, the
as accurate as the patient’s ability to describe the symptoms. pain from a diseased kidney (T10–T12, L1) is felt in the cos-
This subjective information is important in establishing an tovertebral angle and in the flank in the region of and below
accurate diagnosis. the 12th rib. Pain from an inflamed testicle is felt in the gonad
itself.
SYSTEMIC MANIFESTATIONS Referred pain originates in a diseased organ but is felt at
some distance from that organ. The ureteral colic (Figure 3–1)
Symptoms of fever and weight loss should be sought. The
caused by a stone in the upper ureter may be associated with
presence of fever associated with other symptoms of urinary
severe pain in the ipsilateral testicle; this is explained by the
tract infection may be helpful in evaluating the site of the
common innervation of these two structures (T11–T12).
infection. Simple acute cystitis is essentially an afebrile dis-
A stone in the lower ureter may cause pain referred to the
ease. Acute pyelonephritis or prostatitis is apt to cause high
scrotal wall; in this instance, the testis itself is not hyperes-
temperatures (≤40°C [104°F]), often accompanied by violent
thetic. The burning pain with voiding that accompanies
chills. Infants and children who have acute pyelonephritis
acute cystitis is felt in the distal urethra in females and in the
may have high temperatures without other localizing symp-
glandular urethra in males (S2–S3).
toms or signs. Such a clinical picture, therefore, invariably
Abnormalities of a urologic organ can also cause pain in
requires bacteriologic study of the urine.
any other organ (eg, gastrointestinal, gynecologic) that has a
A history of unexplained attacks of fever occurring even
sensory nerve supply common to both (Figures 3–2 and 3–3).
years before may otherwise represent asymptomatic pyelo-
nephritis. Renal carcinoma sometimes causes fever that may
reach 39°C (102.2°F) or more. The absence of fever does not ▶▶Kidney Pain (Figure 3–1)
by any means rule out renal infection, for it is the rule that Typical renal pain is felt as a dull and constant ache in the
chronic pyelonephritis does not cause fever. costovertebral angle just lateral to the sacrospinalis muscle
Weight loss is to be expected in the advanced stages of and just below the 12th rib. This pain often spreads along
cancer, but it may also be noticed when renal insufficiency the subcostal area toward the umbilicus or lower abdominal
due to obstruction or infection supervenes. In children who quadrant. It may be expected in the renal diseases that cause
have “failure to thrive” (low weight and less than average sudden distention of the renal capsule. Acute pyelonephritis
height for their age), chronic obstruction, urinary tract infec- (with its sudden edema) and acute ureteral obstruction (with
tion, or both should be suspected. its sudden renal back pressure) both cause this typical pain.

▲▲Figure 3–1. Referred pain from kidney (dotted areas) and ureter (shaded areas).
It should be pointed out, however, that many urologic renal The physician may be able to judge the position of a ure-
diseases are painless because their progression is so slow that teral stone by the history of pain and the site of referral. If the
sudden capsular distention does not occur. Such diseases stone is lodged in the upper ureter, the pain radiates to
include cancer, chronic pyelonephritis, staghorn calculus, the testicle, since the nerve supply of this organ is simi-
tuberculosis, polycystic kidney, and hydronephrosis due to lar to those of the kidney and upper ureter (T11–T12).
chronic ureteral obstruction. With stones in the midportion of the ureter on the right side,
the pain is referred to McBurney’s point and may therefore
▶▶Ureteral Pain (Figure 3–1) simulate appendicitis; on the left side, it may resemble diver-
ticulitis or other diseases of the descending or sigmoid colon
Ureteral pain is typically stimulated by acute obstruction (pas-
(T12, L1). As the stone approaches the bladder, inflamma-
sage of a stone or a blood clot). In this instance, there is back
tion and edema of the ureteral orifice ensue, and symptoms
pain from renal capsular distention combined with severe col-
of vesical irritability such as urinary frequency and urgency
icky pain (due to renal pelvic and ureteral muscle spasm) that
may occur. It is important to realize, however, that in mild
radiates from the costovertebral angle down toward the lower
ureteral obstruction, as seen in the congenital stenoses, there
anterior abdominal quadrant, along the course of the ureter.
is usually no pain, either renal or ureteral.
In men, it may also be felt in the bladder, scrotum, or testicle.
In women, it may radiate into the vulva. The severity and col-
icky nature of this pain are caused by the hyperperistalsis and ▶▶Vesical Pain
spasm of this smooth-muscle organ as it attempts to rid itself The overdistended bladder of the patient in acute urinary
of a foreign body or to overcome obstruction. retention causes agonizing pain in the suprapubic area. Other

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THE STRAIN THAT MAKES THE CORNING EGG FARM FAMOUS
As The Corning Egg Farm was located within a few miles of New
York City the breeds which laid the white shelled egg were the only
ones worthy of consideration, and, in the study of the question, it
was found there was another important matter confronting the egg
farmer, as to the breed which he should keep, whether a setter, or a
non-setter. On an egg farm, where hundreds of layers are to be kept,
if any of the Asiatics, or so called American Breeds, were kept, they
would be a source of considerable added expense, first, in the way
of loss of eggs during their numerous broody periods; second, in the
necessary buildings in which to carry the “broody biddies” until they
have become sensible, and are in a proper frame of mind to be
returned to the Laying House. This might look on its face a small
affair, but success to The Corning Egg Farm has come through
watching every corner, and while sparing no needed expenditure,
avoiding unnecessary and foolish outlay.
So, to the man who would really meet with a large success, all the
breeds which lay the dark shelled egg, because of their setting
propensity, must be eliminated.
All the members of the Mediterranean family are layers of the
white shelled egg, and are what is termed “non-setting.”
S. C. White Leghorns Outclass All

Before deciding we looked the different members of this family
over with considerable care, and we found that the Single Comb
White Leghorn is the fowl that out-classes all the others for the
purpose of an egg farm. It is a bird, where properly bred, of great
hardiness and stamina. It readily adapts itself to all conditions of
climate, and, where the right “strain” is procured, it is never a
disappointer as to the number, size, and the class of eggs which it
produces. We, therefore, decided to adopt the Single Comb White
Leghorn, and we have outlined, in a previous chapter, how we went
to work to build up the unequaled Corning Strain, by the most careful
selection, and scientific mating.
Prof. Gowell, at the Maine Agricultural Station, carried on his
breeding with Barred Plymouth Rocks, and it is interesting to note
that his average for some eight years, taking his star performers,
was 134.27 eggs per hen for twelve months, while at The Corning
Egg Farm the flocks of fifteen hundred pullets averaged per hen, for
ten months laying, 143.25 eggs in 1909, and 145.11 eggs in 1910.
Here was a difference of two months in time, and yet the large
flocks, taken as a whole, not weeding out a few star performers,
surpassed the twelve months’ record of the Barred Plymouth Rocks
at the Maine Station by almost nine eggs in 1909, and ten eggs in
1910. This significant fact made considerable impression on a
number of breeders in the neighborhood of Boston, with the result
that, in the last two years, The Corning Egg Farm has supplied a
large number of hatching eggs and considerable breeding stock for
farms in New England.
As one gentleman from Boston pointed out, even with the
difference in price between the brown and the white egg, he found
that he could not really afford to continue with the breeds laying the
brown egg, for the Leghorn, in numbers, more than made up for the
slight difference in price between the two colors, in the Boston
Market. And, as he still further pointed out, it took less food to supply
the Leghorn than it did any of the larger breeds, and this, of course,
was another source of economy.
It should be remembered that the “Strain” of any breed is most
important. One may purchase White Leghorns where the inbreeding
has been so great that they are not capable of laying eggs in large
numbers, and the percentage of fertility from the hatching standpoint
in such birds will be a most uncertain quantity. Such chicks as may
be hatched will be far from strong, and the mortality will run into
figures which will dishearten anyone.
Line Breeding—Not Inbreeding

In the building up of a great strain of birds it is necessary to “line
breed,” for, if the old theory of introducing new blood to prevent
inbreeding, and the method of introducing the new blood, was, as is
done in so many places even to-day, by introducing males from other
sources, the entire system falls down. Nothing is accomplished and
time is worse than wasted. The possibility of handing down the
virtues of mother to daughter, and of father to son, is eliminated. If all
the qualities of a given “Strain” are to be handed down line breeding
must be adhered to in the strictest sense. Inbreeding, however, must
be avoided, or disaster will follow.
How Corning Farm Produces Unrelated Cockerels

The Method of The Corning Egg Farm is as follows: a pen of
carefully selected yearling hens is set aside in what is known as “the
pen for the production of unrelated cockerels.” A most carefully
selected cockerel to every twelve hens is placed in the pen.
Incubators are run with eggs from this pen only, and the resulting
chicks are marked before being placed in the Brooder House. The
cockerels which appear with this marking are grown to maturity,
those coming up to our standard being selected to head the breeding
pens for the following season. The marked pullets are placed in the
Laying Houses with the other pullets, but are never selected for
yearling breeders on our own Farm. In pens sold to others we
always furnish unrelated cockerels.
Having hatched a sufficient number of chicks to produce about
four hundred cockerels, no further eggs are set from this pen, and, at
the end of the season, all the birds comprising this pen are sold.
This Method of line breeding hands down the laying quality which
has been so developed, and which is being increased from season
to season in an unbroken line, but inbreeding is absolutely avoided,
and the vigor of the stock is maintained.
Perhaps, in closing the chapter, nothing could be more apt than a
letter received from a Breeder of Crystal White Orpingtons, in the
neighborhood of one of the large Western Cities. The letter-head, in
large type, states, “Breeder of Crystal White Orpingtons, the Great
Winter Layer.” The contents of the letter is as follows:
“As I am now planning to go into the Egg business, and desire to
follow your method as closely as possible, and, while in this locality
there is not such a marked preference for the white egg over the
brown, still the White Leghorn, of a good strain, doubtless outlays
any other breed known, and the shape of its egg is such that it is
superior for table use, to any laid by the dark shelled family. It,
therefore, is my purpose, as rapidly as possible to work into a large
flock of Leghorns, with Corning stock as a basis.”
It will be noted that the gentleman is a breeder of Crystal White
Orpingtons, and prints in large type on his letter-head, “The Great
Winter Layer,” but that when it comes down to “brass tacks,” from the
standpoint of the hen which will produce an egg for table use, and
the hen that will give you the requisite number to make the dollars,
the Breeder of the Crystal White Orpingtons wants to put in the
Corning Strain of Single Comb White Leghorns.
CHAPTER VI
Advantages of the Large Flock System—Reduces
Cost of Housing and Economizes in Time and
Labor
For many years the floor space per hen has been an interesting
study to anyone reading poultry literature, either in books or in
magazine articles.
Some fifteen years ago it was generally considered for a hen to do
at all well she must have at least twenty square feet of floor space.
Later, the number of feet was divided by half, and for some time ten
square feet was considered to be the very least a hen could possibly
do with. Then we come to the four square feet period, and this
created a great deal of controversy. Many writers declared that it was
impossible for any hen, no matter how housed, to do well in such a
restricted space. At times, some visionary writer pictured a flock in
one house, of what was then considered an enormous size. One
Professor of poultry went so far as to state that he had successfully
kept some three hundred hens in one flock, and had obtained most
satisfactory results. This statement, however, was denied by others,
and the Professor wrote an article in which he set forth that, while he
had done this, he would never think of suggesting that the average
poultry-keeper attempt it. In his statement there were some truths
that it is well to remember, namely, that the average poultry-keeper
would not give the flock the care and supervision necessary to keep
it in health. In other words, the poultry-keeper would not attend to the
necessary cleanliness, and disease would break out, and, in the
average poultry house, under such conditions, this would mean the
total annihilation of the flock.
THREE STERILE LAYING HOUSES CONTAINING 4500 PULLETS, WITH A
FLOOR SPACE OF 7680 SQUARE FEET
Draughts the Stumbling Block

As economy of space and labor is one of the main factors in
getting a commercial profit where poultry is operated with, the large
flock system appealed most strongly to The Corning Egg Farm. Long
houses, under one roof, without divisions, had been attempted by
others, and the endeavor to discover the reason for the failures,
where this had been attempted, was a very interesting study. It was
found that the main stumbling block in houses of this type was
draughts. To eliminate the draughts was the problem we then
undertook to solve. It was found that if the houses were built in
sections of twenty feet, and the partitions which divided the house
into roosting closets were extended twelve inches beyond the
dropping boards, and were carried from the floor to the roof, the air
currents were broken up, and the difficulty of draughts was
overcome.
Houses, as we believed in constructing them, were expensive,
unless it was possible to carry a very large number of layers
successfully in them. In studying the two hundred and twenty-five
pullets as they worked contentedly in the No. 1 Laying House, which
was but twelve feet wide, we became convinced that it was perfectly
possible in a house sixteen feet wide by one hundred and sixty feet
in length to carry fifteen hundred layers. This, to be sure, allowed the
hen only a little over two square feet of floor space, with the dropping
boards included. But, as we figured it, the hen also had the entire
house for floor space, and, while it is true that fourteen hundred and
ninety-nine sisters were her near neighbors, they all enjoyed the
same large space to roam in. A house, then, of this size,
accommodating fifteen hundred layers, was not an expensive house
per bird, and, when you consider that the construction was such that
the up-keep was practically nothing, it became not only not an
expensive house, but really a very cheap one.
The success of the fifteen hundred layers in one house proved
itself at once, and we never have seen the slightest necessity for
altering the plan of the Laying House, as we first laid it out.
2,000 Birds to a House

The large flock system works economies, then, in housing, in the
amount of labor necessary to care for the birds, and in gathering the
eggs. And there is no doubt but that a house of considerably greater
length, with a flock ranging as high as two thousand birds, could
successfully be handled. In fact, on one farm which has been in
existence over twenty-five years, a Corning Method Laying House of
two hundred feet in length has been in operation now for twelve
months, and the owners write us that it is the most successful house
on their entire farm, and that as rapidly as possible they are
rebuilding all their Laying Houses, and making them of this type.
CHAPTER VII
What is the Winter Layer?—The Properly Hatched
and Reared Pullet
Many people have a very erroneous idea with regard to getting
Winter eggs. They seem to think any hen should produce eggs in
Winter. The hen generally moults in the early Fall, and Nature has
provided this time of rest for her. The egg organs cease to produce,
for the hen finds she has all she can do to supply the necessary
material for her new dress, and this is a very serious drain on her
system. The natural time, however, for a pullet to begin to lay is
when she reaches maturity, and, as the pullet hatched in the early
Spring, properly cared for, should come into eggs in the early Fall,
the pullet, then, is the Winter layer.
It must still be remembered that the domesticated fowl of to-day is
a bird of evolution. In its wild state a pullet did not begin to lay eggs
in the Fall, and neither did she lay a large number of eggs at any
time. With the coming of Spring, and an abundance of succulent
green food, and large quantities of animal food in the shape of a
great variety of worms and insects, she laid and hatched her brood.
Therefore, to have successful Winter layers, it is necessary to
produce as nearly as possible the Spring-time conditions.
INTERIOR LAYING HOUSE NO. 1 IN 1910
Must Feed Green Food

On The Corning Egg Farm, when the pullets are brought up from
the Range into the Laying Houses, the majority of them have already
been laying on the Range, and they are in fit condition to be brought
strongly into eggs. They are fed a large quantity of succulent green
food, in the form which, perhaps, is more delicious to the hen than
any other, that is, Sprouted Oats. The quantity of animal food in their
mash is increased, and, with the vigorous digging for the grain in the
deep litter, the problem of Winter eggs is solved, and from day to
day, the number of eggs coming from the pullet houses, increases
very rapidly.
On the other hand, the pullet which has completed its first ten
months of laying is well advanced in the moult, and is becoming a
yearling hen. Those qualifying under the drastic examination for
perfect type are selected for the next year’s Breeders, and are
removed to the Breeding Houses, which have been thoroughly
disinfected and put in the most sanitary condition to receive them.
Those not reaching the Corning Standard are marketed, as we sell
culls only to the butcher.
The aim in handling the yearling hen is not to get eggs from her
during the Winter, but to give her a long rest, and to build her up, and
put her in the pink of condition for the coming breeding season, and
it is the aim at The Corning Egg Farm to have as few eggs produced
as possible from the breeding pens until about the first of January,
when an increased amount of animal food is added to the daily ration
for the purpose of bringing the hens into eggs, and within a few days
there is a very rapid increase in the number of eggs from these pens.
It must be remembered that the profit in Winter eggs is made from
pullets, and to be successful in this line the Laying Houses must be
well stocked with them.
Yearling and two year old hens are the proper breeding females.
The Corning Egg Farm Method is one of continuous rotation, as
follows:
Incubator to Brooder House.
Brooder House to Range.
Range to Laying House. Those selected as coming up to the
Corning Standard go to the Breeder House.
At the end of the second year the Breeders are all sold for
foundation stock.
This gives an opportunity to the public to procure the very best
Breeders at a most reasonable price.
CHAPTER VIII
A Great Laying Strain—The Selection of Breeders
to Produce It
The first requisite is to breed from a mature animal, from a real
yearling hen. The term “yearling hen” is a misnomer, for, when she is
twelve months of age she has not as a rule developed into a true
yearling hen. The female has five months of growth, ten months of
laying, and then she moults, which process varies in duration from
eight to ten weeks.
Eighteen Months Old

When she has completed the moult, her entire anatomy has
undergone a change, and she is a mature animal, about eighteen
months of age, a fit specimen to reproduce her kind, and her off-
spring will be strong and vigorous youngsters.
The great mortality one reads of among chicks can be traced more
to breeding from immature females than to any other cause.
The general method of selecting breeders for a great many years
has been by the use of “trap nests.” Surely the use of a mechanical
device is a poor method to determine what hens are proper for
breeding purposes, and really the trap nest tells you nothing.
In every pen there are daily a number of eggs which are not laid in
the nest at all. To what particular hen does the attendant credit eggs
found in hollows scooped out in corners under the dropping boards?
It is a peculiarity of “Biddy” that where she sees an egg she almost
always decides it is a good and proper place for her to lay another.
Thus, on some days, where trap nests are in use, it may be
necessary to make a great number of guesses as to which hen did
not lay in the traps, but on the floor.
Trap Nests a Failure
There is another reason why trap nests really tell you nothing.
Take two females of a pen whose numbers are one and two. For the
first few weeks No. 1 surpasses her sister No. 2 in the production of
eggs. To this pen, clover has been the green food fed, and of this
ingredient the farm has run short. The shipment has been expected
daily but did not arrive, and, because of that failure, for four or five
days no other green food was provided. Then cabbage was resorted
to to take the place of the clover. The pen having been without green
food for a number of days was fairly greedy for it, and good, crisp
cabbage suits the palate of many hens exactly, and they are very apt
to overdo the matter in eating it. A great layer must be a large eater,
and so hen No. 1 gorged herself on the cabbage. Her digestive
organs were upset, and for a number of weeks she ceased laying,
while hen No. 2 continued to shell out a fair number of eggs. The
owner of these birds, when it came time for the selection of the
breeders, expressed his great disappointment over hen No. 1. She
had started so well, and then had blown up entirely, and so she is
passed up, and hen No. 2 is accepted as a breeder.
ONE OF THE BREEDING HOUSES JUST AFTER MATING 1910
Now, if the anatomy of these two birds had been studied, it would
have been found at once that hen No. 1 was much better qualified to
take a place in the breeding pen than hen No. 2. The mere fact that
the trap nest record of any female shows a phenomenal number of
eggs laid in ten or twelve months does not necessarily prove that
she is a proper animal to breed from. Post-mortem examinations
show in many cases that they are freaks, and, while they have laid a
great number of eggs, there was much to be desired in regard to the
eggs, as to their size, shape, and color. As a matter of fact it would
have been a great mistake to have bred from such an individual.
Type Reproduces Type

It must be remembered that type produces type, and the only
proper way to select birds for the breeding pen which will produce
progeny capable of great egg production is to thoroughly understand
their anatomy. It is impossible to produce a great performer in any
line unless the animal is of a build capable of the performance. No
one would expect to breed a two-minute trotter from a Shetland
Pony.
The hen which is capable of becoming an ideal layer must have a
deep keel, a long body, and, as she faces out, she must have an
appearance of broadness, and must be the shape of a wedge back
to the point where the wings join the body.
The Large Flock System is carried on in the Breeding Pen on The
Corning Egg Farm, and it has been most successful. It has been
found that the small pen does not produce the high fertility
continuously which the Large Flock System does. During the season
of 1910, for long periods, the fertility ran as high as 96%, and as
early as the first of March it was above 90%. In the season of 1911,
eggs incubated in the early part of February, ran above 91%, and
during the season there were times when the fertility reached 97%.
The Breeding Pens are mated up two weeks before eggs are to be
used for incubation, and early hatched cockerels are used to head
these Breeding Pens. It has been found that the mating of cockerels
with yearling hens produces a very decided predominance of pullets,
and the youngsters are strong and vigorous from the start.
The proportion of mating is one to twelve, and the records of The
Corning Egg Farm show that by this method of mating the number of
cockerels produced, through the years that the Farm has been in
operation, has been as low as one-quarter, and as high as one-third.
The males to head the pens are selected with the same care that
the hens are. They are all perfect birds, of large size, and conform as
closely as possible to the standard requirements, without interfering
with the paramount aim of producing a Great Layer.
CHAPTER IX
What is the Best Time to Hatch?
The question which is the title of this chapter is asked over and
over again. You see it propounded to the editor of almost every
poultry paper in the country. And it is a difficult one to answer,
because the various needs of different people are so diversified.
April and May are doubtless the natural hatching seasons for all
varieties. Climatic conditions are then kinder, the food which is
necessary for the production of many eggs, and eggs of the strong
hatchable kind, is supplied by Nature in great abundance, and the
young chick coming into life in these months finds a great variety of
natural food of the very best kind for growth awaiting it. In Spring
eggs run strongly fertile, and in every way Nature seems to lend
herself to successful hatching, and the starting of the young chick
properly on its journey.
The man, however, who is operating an egg farm, and has made
contracts for the delivery of a continuous supply of eggs to exacting
customers, cannot well afford to wait until these months to hatch in,
for it is necessary for him to have a large number of pullets reaching
maturity and beginning to lay, before his last year’s pullets reach the
moulting period and stop egg production. To accomplish this it is
necessary to have in his brooder house, by not later than the first
week of March, a goodly number of yellow babies. From that time on
he must keep them coming, so as to have a sufficient number a few
weeks apart to take the place of the yearling hens going into the
moult. In this way he will succeed in keeping up a continuous flow of
eggs.
It is true there is a danger in these early hatched pullets. They may
go into what is called the Winter moult, after laying well into the
month of December, but they will not all moult, and before there is a
marked shrinkage the later hatches will be laying strongly.
The moult which occurs with early hatched birds does not last as
long as the moult coming in the regular season. The birds soon
return to the nest, and the house rapidly jumps back to a very large
output of eggs for the coming Spring months. Thus the great
increase in numbers helps to offset the decrease in price, and to
equalize the bank account.
It must be remembered, however, that Leghorns hatched up to the
25th of June make good Winter layers provided they are properly
cared for, and given the food and attention which produces a great
growth, and under such conditions one will find no difficulty in getting
them into laying eggs readily by the time they are five months of age.
An Interesting Experiment in Late Hatching

In the season of 1910 The Corning Egg Farm made a very
interesting experiment, in a large way, so far as late hatching goes.
We incubated two large batches of eggs, the first being set so that
the chicks hatched from the 18th to the 26th of July; the second
batch completed incubation August 15th. The resulting pullets from
these two hatches were some fifty odd over twelve hundred. We
carried them on Range until December 1st, and then placed them in
a Laying House by themselves. They had not begun to lay on Range
so far as we were able to discover, although many of the pullets had
the appearance of eggs. Almost from the start, after they were
placed in the Colony Houses, we fed them, in addition to the regular
Range ration, a good supply of Sprouted Oats each day. This was
done for the reason that of course the succulent green food had
passed away, and we consider it of vital importance that growing
birds be given the opportunity to gather a large supply of succulent
green food. The records show that within three days after the pullets
were placed in the Laying House we began to gather from one to
three eggs a day. Before December was over the house was
producing 10%; January saw 35% output of eggs, and before
February was very far advanced we were doing better than 60%.
There was a time in March when the House was yielding a 75%
output.
SPROUTED OATS CELLAR
These birds laid strongly all Summer, and we were interested in

noting when they would start to moult. We had seen the statement
made a number of times that late hatched pullets were very late
moulters. In our experience, however, this did not prove to be true,
for this pen of birds moulted at just about the same time, and in the
same proportion, as the earlier hatches did.
We had frequently seen it stated that birds hatched in the very last
week of August, or the first week in September, would produce eggs
at the same time that the June hatched pullets would begin to
produce them. Our experience with June hatches, and we have had
four years of it, disproves this statement absolutely. We find that the
June hatched pullet, properly cared for, comes in quite as rapidly as
those hatched in April and May.
We do not wish to go on record as advocates of July and August
hatching, but we simply wish to show what could be accomplished if
a Breeder met with some misfortune, and was compelled to hatch
late or not at all.
CHAPTER X
Succulent Green Food—Satisfactory Egg
Production Impossible Without It
A goodly supply of green food is necessary to all birds, the
growing chicken as well as the yearling hen, for it is a great aid to
digestion, helping to properly assimilate all foods as they are taken
into the crop, and passed through the great grinding mill of a
chicken.
There is no possible hope of a full egg supply from any Laying
House where a large quantity of green food is not fed daily. It may be
fed in many forms. Clover or Alfalfa (and we are now speaking first
of the Winter supply of green food) may be procured in a dry state,
and by properly scalding it with hot water it may be made to almost
live again, so far as its freshness and delightful odor go. In many
cases the preparation of Clover or Alfalfa spoils it. The water should
be quite at the boiling point, and it should be poured over, preferably
it should be put on with a sprinkling can. The method at The Corning
Egg Farm is to place whichever we are using of the Clover family in
pails, a given number for each Laying House, and as they stand in
rows the hot water is applied with a sprinkling can. The contents are
not allowed to steep, but as soon as the second wetting of the long
row of pails is reached they are placed on the delivery wagon and at
once taken to their destination. When the contents are emptied from
the pails they will be steaming hot, too hot for the birds to take at
first, and you will find them standing in a ring around the Clover, and
from time to time testing the heat. As soon as it is cool enough they
will devour it with great avidity.
Where Alfalfa is fed some flocks give considerable difficulty at first
as they do not seem to relish it, but after a short time they seem to
acquire the taste, and become very fond of it. It contains a higher
amount of protein than the ordinary Clover which can be bought in
the market, but in purchasing Alfalfa products one should be careful
not to buy a large quantity of dirt, but get what is known as “short
cut,” and have it carefully sifted.
By many people cabbages are considered a most excellent green
food for Winter use, but if they are chopped up and fed to the layers
considerable caution should be used in the feeding. They are very
apt to upset the digestive organs of the birds, and that means a very
decided decrease in the number of eggs. This is equally true of
Mangle beets and other roots which in many cases are used.
Sprouted Oats Best

At The Corning Egg Farm we are strong believers in Sprouted
Oats as a green food, and we now maintain a cement Cellar, with
good drainage, which is used for nothing else. The method of
sprouting oats is really very simple, and does not require the
arduous labor which one would imagine from numerous articles
written on the subject.
How They Are Grown on the Farm

We have frames three by six feet in size, built of ordinary boards,
but not matched material. The sides are about four inches high.
These frames are laid on the floor of the Cellar, and each frame is
filled with forty-eight quarts of oats spread evenly over the bottom.
We have a large sprinkler attached to the hose, and the oats are
thoroughly wet as they lie in the trays, and this wetting is repeated
every morning. In a temperature from fifty to sixty degrees we find
that the oats have started to sprout about the third day, and from this
on the growth is very fast. Parts of the oats in the frame will swell two
or three inches in places, above the surrounding mass of oats, and
we make it a practice to place the sprinkler directly on top of this
swelling, and it is found by so doing that the frame in a short time will
present a very even growth.
If the Sprouted Oats are fed when the green tops are from one
and a half to two inches in length the chemical quality of the oat is
not lost, and we really get a double ration when it is fed. If allowed to
go beyond this length, they are then just an ordinary green food.
In many instances we have noticed writers advocating soaking the
oats overnight, and then, for the next few days, to periodically stir
them. And in other cases writers advise, when they are placed in the
frames to turn the oats over. This is a serious mistake, for anyone
can readily see that the tender shoots, which grow most rapidly after
the third day, would be broken off, and where this occurs the oats will
rot.
Oats, of course, can be sprouted in sheds, or even out-of-doors, if
they are covered up so that the sun will not dry them out too rapidly.
A frame should be made in such a manner that the water sprayed
over the oats will slowly drain away. There are a number of different
contrivances now being placed on the market for sprouting oats, and
we have no doubt that, on small plants, some of them would prove
quite satisfactory. Where it is desired to sprout oats in a small way, in
the Cellar of one’s house, a rack can be built with run-ways for the
trays to slide on, with a space of two inches between the trays. By
thoroughly sprinkling the top tray the water will run down through
from one tray to another, and, as the growth progresses, the more
advanced ones can be moved up from the bottom of the rack, as
they require less water than those in a less advanced stage.
The oats sprout more quickly if grown and sprinkled in a fairly dark
place, and it must be remembered that too warm a temperature will
rot the mass after the growth has reached its fourth or fifth day.
Timothy and Clover Cut Green

As one enters The Corning Egg Farm, on the left of the drive,
there is about an acre of Timothy and Clover. This acre has been
very heavily fertilized and brought up to a high state of cultivation.
The Timothy and Clover grow so rapidly, and the growth comes in
such abundance almost before the snow is off the ground, that
cutting it as we do, so many rows each morning, it is impossible to
cross the entire plot before that which was first cut has almost grown
beyond the succulent point. To make a change for the hens we cut
this in the early Spring, and pass it through the Clover Cutter,

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Smith & Tanaghoâ€™s General Urology

Smith & Tanagho’s

Jack W. McAninch, MD, FACS, FRCS(E)(Hon)

Tom F. Lue, MD, FACS, ScD (Hon)

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20 Renal Parenchymal Neoplasms 329 31 Disorders of the Adrenal Glands 509

21 Cancer of the Prostate Gland 351 32 Disorders of the Kidneys 521

22 Genital Tumors 377 33 Diagnosis of Medical Renal Diseases 539

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42 Disorders of the Female Urethra 659 46 Genital Gender-Affirming Surgery:

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Peter R. Carroll, MD, MPH Arpita Desai, MD

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Michael DiSandro, MD Kirsten L. Greene, MD, MS

Daniela Franz, MD Hedvig Hricak, MD, PhD

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John N. Krieger, MD Anobel Y. Odisho, MD, MPH

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Katsuto Shinohara, MD David Tat, DO

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Jack W. McAninch, MD, FACS, FRCS(E) (Hon)

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CALICES, RENAL PELVIS, AND URETER

1. Calices—The tips of the minor calices (8–12 in number)

▶▶Histology (Figure 1–4) ▶▶Gross Appearance

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B. Relations ▶▶Histology (Figure 1–10)

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▲▲Figure 1–11. Section of the prostate gland shows the

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▶▶Blood Supply EPIDIDYMIS

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The testis is covered anteriorly and laterally by the visceral SCROTUM

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▶▶Blood Supply ▶▶Blood Supply

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Emil A. Tanagho, MD; Hiep T. Nguyen, MD;

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Anomalies of the Nephric System