Download Download

Total Page:16

File Type:pdf, Size:1020Kb

Download Download HISTOPATHOLOGICAL TYPES OF OVARIAN NEOPLASMS IN UNIVERSITY COLLEGE HOSPITAL, IBADAN BETWEEN JANUARY 1991 AND JUNE 2013 BY DR. MUSTAPHA AKANJI AJANI, MBBS (OGBOMOSO) DEPARTMENT OF PATHOLOGY, UNIVERSITY COLLEGE HOSPITAL, IBADAN [email protected] /08039125255 A DISSERTATION SUBMITTED TO THE NATIONAL POSTGRADUATE MEDICAL COLLEGE OF NIGERIA IN PARTIAL FULFILMENT OF THE REQUIREMENTS FOR THE AWARD OF THE FELLOWSHIP OF THE NATIONAL POSTGRADUATE MEDICAL COLLEGE OF NIGERIA (FMCPath) OCTOBER 2014 i DECLARATION This is to certify that this study titled HISTOPATHOLOGICAL TYPES OF OVARIAN NEOPLASMS IN UNIVERSITY COLLEGE HOSPITAL, IBADAN BETWEEN JANUARY 1991 AND JUNE 2013 was performed by me in the Department of Pathology, University College Hospital, Ibadan. This project has not been submitted to any other College for consideration ----------------------------------- AJANI, MUSTAPHA AKANJI MBBS (OGBOMOSO) ii ATTESTATION This is to certify that we supervised Dr M. A. Ajani in the conduct of the study entitled HISTOPATHOLOGICAL TYPES OF OVARIAN NEOPLASMS IN UNIVERSITY COLLEGE HOSPITAL, IBADAN BETWEEN JANUARY 1991 AND JUNE 2013. ---------------------------------------------- PROFESSOR E. E. U. AKANG MBBS (Ib), FWACP, FMCPath ----------------------------------- DR. C. A. OKOLO MBBS, FMCPath iii DEDICATION This project is dedicated to: the Almighty God, my present help; my late cheerful and kind - hearted mother, Mrs Amudat Ajani (Nee Lasisi). You sold all you had so that I could be educated. You taught me to be diligent in all that I do. Even in death, you will always be loved. iv ACKNOWLEDGEMENT Who am I without Him? My foremost and deepest appreciation goes to Almighty God-my greatest inspiration, who has made this work a possibility. I acknowledge the efforts of my supervisors, Prof EEU Akang and Dr CA Okolo, for their guidance and dedication to this work. My gratitude also goes to my other teachers in the Department of Pathology: Prof JO Ogunbiyi, Dr AO Oluwasola, Dr GO Ogun, Dr AO Adeoye, Dr UO Eze and Dr A Salami for imparting my life. I wish to thank Mr S Ajagboye and Mr SP Otegbade of the Department of Pathology for the technical assistance they rendered with the slides used for this study. I also wish to acknowledge my fellow resident doctors for their support and encouragement. My gratitude goes to my lovely wife, Dr TA Ajani for her support throughout all these years and also to my lovely children; Esther Ajani and Daniel Ajani for their encouragement. v TABLE OF CONTENTS Page TITLE PAGE i DECLARATION ii ATTESTATION iii DEDICATION iv ACKNOWLEDGEMENT v TABLE OF CONTENTS vi–vii LIST OF FIGURES viii–ix LIST OF TABLES x LIST OF APPENDICES xi SUMMARY xii–xiii CHAPTER ONE Introduction 1– 2 Justification 3 Aim and Objectives 4 vi CHAPTER TWO Literature Review 5– 21 CHAPTER THREE Materials and Methods 22– 23 CHAPTER FOUR Results 4.1 General Findings 24–25 4.2 Age 25–26 4.3 Location 26–28 4.4 Specific Ovarian Neoplasms 28 –32 4.5 Childhood Ovarian Neoplasms 33 List of Figures and Tables 34 –63 CHAPTER FIVE Discussion 64–73 Conclusion 74 REFERENCES 75-80 APPENDICES 81- 83 vii LIST OF FIGURES Page Figure 1- Age distribution of Ovarian Neoplasms 34 Figure 2 – Photomicrograph of a case of Mucinous Cystadenoma (X 400) 35 Figure 3 – Photomicrograph of a case of Benign Brenner Tumour (X 400) 36 Figure 4 – Photomicrograph of a case of Borderline Serous Tumour (X 100) 37 Figure 5 – Photomicrograph of a case of Papillary Serous Cystadenocarcinoma showing predominant papillary pattern (X 400) 38 Figure 6- Photomicrograph of a case of Papillary Serous Cystadenocarcinoma showing psammoma bodies (X 400) 39 Figure 7 – Photomicrograph of a case of Mucinous Cystadenocarcinoma (X100) 40 Figure 8 – Photomicrograph of a case of Malignant Brenner Tumour (X400) 41 Figure 9 – Photomicrograph of a case of Mature Cystic Teratoma (X 100) 42 Figure 10 – Photomicrograph of a case of Struma Ovarii (X 100) 43 Figure 11 – Photomicrograph of a case of Choriocarcinoma (X 100) 44 Figure 12 – Photomicrograph of a case of Dysgerminoma (X100) 45 Figure 13 – Photomicrograph of a case of Yolk sac tumour (X 100) 46 Figure 14 – Photomicrograph of a case of Granulosa Cell Tumour (X 400) 47 viii Figure 15 – Photomicrograph of a case of Metastatic Adenocarcinoma (X 400) 48 Figure 16 – Photomicrograph of a case of Burkitt Lymphoma (X400) 49 ix LIST OF TABLES Page Table 1 – Age distribution of 822 patients with primary ovarian neoplasms 50 Table 2 – Age distribution of 46 patients with secondary ovarian neoplasms 51 Table 3 – Age distribution of 516 patients with benign/borderline ovarian neoplasms 52 Table 4 – Age distribution of 352 patients with malignant ovarian neoplasms 53 Table 5 – Correlation between location of ovarian neoplasms and age 54 Table 6 – Frequency of Surface epithelial tumours 55 Table 7 – Frequency of Germ cell tumours 56 Table 8 – Frequency of Sex cord Stromal tumours 57 Table 9 – Frequency of Primary and Secondary ovarian neoplasms 58 Table 10 – Age distribution of Childhood ovarian neoplasms 59 Table 11 – Comparison of distribution of benign, borderline and malignant ovarian neoplasms seen in the present study with other studies 60 Table 12 – Comparison of Histological types seen in the present study with other studies 61 Table13 – Relative frequencies of the eight commonest benign ovarian tumours in the present study compared with other studies 62 Table 14 – Relative frequencies of the eight commonest malignant ovarian tumours in the present study compared with other studies 63 x LIST OF APPENDICES Page Appendix 1 2003 WHO Histological Classification of Tumours of the Ovary 81- 82 Appendix 2 Ethical Approval 83 xi SUMMARY Design- This was a retrospective study carried out at the Department of Pathology, University College Hospital, Ibadan. Aim- The aim of this study was to determine the histopathological pattern of ovarian neoplasms seen at the University College Hospital, Ibadan, Nigeria. Methods- Histologically confirmed cases of ovarian neoplasms diagnosed at the University College Hospital (UCH), Ibadan between January 1991 and June 2013 were used for the study. Cases with inadequate clinical or pathology data and those whose blocks and or slides could notbe retrieved were excluded from the study. Data were obtained from the records of the Department of Pathology. The cases were histologically classified using the 2003 WHO histological classification of tumours of the ovary. The data obtained were subjected to statistical analysis using the Statistical Package for Social Sciences version 20. Results- A total of 868 cases of ovarian neoplasm were included in this study. Five hundred and ten (58.8%) were benign, 351 (40.6%) were malignant and 6 (0.7%) were borderline tumours. Three hundred and sixty-two (41.7%) cases were right sided, 297 (34.2%) were left sided and 209 (24.1%) were bilateral. Eight hundred and twenty-two (94.7%) cases were primary ovarian tumours and 46 (5.3%) constituted the secondary ovarian neoplasms. The age range was from 4 to 92 years with the mean age of 39.2 (S. D = 15.8 years). The peak age of occurrence of ovarian neoplasms was in the fourth decade. Surface epithelial tumours were the most common histological type of ovarian neoplasms constituting 359 (41.4%) closely followed by Germ cell tumours 313 (36.1%). Mature cystic teratoma was the commonest benign ovarian tumour accounting for 279 (32.1%) cases. It showed a wide range of occurrence with peak occurrence xii between 20 and 29 years. Serous cystadenocarcinoma was the commonest malignant ovarian tumour accounting for 117 (13.5%) of all ovarian neoplasms with peak age of occurrence between 50 and 59 years. Conclusion- Surface epithelial tumours were the most common ovarian neoplasm followed by germ cell tumours. This pattern is observed in most parts of Nigeria, some African and Asian countries, and in the Western world. Keywords: Histopathological pattern, ovarian neoplasms, Ibadan, Nigeria xiii CHAPTER ONE 1.1 INTRODUCTION Ovarian tumours are common forms of neoplasms in women. There are many types of ovarian tumours, both benign and malignant. About 80% of ovarian neoplasms are benign, and these occur mostly in young women between the ages of 20 and 45 years. The malignant tumours are more common in older women between the ages of 40 and 65 years.1 Malignant ovarian tumours account for about 30% of female genital cancers. Ovarian carcinoma is the fourth most common female cancer and the fourth leading cause of cancer related deaths in females.2, 3, 4, 5 Ovarian tumours are generally difficult to detect until they are of advanced stage or are large in size. This is primarily due to the fact that symptoms are vague and most cases are asymptomatic and therefore they manifest when advanced. Another reason is the fact that no definite screening program exists.6 The proposed causal relationship between ovarian stimulation and neoplasia is based on three main hypotheses proposed by Fathalla. The first hypothesis suggests that epithelial ovarian carcinoma results from repeated ovulations, where the cumulative effects of each minor trauma on the ovarian epithelium can lead to malignant transformation. This proposes that the risk of ovarian cancer is directly proportional to the number of ovulatory cycles between the menarche and the menopause. The second hypothesis suggests that persistent exposure of the ovary to endogenous or exogenous gonadotrophins or in conjunction with secondarily elevated oestradiol concentrations may be directly carcinogenic. The third hypothesis relates to the production of chemical carcinogens within the local ovarian environment after stimulation with gonadotrophins and oestrogens.6 1 Determination of various histological patterns of ovarian tumours is very important in diagnosis, treatment as well as prognostication of ovarian tumours. Prognosis of the tumours can also be predicted from the degree of differentiation of the tumours. The stage and laterality of the tumour also indicates their nature; for example, tumours in the sex cord stromal category are almost always confined to a single ovary.
Recommended publications
  • Male Reproductive System Sexual Reproduction Requires Two Types Of
    Male Reproductive system Sexual reproduction requires two types of gametes or sex cells. In the male these cells are the spermatozoa and in the female they are the ova. The reproductive systems are unique in three respects 1. They are specialized in perpetuating the species and passing genetic information. 2. The anatomy and physiology between the male and female reproductive systems are different. 3. They exhibit latent development under hormonal control. The structures of the male reproductive system can be divided into three categories. 1. Primary sex organs - the gonads (testes). These produce sperm and sex hormones. 2. Secondary sex organs - the structures necessary for caring for and transportation of the sperm. A. Sperm transporting ducts 1. epididymus 2. ductus deferens 3. ejaculatory ducts 4. urethra B. Accessory glands 1. seminal vesicle 2. prostate gland 3. bulbourethral (Cowper's) glands C. Copulatory organ - penis. Also includes the scrotum (the skin enclosing the testes) 3. Secondary sex characteristics - These are not reproductively necessary, but are considered sexual attractants. They include things such as body hair, body physique, and voice pitch. Sexual determination - Sex is determined at the time of conception. As we will see, all ova have an x chromosome and sperm are 50:50 X and Y. If an ova is fertilized by an x sperm then we have a female. If an ova is fertilized by a Y sperm then we have a male. Sometimes we see more than one X in an ovum. As long as there is a Y chromosome we will have a male. ie. XXXY = male.
    [Show full text]
  • Mechanisms of Gonadal Morphogenesis Are Not Conserved Between Chick and Mouse ⁎ Ryohei Sekido , Robin Lovell-Badge
    Developmental Biology 302 (2007) 132–142 www.elsevier.com/locate/ydbio Mechanisms of gonadal morphogenesis are not conserved between chick and mouse ⁎ Ryohei Sekido , Robin Lovell-Badge Division of Developmental Genetics, MRC National Institute for Medical Research, The Ridgeway, Mill Hill, London NW7 1AA, UK Received for publication 3 June 2006; revised 16 August 2006; accepted 5 September 2006 Available online 9 September 2006 Abstract To understand mechanisms of sex determination, it is important to know the lineage relationships of cells comprising the gonads. For example, in mice, the Y-linked gene Sry triggers differentiation of Sertoli cells from a cell population originating in the coelomic epithelium overlying the nascent gonad that also gives rise to uncharacterised interstitial cells. In contrast, little is known about origins of somatic cell types in the chick testis, where there is no Sry gene and sex determination depends on a ZZ male/ZW female mechanism. To investigate this, we performed fate mapping experiments in ovo, labelling at indifferent stages the coelomic epithelium by electroporation with a lacZ reporter gene and the underlying nephrogenous (or mesonephric) mesenchyme with chemical dyes. After sex differentiation, LacZ-positive cells were exclusively outside testis cords and were 3βHSD-negative, indicating that the coelomic epithelium contributes only to non-steroidogenic interstitial cells. However, we detected dye-labelled cells both inside and outside the cords. The former were AMH-positive while some of the latter were 3βHSD- positive, showing that nephrogenous mesenchyme contributes to both Sertoli cells and steroidogenic cells. This is the first demonstration via lineage analysis that steroidogenic cells originate from nephrogenous mesenchyme, but the revelation that Sertoli cells have different origins between chick and mouse suggests that, during evolution, mechanisms of gonad morphogenesis may diverge alongside those of sex determination.
    [Show full text]
  • ANA214: Systemic Embryology
    ANA214: Systemic Embryology ISHOLA, Azeez Olakune [email protected] Anatomy Department, College of Medicine and Health Sciences Outline • Organogenesis foundation • Urogenital system • Respiratory System • Kidney • Larynx • Ureter • Trachea & Bronchi • Urinary bladder • Lungs • Male urethra • Female urethra • Cardiovascular System • Prostate • Heart • Uterus and uterine tubes • Blood vessels • Vagina • Fetal Circulation • External genitalia • Changes in Circulation at Birth • Testes • Gastrointestinal System • Ovary • Mouth • Nervous System • Pharynx • Neurulation • GI Tract • Neural crests • Liver, Spleen, Pancreas Segmentation of Mesoderm • Start by 17th day • Under the influence of notochord • Cells close to midline proliferate – PARAXIAL MESODERM • Lateral cells remain thin – LATERAL PLATE MESODERM • Somatic/Parietal mesoderm – close to amnion • Visceral/Splanchnic mesoderm – close to yolk sac • Intermediate mesoderm connects paraxial and lateral mesoderm Paraxial Mesoderm • Paraxial mesoderm organized into segments – SOMITOMERES • Occurs in craniocaudal sequence and start from occipital region • 1st developed by day 20 (3 pairs per day) – 5th week • Gives axial skeleton Intermediate Mesoderm • Differentiate into Urogenital structures • Pronephros, mesonephros Lateral Plate Mesoderm • Parietal mesoderm + ectoderm = lateral body wall folds • Dermis of skin • Bones + CT of limb + sternum • Visceral Mesoderm + endoderm = wall of gut tube • Parietal mesoderm surrounding cavity = pleura, peritoneal and pericardial cavity • Blood &
    [Show full text]
  • Actinomycosis Israeli, 129, 352, 391 Types Of, 691 Addison's Disease, Premature Ovarian Failure In, 742
    Index Abattoirs, tumor surveys on animals from, 823, Abruptio placentae, etiology of, 667 828 Abscess( es) Abdomen from endometritis, 249 ectopic pregnancy in, 6 5 1 in leiomyomata, 305 endometriosis of, 405 ovarian, 352, 387, 388-391 enlargement of, from intravenous tuboovarian, 347, 349, 360, 388-390 leiomyomatosis, 309 Acantholysis, of vulva, 26 Abdominal ostium, 6 Acatalasemia, prenatal diagnosis of, 714 Abortion, 691-697 Accessory ovary, 366 actinomycosis following, 129 Acetic acid, use in cervical colposcopy, 166-167 as choriocarcinoma precursor, 708 "Acetic acid test," in colposcopy, 167 criminal, 695 N-Aceryl-a-D-glucosamidase, in prenatal diagnosis, definition of, 691 718 of ectopic pregnancy, 650-653 Acid lipase, in prenatal diagnosis, 718 endometrial biopsy for, 246-247 Acid phosphatase in endometrial epithelium, 238, endometritis following, 250-252, 254 240 fetal abnormalities in, 655 in prenatal diagnosis, 716 habitual, 694-695 Acridine orange fluorescence test, for cervical from herpesvirus infections, 128 neoplasia, 168 of hydatidiform mole, 699-700 Acrochordon, of vulva, 31 induced, 695-697 Actinomycin D from leiomyomata, 300, 737 in therapy of missed, 695, 702 choriocarcinoma, 709 tissue studies of, 789-794 dysgerminomas, 53 7 monosomy X and, 433 endodermal sinus tumors, 545 after radiation for cervical cancer, 188 Actinomycosis, 25 spontaneous, 691-694 of cervix, 129, 130 pathologic ova in, 702 of endometrium, 257 preceding choriocarcinoma, 705 of fallopian tube, 352 tissue studies of, 789-794 of ovary, 390, 391 threatened,
    [Show full text]
  • Testicular Tumors: General Considerations
    TESTICULAR TUMORS: 1 GENERAL CONSIDERATIONS Since the last quarter of the 20th century, EMBRYOLOGY, ANATOMY, great advances have been made in the feld of HISTOLOGY, AND PHYSIOLOGY testicular oncology. There is now effective treat- Several thorough reviews of the embryology ment for almost all testicular germ cell tumors (22–31), anatomy (22,25,32,33), and histology (which constitute the great majority of testicular (34–36) of the testis may be consulted for more neoplasms); prior to this era, seminoma was the detailed information about these topics. only histologic type of testicular tumor that Embryology could be effectively treated after metastases had developed. The studies of Skakkebaek and his The primordial and undifferentiated gonad is associates (1–9) established that most germ cell frst detectable at about 4 weeks of gestational tumors arise from morphologically distinctive, age when paired thickenings are identifed at intratubular malignant germ cells. These works either side of the midline, between the mes- support a common pathway for the different enteric root and the mesonephros (fg. 1-1, types of germ cell tumors and reaffrms the ap- left). Genes that promote cellular proliferation proach to nomenclature of the World Health or impede apoptosis play a role in the initial Organization (WHO) (10). We advocate the use development of these gonadal ridges, includ- of a modifed version of the WHO classifcation ing NR5A1 (SF-1), WT1, LHX1, IGFLR1, LHX9, of testicular germ cell tumors so that meaningful CBX2, and EMX2 (31). At the maximum point comparisons of clinical investigations can be of their development, the gonadal, or genital, made between different institutions.
    [Show full text]
  • 1- Development of Female Genital System
    Development of female genital systems Reproductive block …………………………………………………………………. Objectives : ✓ Describe the development of gonads (indifferent& different stages) ✓ Describe the development of the female gonad (ovary). ✓ Describe the development of the internal genital organs (uterine tubes, uterus & vagina). ✓ Describe the development of the external genitalia. ✓ List the main congenital anomalies. Resources : ✓ 435 embryology (males & females) lectures. ✓ BRS embryology Book. ✓ The Developing Human Clinically Oriented Embryology book. Color Index: ✓ EXTRA ✓ Important ✓ Day, Week, Month Team leaders : Afnan AlMalki & Helmi M AlSwerki. Helpful video Focus on female genital system INTRODUCTION Sex Determination - Chromosomal and genetic sex is established at fertilization and depends upon the presence of Y or X chromosome of the sperm. - Development of female phenotype requires two X chromosomes. - The type of sex chromosomes complex established at fertilization determine the type of gonad differentiated from the indifferent gonad - The Y chromosome has testis determining factor (TDF) testis determining factor. One of the important result of fertilization is sex determination. - The primary female sexual differentiation is determined by the presence of the X chromosome , and the absence of Y chromosome and does not depend on hormonal effect. - The type of gonad determines the type of sexual differentiation in the Sexual Ducts and External Genitalia. - The Female reproductive system development comprises of : Gonad (Ovary) , Genital Ducts ( Both male and female embryo have two pair of genital ducts , They do not depend on ovaries or hormones ) and External genitalia. DEVELOPMENT OF THE GONADS (ovaries) - Is Derived From Three Sources (Male Slides) 1. Mesothelium 2. Mesenchyme 3. Primordial Germ cells (mesodermal epithelium ) lining underlying embryonic appear among the Endodermal the posterior abdominal wall connective tissue cell s in the wall of the yolk sac).
    [Show full text]
  • Sex Determination
    Sex Determination • Most animal species are dioecious – 2 sexes with different gonads • Females: produce eggs in ovaries • Males: produce sperm in testes • Exception • Hermaphrodites: have both types of gonads • Many animals also differ in secondary traits What Determines Sex? • Individual differentiates into male or female • Causes – Genetic factors (sex chromosomes) – occur at fertilization – Environmental factors – occur after fertilization How Do Vertebrate Gonads Develop? • Gonad differentiation – first morphological difference between males and females • Gonads develop from intermediate mesoderm • Paired structures What is a Bipotential Gonad? • Indifferent gonad develops – 4-6 wks in human = “bipotential stage” – genital ridge forms next to developing kidney (mesonephric ridge) Structure of the Indifferent Gonad • Sex cords form – Columns of epithelial cells penetrate mesenchyme – Primordial germ cells migrate from posterior endoderm – Become surrounded by sex cords What is the Fate of the Sex Cords? • Initially in central area (medulla, medullary) – Will develop in male – Proliferate • In outer area (cortex, cortical) – Develop in female • Normally binary choice Differentiation of the Gonad • Into testes or ovaries – primary sex determination – does not involve hormones network of internal sex cords (at new cortical sex cords puberty: --> seminiferous tubules, cluster around each germ cell Sertoli cells Male Differentiation • Male sex cords or testis cords proliferate and cortex becomes thick layer of extracellular matrix • Male
    [Show full text]
  • Animal and Veterinary Science Department University of Idaho
    Animal and Veterinary Science Department University of Idaho EMBRYOGENESIS AND SEXUAL DIFFFERENTIATION AVS 222 (Instructor: Dr. Amin Ahmadzadeh) Chapter 4 I. DIFFERENTIATION Primitive group of unspecialized cells develop a functional and specialized group of cells that provide a common function A. Involves Formation of Three Germ Layers 1. Embryonic tissue, which form all adult tissues and organs B. Germ Layers Formed During Gastrulation (re-arrangement of the embryonic cells) C. Three Germ Layers: (Table 4-1) 1. Ectoderm: in general, form exterior tissues (Figure 4-1, adapted from Senger ©) a. Skin, hair, sweat glands b. Mammary glands c. Hypothalamus, anterior and posterior pituitary d. Part of the reproductive tract (male and female) 2. Mesoderm: in general, forms structural tissue (Figure 4-1) a. Muscle, Skeletal system, blood vessels b. Reproductive system gonads, uterus, cervix, part of vagina, accessory sex glands e. Renal system 3. Endoderm: in general, form internal organs (Figure 4-1) a. Digestive system, Liver, lungs b. Majority of glands II. SEXUAL DIFFERENTIATION AND DETERMINATION A. Genetic differentiation 1. An individual’s sex is genetically determined by the presence of a Y chromosome 2. Genetic differentiation takes place at fertilization when a sperm delivers either an X (female) or Y (male) chromosome to the oocyte 3. Sex determination gene of the Y chromosome causing the undifferentiated gonad develop into the testis is Sry gene 4. Sry gene of the Y chromosome responsible for the expression of substance called testis determining factor (TDF) secreted by the sex cords. 6. TDF controls the pathway towards either male or female development.
    [Show full text]
  • Reproduction Block Embryology Team
    Reproduction Block Embryology Team Lecture 1: Development of the Male Reproductive Organs Abdulrahman Ahmed Alkadhaib Lama AlShwairikh Nawaf Modahi Norah AlRefayi Khalid Al-Own Sarah AlKhelb Abdulrahman Al-khelaif Done By: Sarah AlKhelb , Nawaf Modahi & Abdulrahman Al-khelaif Revised By: Lama AlShwairikh & Abdulrahman Ahmed Alkadhaib Objectives: At the end of the lecture, students should be able to: List the causes of differentiation of genitalia into the male type. Describe the origin of each part of the male internal & external genitalia. List the causes & describe the events of descent of testis. List the common anomalies of male genital system & describe the causes of each of them. Red = important Green= team notes P.S. 16 pages may seem too many, but the actual work is 10 pages. So, don’t worry about it, and hopefully you’ll find the lecture easy to understand. Best of luck! MALE GENITAL SYSTEM Gonad: Testis. Genital Ducts: Epididymis. Vas deferens. Urethra. Genital Glands: Seminale vesicle (Seminal gland) Prostate. Bulbourethral Glands. DEVELOPMENT OF GONADS During 5th week: Gonadal development occurs. Until 7th week: gonads are similar in both sexes. Gonads are derived from 3 sources: 1. Mesothelium (mesodermal) epithelium lining the coelomic cavity) 2. Underlying mesenchyme 3. Primordial germ cells INDIFFERENT GONADS Gonadal ridge: a bulge on the medial side of mesonephros produced by: 1. Proliferation of mesothelium (cortex) 2. Proliferation of mesenchyme (medulla) Gonadal (primary sex) cords: The proliferating mesothelial cells (of the gonadal ridge) fuse and penetrate the underlying mesenchyme to form gonadal cords. Primordial germ cells: endodermal cells of the yolk sac migrate along dorsal mesentery of hindgut to gonadal ridges & become incorporated into gonadal cords.
    [Show full text]
  • Development of the Genital System Development of the Gonads
    Development of the Genital System Development of the gonads Dr Ahmed Salman The gonads develop form three sources (the first two are mesodermal, the third one is endodermal ) . 1.Proliferating coelomic epithelium on the medial side of the mesonephros. 2. Adjacent mesenchyme dorsal to the proliferating coelomic epithelium. 3. Primordial germ cells (endodermal), which develop in the wall of the yolk sac and migrate along the dorsal mesentery to reach the developing gonad. DR AHMED SALMAN The indifferent stage of the developing gonads - The coelomic epithelium (on either side of the aorta) proliferates and becomes multi layered and forms a longitudinal projection into the coelomic cavity called the genital ridge. - The genital ridge forms a number of epithelial cords called the primary sex cords that invade the underlying mesenchyme, which separate the cords from each other. - Up to the 6th or 7th week, the developing gonad cannot be differentiated into testis or ovary. DR AHMED SALMAN DR AHMED SALMAN Development of the testis and its descent Under the effect of the testis determining factor (T.D.F) present on the short arm of Y - chromosome, the undifferentiated gonad is switched to form a testis. 1. The coelomic epithelium. - The primary sex cords elongate to form testis cords (future seminiferous tubules) which undergo three important events : • Ventrally, they lose contact with the surface epithelium by the developing tunica albuginae. • Dorsally, they communicate with each other to form rete testis. • Internally, they are invaded by the primitive germ cells. DR AHMED SALMAN The testis cords become lined by two types of cells: A.
    [Show full text]
  • Development of Gonads and Sex Differentiation
    Development of gonads and sex differentiation Development of gonads and sex differentiation Chromosomal and genetic sex is established at fertilization and depends upon whether an X-bearing sperm or a Y-bearing sperm fertilizes the X-bearing ovum. The type of gonads that develop, gonadal sex, is determined by the sex chromosome complex (XX or XY). Sex differentiation is a complex process that involves many genes, including autosomal ones. The key to sexual dimorphism is the Y chromosome. This chromosome has a strong testis-determining effect on the medulla of the indifferent gonad. It contains the testis- determining gene, the SRY (sex-determining region on Y) gene on its short arm (Yp11). The protein product of this gene is a transcription factor initiating a cascade of downstream genes that determine the fate of rudimentary sexual organs. The SRY protein is the testis-determining factor. When the transcription factor is expressed in the somatic support cells of the indifferent presumptive gonad, male development occurs. This step is called primary sex determination. If the factor is absent or defective, female development takes place. The sexual genotype is responsible for directing gonadal development (testis versus ovary). The type of gonads present then determines the type of sexual differentiation that occurs in the genital ducts and external genitalia. It is the androgen testosterone, produced by the testes, that determines maleness. Although the chromosomal and genetic sex of an embryo is determined at fertilization by the kind of sperm that fertilizes the ovum, male and female morphological characteristics of sex do not begin to develop until the 7th week.
    [Show full text]
  • Embryology /Organogenesis
    Embryology /organogenesis/ Development and teratology of reproductive system Male or female sex is determined by spermatozoon Y in the moment of fertilization SRY gene, on the short arm of the Y chromosome, initiates male sexual differentiation. • The SRY initiates transformation of indifferent gonads into testes, which produce hormones supporting development of male reproductive organs. • Developed testes produce: - testosterone (T) - stimulates Wolffian ducts development (epididymis with ductuli efferentes + ductus epididymidis and deferent ducts) and - anti-Müllerian hormone (AMH) - suppresses Mullerian ducts development (oviduct, uterus, and upper vagina). • Indifferent stage – until week 7 - 10 • Differentiated stage 1) Development of gonads 2) Development of reproductive passages 3) Development of external genitalia Development of gonads mesonephric ridge (laterally) Dorsal wall of body: urogenital ridge genital ridge (medially), consisting of mesenchyme and coelomic epithelium (Wolffian duct) gonad Embryo, week 5 Three sources of gonad development: 1 – mesenchyme of gonadal ridges (plica genitalis) 2 – coelomic epithelium (mesodermal origin) 3 – gonocytes (primordial cells) gonocytes Primordial germ cells – gonocytes – in endoderm of dorsal wall of yolk sac. Gonocytes migrate along dorsal mesentery of hindgut into the gonadal ridges and induce (!) gonad development. Dorsal mesentery with gonocytes Embryo, weeks 4-6 Indifferent gonad development • Gonocytes induce coelomic epithelium to proliferate - primary proliferation gonocytes, cells of coelomic epithelium in mesenchyme form together: primary sex cords coelomic epith. proliferates and forms cords in mesenchyme of indifferent gonad,gonocytes invade cords. Primary proliferation (in male and female) TESTIS Secondary proliferation (only in female) seminiferous tubules INDIFFERENT tunica GONAD albuginea primary sex cords = medullary cords OVARY ovarian follicles secondary sex cords ONLY = cortical cords in ovary TESTIS: Primary sex cords tubuli semuniferi contorti Gonocytes spermatogonia Coelomic ep.
    [Show full text]