L40, 41, 42 - Reproductive System PDF

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American University of Antigua

Dr.Pugazhandhi Bakthavatchalam

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reproductive system anatomy physiology human biology

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This document is a lecture presentation on the reproductive system, suitable for undergraduate anatomy and physiology students. It covers topics including sperm production, semen composition, male and female reproductive hormones.

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L40, 41 & 42- REPRODUCTIVE SYSTEM Dr.Pugazhandhi Bakthavatchalam Assistant Professor of Anatomy and Physiology, AUACAS, American University of Antigua LEARNING OUTCOMES At the end of this lecture, students should be able to  Describe the Composition of semen  Describe the physiology of ejacula...

L40, 41 & 42- REPRODUCTIVE SYSTEM Dr.Pugazhandhi Bakthavatchalam Assistant Professor of Anatomy and Physiology, AUACAS, American University of Antigua LEARNING OUTCOMES At the end of this lecture, students should be able to  Describe the Composition of semen  Describe the physiology of ejaculation  Describe the Male sex hormones: actions of testosterone during fetal life, puberty and adult life, regulation and testosterone secretion.  Describe the Female reproductive cycle: ovarian cycle, uterine cycle, hormonal changes during the reproductive cycle.  Describe the Female sex hormones: actions of estrogen and progesterone and its regulation. SPERM PRODUCTION Each testis is a mass of more than 800 tightly looped and folded vessels known as seminiferous tubules. Inside each tubule, sperm begin as blob-like cells called spermatogonia lining the inner wall. These pass through a larger stage, as primary spermatocytes, then become smaller as secondary spermatocytes, and begin to develop tails as spermatids. The spermatids finally develop into ripe sperm with long tails. Thousands of sperm are produced every second, each taking about two months to mature. DIFFERENCE IN SEMEN AND SPERM Semen, also known as seminal fluid, is much more than just sperm. Sperm is only about 5 to 10% of any given male single ejaculation and the rest is fructose, fatty acids, and proteins to nourish the sperm during their journey. Sperm Count A man will produce roughly 525 billion sperm during his whole lifetime and close to 1 billion per month. There are around 200 to 500 million sperm in an average in a single human ejaculation Sperm develop in the testes and consist of a head, a midpiece, and a tail. The head contains the nucleus with densely coiled chromatin fibers (chromosomes), with a front section – the Acrosome that contains enzymes for penetrating the female egg. The midpiece has a central filamentous core with many Mitochondria spiraled around it, to give it energy to move the tail which propels it forward. Physiology of erection and ejaculation  Normal sexual function in males requires:  Intact libido  Ability to achieve and maintain penile erection  Ejaculation  Detumescence Sexual response cycle  Excitement phase  Erection and heightened sexual awareness  Plateau phase  Intensification and body responses (HR,  BP,  RR, muscle tension)  Orgasmic phase  Ejaculation and other responses that culminate in  sexual excitement  Resolution phase  Return to pre-arousal state Innervation  Erectile response mediated by a combination of:  Central (psychogenic) innervation CNS stimulates or antagonises spinal pathways that mediate erection and ejaculation  Peripheral (reflexogenic) innervation  Sexual arousal  Tactile stimulation Sensory nerves from skin + glans form dorsal nerve of penis Travel via pudendal nerve  Psychogenic stimuli Limbic system – transmitted via ANS  Neural input (Spinal reflex)  Tactile stimulation reflexively triggers  PSNS vasodilator activity These PSNS neurons arise from S2-4 and travel in pelvic splanchnic nerves Act on endothelial cells to release NO – induces vascular smooth muscle relaxation and  blood flow Prostaglandins are released in cavernosa and aid in SMC relaxation  SNS inhibition  Leads to erection Erection  Vascular phenomenon – involves 3 cylindrical vascular cords running the length of the penis Corpus cavernosa Corpus spongiosum  Normally the blood vessels supplying these are constricted and thus there is little blood within these cords  In order to achieve erection, these inflow vessels dilate, the penis becomes rigid, and thus compresses the emissary veins draining the penis, leaving the corpora as noncompressible cylinders from which blood does not escape (Corpus spongiosum) Ejaculation  Emission  Mediated via SNS impulses T11-L2 spinal segments via hypogastric + pelvic plexuses Contraction of epididymis, ductus deferens, seminal vesicles + prostate Internal vesical sphincter tightly closed Prevents semen entering bladder/urine being expelled during ejaculation  Expulsion  Expulsion of semen from posterior urethra  Mediated by somatic motor impulses via pudendal nerve Rhythmic contraction of bulbospongiosus and ischiocavernosus muscles Leads to increased pressure in penis and expulsion of semen  Detumescence- returning back to the flaccid state  Mediated by: NA from SNS nerves Endothelin from vascular endothelium SMC contraction induced by postsynaptic adrenergic receptors  Increased venous outflow – leads to restoring of flaccid state Maturation of sperm in the epididymis: -After formation in the seminiferous tubules, the sperm require several days to pass through the epididymis (still non-motile). - After the sperm have been in the epididymis for some 18 to 24 hour, they develop the capability of motility (some inhibitory proteins in the epididymal fluid prevent final motility until after ejaculation). Storage of sperm: The 2 testis of adult human form up to 120 million sperm each day. -Small amount stored in the vas deferns. – the majority stored in the epididymis, maintaining their fertility for at least a month. The sperm are kept inactive state by multiple inhibitory substances in the secretion of the ducts. After ejaculation, the sperm becomes motile & capable of fertilizing the ovum “maturation”. - The sertoli cells and epithelium of the epididymis secrete nutrient fluid which contains (testosterone & estrogens), enzymes & nutrients essential for sperm maturation. Physiology of mature sperm: Mature sperm are motile & capable of fertilizing the ovum & their activity is enhanced in a neutral to slightly alkaline medium & depressed in mildly acidic medium. The life expectancy of ejaculated sperm in the female genital tract is only 1 to 2 days Function of the seminal vesicles: - secrete mucoid material containing fructose, citric acid & nutrient substances & large quantities of prostaglandins & fibrinogen. Function of the prostate gland: The prostate gland secretes thin milky fluid contains Ca2+, citrate ion, phosphate ion, a clotting enzyme & profibrinolysin. The alkaline prostatic fluid is important for successful fertilization of the ovum. Effect of sperm count on fertility:  The quantity of ejaculated semen during coitus about 3-5 ml  each milliter contains about 120 million sperm (normal sperm count vary between 35 million to 200 million sperm/ml). Sperm count below 20 million/ml leads to infertility. Effect of sperm morphology and motility on fertility:  Sometimes sperm count is normal but still infertile when about one half of the sperm having abnormal shape.  Sometimes the shape of the sperm is normal but they either relatively non-motile or entirely non-motile which causes infertility. Hormonal factors that stimulate spermatogenesis: 1-Testosterone: secreted by the leydig cells which located in the interstitium of the testis, is essential for the growth and division of the testicular germinal cells. 2-Luteinizing hormone (LH) secreted by the anterior pituitary gland, stimulates the leydig cells to secrete testosterone. 3-Follicle stimulating hormone: FSH also secreted by the anterior pituitary gland, stimulates the sertoli cells, stimulate the conversion of spermatids to sperm (also important for spermatogenesis). 4-Estrogen: formed from testosterone by the sertoli cell under FSH stimulation also essential for spermatogenesis. 5-Growth hormone (also other body hormones) is necessary for controlling metabolic functions of the testis. GH promotes early division of spermatogonia in the absence of GH (pituitary dwarfs), the spermatogenesis is severely deficient or absent  infertility. Male sexual act: Stages of male sexual act: 1-Penile erection. Erection is caused by parasympathetic impulses that pass from the sacral portion of the spinal cord through the pelvic nerves to the penis. 2-Lubrication, Parasympathetic impulses cause the urethral glands &bulbourethral glands to secrete mucous. 3-Emission and ejaculation. Function of the sympathetic nerves. Emission begins by contraction of the vas deferens & ampulla to cause expulsion of the sperm in the internal urethra. Contraction of the prostate &seminal vesicles to expel their fluid in the urethra. All these fluid mix in the internal urethra with the mucous secreted by the bulbourethral glands to form the semen. This process at this point is called emission. Testosterone and other male sex chromosomes: secretion, metabolism and chemistry of the male sex hormone: Secretion of testosterone by the interstitial cell of Leydig in the testis. The testis secretes several male sex hormone called androgens including testosterone, dihydrotestosterone and androstenedione. Testosterone is more abundant form while dihydrotestosterone is more active. Testosterone is converted into dihydrotestosterone in the target cells. Functions of testosterone: It is responsible for the characteristic masculine body. During fetal life the testis are stimulated by placenta chorionic gonodotropin to produce testosterone throughout fetal life & the 10 weeks after birth then no more testosterone production during childhood. At puberty under the anterior pituitary gonadotropic hormones stimulation throughout life then decline beyond 80 years to 50%. Function of testosterone during fetal development: Testosterone secreted by the genital widges & later by the fetal testis is responsible for development of the male body characteristics including the formation of penis & scrotum & prostate gland, seminal vesicles & male genital ducts & suppressing the formation of female genital organs. Effect of testosterone to cause descent of the testis: The testis descend into the scrotum during the last 2 to 3 months of gestation when the testis begin secreting reasonable quantities of testosterone. Effect pf testosterone on development of adult primary and secondary sexual characteristics: 1-After puberty, the increasing amounts of testosterone cause enlargement of the penis, scrotum & testis & secondary sexual characteristics. 2- Effect on the distribution of body hair: Testosterone causes growth of hair: 1) over the pubis, 2) upward along the linea alba of the abdomen to the umbilicus; 3) on the face; 4) on the chest; 5) less often on other regions such as the back. 3-Baldness: Testosterone decreases the growth of hair on the top of the head. Two factors 1) genetic background; 2) large quantities of androgenic hormones. 4-Effect on voice: It causes hypertrophy of the laryngeal mucosa, enlargement of the larynx (typical adult masculine voice) 5-Testosterone increases thickness of the skin and can contribute to development of acne: Testosterone increases the thickness of skin over the body & subcutaneous tissues. Also it increases the secretion of the sebaceous glands & sebaceous glands of the face causing acne. 6-Testosterone increased protein formation and muscle development: Increase muscular development after puberty by 50% in muscle mass over that in female. Also increase in protein in non-muscle parts of the body. These effect due to the anabolic effect of testosterone. 7- Testosterone increases bone matrix and causes Ca2+ retention: Bones grow thicker & deposit additional Ca2+. Thus it increases the total quantity of bone matrix & causes Ca2+ retention (anabolic effect). Testosterone has specific effect on the pelvis 1) narrow the pelvic outlet; 2) lengthen it; 3) cause the funnel- like shape instead of the broad ovoid shape of the female pelvis. It causes the epiphyses of the long bones to unite with the shafts of the bones & early closure of the epiphyses. Cryptorchidism: Failure of the testes to descend in the scrotum which normally occur during fetal life.  They should be treated before puberty because of higher incidence of malignant tumors. The menstrual cycle is the body’s way of preparing for pregnancy. It is controlled by chemicals called hormones. Several hormones are involved in the menstrual cycle of a woman: follicle stimulating hormone (FSH) causes the maturation of an egg in the ovary. luteinising hormone (LH) stimulates the release of the egg. oestrogen is involved in repairing and thickening the uterus lining Progesterone maintains the uterus lining LH is secreted by the pituitary gland. When its level reaches a peak it stimulates the release of a mature egg from the ovary - ovulation FSH is secreted by the pituitary gland. It makes eggs mature and The level of oestrogen stimulates the ovary to rises. This inhibits the After the egg is released the produce oestrogen. production of more FSH level of progesterone rise and and stimulates the build up maintains the lining of the uterus of the lining of the uterus - in preparation for the proliferation implantation of the fertilised egg. Uterus lining breaks down - menstruation Lining of uterus Lining builds up maintained 4 hormones involved: FSH The Menstrual Cycle Oestrogen LH Progesterone The main events in the cycle are: 1) Menstruation – uterus lining breaks down, blood and cells are lost (Day 1- 4) 2) Proliferation – repair of the uterus lining (6-13) 3) Ovulation – release of an egg from the ovary – day 14 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 Cycle starts again References Susan. 2008. Gray’s Anatomy- The Anatomical Basis of clinical Practise. 40th edition. New York: Elsvier. Snell, R.S. 2008. Clinical Anatomy by Regions. 8th edition. Philadelphia: Lippincott Williams & Wilkins. Ellis, H. 2006. Clinical Anatomy- A revision and Applied Anatomy for Clinical Students. 11th edition. Victoria: Blackwell Publishing. Moore, K.L., Dalle,A.F. & Agur, A.M. 2010. Clinically Oriented Anatomy. 6th edition.Philadelphia: Lippincott Williams & Wilkins.

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