Review

Human Life Cycle Mitosis

Stages of Mitosis

Meiosis
Crossing-Over Stages of Meiosis

Chromosomal Inheritance Autosomal Syndromes Sex Chromosomal Syndromes

Human Life Cycle

Mitosis ensures every cell has a complete number of chromosomes. Meiosis reduces the chromosome number by half in gametes.
Sperm and egg (gametes) are haploid (n). Somatic cells are diploid (2n).

Human Life Cycle

Mitosis
Mitosis occurs in humans when tissues grow or when repair occurs, and produces daughter cells with the same number of chromosomes as the parental cells.
Sister chromosomes separate, and one of each kind of chromosome goes into each daughter cell.

Mitosis Overview

Cell Cycle
Cell cycle consists of:
Interphase. Mitosis. Cytokinesis.

Interphase is the interval of time between cell divisions, and is the phase the cell is in the longest.

Stages of Mitosis
Prophase.
Centrioles outside nucleus move away from each other. Spindle fibers appear. Nuclear envelope fragments.

Metaphase.
Spindle fully-formed. Chromosomes align at the equator.

Stages of Mitosis
Anaphase.
Sister chromosomes separate and daughter chromosomes move to the poles.
Spindle fibers shorten and pull chromosomes towards the poles.

Telophase.
Chromosomes arrive at the poles. Chromosomes become indistinct chromatin. Two daughter cells.

Meiosis
Meiosis requires two nuclear divisions and results in four daughter cells, each with half the number of parental chromosomes.
Humans have 23 pairs of homologous chromosomes.
During meiosis I synapsis occurs allowing crossing-over.
Exchange of genetic material between chromatids.

Crossing-Over

Meiosis
At the beginning of Meiosis II, chromosomes are dyads because each is composed of two sister chromatids. During Meiosis II, sister chromatids separate in each of the cells from Meiosis I. Each of the resulting four daughter cells has the haploid number of chromosomes.

Meiosis Overview

The Importance of Meiosis

Three ways individuals are assured a different genetic combination than either parent.
Crossing-over recombines genes on sister chromosomes of homologous pairs. Following meiosis, gametes have all possible chromosome combinations. At fertilization, sperm and egg carry varied chromosome combinations.

Spermatogenesis and Oogenesis

Spermatogenesis occurs in the testes of males and produces haploid sperm.
Once started, continues to completion.

Oogenesis occurs in the ovaries of females, and produces haploid eggs.

Does not necessarily go to completion.

Stages of Meiosis
First Division.
Prophase I - Spindle appears, and nuclear envelope fragments. Metaphase I - Tetrads line up at equator. Anaphase I - Homologous chromosomes of each pair separate and move to opposite poles of the spindle. Telophase I - Spindle disappears and nuclear envelope reforms. Cytokinesis - Plasma membrane furrows.

Stages of Meiosis
Second Division.
Prophase II - Spindle appears and nuclear envelope disassembles. Metaphase II - Dyads line up at equator. Anaphase II - Sister chromatids separate and move towards poles. Telophase II - Spindle disappears and nuclear envelope reforms. Cytokinesis - Plasma membrane furrows.
Four haploid daughter cells produced.

Chromosomal Inheritance
Humans have 22 pairs of autosomes, and one pair of sex chromosomes.
Abnormal chromosome number or structure often leads to a syndrome.

Amniocentesis and Chorionic Villi Sampling can be used to obtain a genetic sample to produce a karyotype.
Visual display of chromosomes arranged by size, shape, and banding pattern.

Human Karyotype Preparation

Autosomal Syndromes
Nondisjunction occurs:
During Meiosis I when both members of a homologous pair go to the same daughter cell. During Meiosis II when sister chromosomes fail to separate and both daughter chromosomes go to the same gamete.

Autosomal Syndromes
Down Syndrome.
Trisomy 21. Incidence increases with mothers age.

Cri du Chat Syndrome.

Chromosomal deletion.

Sex Chromosomal Syndromes

Fragile X Syndrome. Abnormal Sex Chromosome Number.
Turner Syndrome.
XO.

Klinefelter Syndrome.
Two or more X chromosomes with a Y.

Poly-X Females.
More than two X chromosomes.

Jacobs Syndrome.
XYY.

Turner and Klinefelter Syndromes

Reproduction

Outline
Sexual reproduction Sex determination Development of sexual accessory organs and external genitalia Male Reproductive System
Testes and Sperm Hormonal Regulation

Sexual reproduction
In sexual reproduction, germ cells or gametes (sperm and ova), are formed within the gonads (testes and ovaries) by a process of reduction divisions or meiosis The normal number of chromosomes in most human cells forty six is halved, so that each gamete receives twenty- three chromosome s Fusion of a sperm and ovum in the act of fertilization results in restoration of the original chromosomes number of forty-six in the fertilized egg ( the zygote) Growth of the zygote into an adult occurs by means of mitotic cell divisions When this individual reaches puberty, matures sperm or ova will be formed by meiosis within the gonads so that the life cycle can be continued

Sexual Reproduction in Human

testis
meiosis

ovary
meiosis fertilization

sperms

eggs (ova)

zygote embryo foetus baby

Sex Determination
When a diploid cell undergoes meiotic division, its daughter cells receive only one chromosome from each homologous pair of chromosomes ( haploid) Since female have two X chromosomes, however all of the ova will normally contain one X chromosome. Whereas sperm are X bearing and others are Y bearing, the chromosomal sex of the zygote is determined by the sperm If a Y bearing sperm fertilizes the ovum the zygote will be XY and male, if an X-bearing sperm fertilizes the ovum, the zygote will be XX and female

Formation of Testes and ovaries

The gonads of males and females appear similar for the first forty days of development following conception at this stage in development the gonads have the potential to become either testes or ovaries The hypothetical substance that promotes their conversion to testes has been called the testis determining factors (TDF).

Formation of Testes and ovaries

It has long been recognized that male sex is determined by the presence of a Y-chromosome (H-Y antigen) induces development of testes Whereas the absence of a Y-chromosome (No H-Y antigen ) allows the development of ovaries Scientists have discovered that, in rare male babies with xx genotypes, ones of the x chromosomes contain a segment of the Y chromosome. This error occurred during meiotic cell division which formed the sperm. Similarly , rare female babies with xy genotypes were found to be missing the same portion of the Y chromosome that was erroneously inserted into the X chromosome of XX males

Formation of Testes and ovaries

Through these and others observations, it has been shown that the gene for the testis determining factors is located on the short arm of the Y chromosome A segment of this region less than 250 bases long has recently been identified as a likely TDF gene

Formation of Testes and ovaries

Seminiferous tubules appear very early in embryonic development ( between 43-50 days following conception) At about 65 the leydig cells appear in the embryonic testes. In contrast to the rapid development of the testes, the functional units of the ovaries called the ovarian follicles do not appear until the second trimester of pregnancy( at about day 105).

Formation of Testes and ovaries

The early appearing leydig cells in the embryonic testes secrete large amout of male sex hormones, or androgens. The major androgen secreted by these cells is testosterone Testosterone secretions begins as early as nine to ten weeks after conception, reach a peak at twelve to fourteen weeks, and declines to very low by the end of the second trimester(21 week)

 The embryonic testes secretes testosterone, which induces development of male reproductive tract from wolffians ducts. Testosterone is not the active agent within target organs. Inside the target cells, testosterone is converted by an enzyme called 5 alpha reductase into the active hormone known as dihydrotestosterone (DHT), which induces development of male genitalia In addition , the testes secrete mullerian inhibiting factors (MIF), which cause regression of the mullerian ductus The absence of testes , testosteron, DHT and MIF allows wolffian ducts to regress, the development of female genitalia and the formation of the female reproductive tract from the mullerian ducts.

Formation of Testes and ovaries

As the testes develop they move within abdominal cavity and gradually descend into the scrotum Descend of the testes is sometime not complete until shortly after birth The cooler temperature of the scrotum, which is ussually 3-4 degrees celsius lower than the temperature of the body cavity, is needed for spermatogenesis This requirment is ilustrated by the fact that spermatogenesis does not occur in male with undescended testes called cryptorchidism ( crypt= hidden , orchid= testes)

Male Anatomy
Intratesticular
Seminiferous tubule Efferent ducts (collection ducts) Epididymis (maturation; short term storage)

Extratesticular
Vas deferens (vasectomy) Ampulla (situated just above SV; storage) Seminal vesicles (site of seminal fluid production and storage)

Reproductive Anatomy of the Human Male

The scrotum and the penis are the external components of the reproductive system.

The internal reproductive organs consist of gonads, accessory sex glands, and ducts.

Testes
Testes begin to develop inside the abdominal cavity and descend into the scrotal sacs during last two months of fetal development Scrotum helps regulate temperature of testes. Lower temperature necessary for functional sperm Composed of seminiferous tubules (site of sperm production)

Testes
The testes have two primary functions 1. Spermatogenesis the process of producing mature sperm 2. Steroidogenesis the synthesis of testosterone Both processes are regulated by the pituitary gonadotropin LH and FSH Testosterone is the primary sex hormone in the male and is responsible for primary and secondary sex characteristics

Endocrine Regulation of Reproduction

The embryonic testes during the first trimester of pregnancy are active endocrine glands, secrete high amount of testosterone needed to masculinize the male embryo's external genitalia and sex accessory organs. After parturition FSH And LH increase at about 6 months of age. (Similar in event female) the subsequent increase in testicular steroidogenesis and androgen secretion may result in the sexual differentiation of the brain

Endocrine Regulation of Reproduction

There is no differences in the blood concentrations of sex steroid (androgen & esterogen) in pre pubertal boy or girls very low level and remaining low until the beginning of puberty This doesnt to be due to deficiencies in the ability of gonads to produces these hormones, but rather to lack of sufficient stimulation During puberty the gonads secrete increased amounts of sex steroid hormones as a result of increased stimulation by gonadotropic hormones from anterior pituitary gland

Puberty
Adrenarche ( increase in adrenal androgens) which usually occurs at approximately 8 years of age, is harbinger of the onset of the puberty Evidence suggest that, rise in gonadotropin secretion at 10-14 years of age is result two process: 1. Maturational of hypothalamus and other region of brain that leads to increase GnRH secretion 2. Decrease the sensitivity of the hypothalamus and pituitary to negative feed back effects of steroid sex hormones.

Puberty
During late puberty there is pulsatile secretion of gonadotropins (FSH &LH) secretion increase during periods of sleep and decrease during period of wakefulness. Increased gonadotropin secretion stimulate a rise in sex steroid secretion from gonads (testosteron and estradiol -17)

Hormonal Regulation of Male Reproductive Function

1. The hypothalamus release gonadotropin releasing hormone (GnRH)which controls the release of the anterior pituitary gonadotropins FSH and LH. GnRH reaches the anterior pituitary cells via the blood of the hypophyseal portal system 2. Binding of GnRH to pituitary cell prompts them to secrete FSH and LH into the blood 3. FSH stimulate spermatogenesis in the testes indirectly by stimulating Sertoli cells to release androgen binding protein (ABP).

The hypothalamus- pituitary- testicular (HPT) axis is

Hormonal Regulation of Male Reproductive Function

4. LH binds to the interstitial cells and stimulate them to secrete testosteron. Locally testosteron serves as the final trigger for spermatogenesis. Testosteron entering the bloodstream exerts a number of effects at other body sites 5. Both the hypothalamus and anterior pituitary are subject to feedback inhibition by blood borne hormones. Testosteron inhibits hypothalamic release of GnRH and may act directly on the anterior pituitary to inhibit gonadotropin release. Inhibin acts directly on the anterior pituitary and inhibits the secretion of FSH

Stimulasi from other area of the brain

 The testes consist of two parts

1. The seminiferous tubules, where spermatogenesis occurs 2. The interstitial tissue , which contains androgen-secreting leydig cells

Each seminiferous tubule is composed of two somatic cell types ( myoid cells and sertoli cells) and germ cells. The seminiferous tubule is surrounded by a basement membrane with myoid cells on its perimeter

Semiferous Tubule

Seminiferous Tubule

Sertoli Cells
The Sertoli cells are the only nongerminal cell type in the tubules They form a continuous layer , connected by tight junctions, around the circumference of each tubule. In this way the sertoli cells constitute a blood testis barrier, because molecules from the blood must pass through the cytoplasm of the sertoli cells before entering germinal cells. This barrier normally prevents the immune system from becoming sensitized to antigen in the developing sperm, and thus prevents autoimmune destruction of the sperm

Sertoli Cells
The cytoplasm of the sertoli cells extends through the width of the tubule and envelops the developing germ cells, so that it is difficult to tell where the cytoplasm of the sertoli and germ cells is separated Sertoli cells phagocytose residual bodies (excess cytoplasm resulting from transformation of spermatid to spermatozoa) Provide structural support and nutrition for germ cells, secrete fluids and assist in spermiation

 At puberty the capacity of sertoli cells to bind FSH and testosteron increase Receptor for FSH present only on the plasma membranes of Sertoli cells, are glycoproteins linked to adenylate cyclase via G proteins. FSH exerts multiple effects on the sertoli cells FSH stimulate the production of androgen binding protein and plasminogen activator, increase secretion of inhibin and induces aromatase activity for conversion of androgen to esterogens. ABP has a high affinity for dihydrotestosterone and testosterone

Leydig Cells
The large polyhedral cells that are often found in clusters nears blood vessels in the interstitium between seminiferous tubules. They are equipped to produce steroid because they have numerous mitochondria, a prominent smooth ER, and conspicuous lipid droplets. Leydig cells have LH receptors, and the major effect of LH is to stimulate androgen secretion via CAMP dependent mechanism The main product is testosteron, but two other androgens of less biological activity , DHEA and androstenedione

 There are bi-directional interactions between Sertoli and leydig cells. The Sertoli cell is incapable of producing testosterone but contains testosterone receptors as well as FSH dependent aromatase The leydig cell does not produce estradiol but contain receptors for it, and estradiol can suppress the response of the leydig to LH Testosterone diffuses from the leydig cells, crosses the basement membrane, enters the sertoli cell, and bind to ABP as a result,androgen level can reach high local concentrations in the seminiferous tubules. Testosterone is obligatory for spermatogenesis and proper functioning of sertoli cells.

Spermatogenesis is the production of mature sperm cells from spermatogonia A continuous and prolific process in the adult male Occurs in seminiferous tubules As spermatogenesis progresses the developing sperm cells move from the wall to the lumen of a seminiferous tubule The time required to produce mature spermatozoa from the earliest stage of spermatogonia is 65 to 70 days. New cycles are initiated at regular time intervals (very 2 to 3 weeks) before the previous ones are completed Approximately 200 million spermatozoa are produced daily in the adult human testes , which is about the same number of sperm present in a normal ejaculate

This process can be divided into three phases: 1. Cellular proliferation by mitosis 2. Two reduction divisions by meiosis to produce haploid spermatids 3. Cell differentiation by process called spermiogenesis, in which the spermatids differentiate into spermatozoa Spermatogenesis is initiated shortly before puberty, under the influence of the rising levels of gonadotropins and testosterone, and continues throughout life, with a slight decline during old age

Testosterone is Essential for Sperm Production and maturation Spermatogenesis requires high intratesticular levels of testosterone, secreted from the LH stimulated Leydig cells. The testosterone diffuse across the basement membrane of the semeniferous tubule, crosses the blood testes barrier and complexes with ABP. Sertoli cells contains receptors for FSH and testosterone FSH is thought to be required for the initiation spermatogenesis before puberty. When adequate sperm production has been achieved, LH alone or testosterone alone is sufficient to maintain spermatogenesis

The formation of a mature spermatozoa the acrosome contains proteolityc enzymes such as hyaluronidase, acrosin, neuraminidase, phospholipaseA and esterases. They are inactive until the acrosome reaction occurs upon contact of the sperm head with the egg. Their proteolytic action enables sperm to penetrate through the egg membranes. Mitochondria that supply energy for sperm metabolism and locomotion The tail composed of 9+2 arrangement of microtubules, which is typical of cilia and flagella, and is surrounded by a fibrous sheath that provide some rigidity.the tail propels the sperm by a twisting motion

 Mature sperm have three distinct parts.

Head. Nucleus covered by acrosome. Middle Piece. Provide energy for movement. Tail. Flagellum for movement.

Epididymis
The seminiferous tubules are connected at bots ends to the rete testis. Spermatozoa and tubular secretions are moved to this area and are drained via the efferent ductules into the epididymis Spermatozoa that enter the head of the epididymis are non motile. In the epididymis sperm gain motility and undergo other maturational changes ( sperm that leave the epididymis are more resistant to changes in PH and temperature, are motile, and gain the ability to fertilize ovum) . For temporarily storage of sperms between ejaculations During copulation, muscles of epididymis contract to release sperms

Testis and epididymis

epididymis

vas deferens (sperm duct)

Efferent ductules
Rete testis

sperm tubules

Ductus defferent / Vas defferent

The vas defferens carries sperm from the epididymis out of the scrotum into body cavity Sperma can be stored within widened area of the vas deffererent known as ampulla

Male Reproductive System

secrete seminal fluid

seminal vesicle prostate gland Cowpers gland

The Seminal Vesicles

Located near bladder A pair of seminal vesicle contribute about 60% of total semen volume Seminal fluid is thick, yellowish, and alkaline.It contains mucus, fructose, ascorbic acid, inositol, 5 amino acid, coagulating enzyme ( fibrinogen),and prostaglandins.

Functions of Seminal Fluid

To provide a medium for the sperms to swim To activate and nourish the sperms /Energy
source for sperm(fructose)

To neutralize the acidity in the female reproductive tract

The Prostate Gland

Secretes directly into the urethra.

Prostatic fluid is a milky, slighly acid fluid that contains citrate, anticoagulan fibrinolysin and enzymes acid phosphatase

Prostate gland
Encapsulates the urethra and ejaculatory duct Secretes directly into the urethra. Prostatic fluid is a milky, contains citrate, anticoagulan fibrinolysin and enzymes acid phosphatase Secretion raises pH of sperm

 The seminal vesicles and prostate are androgen dependent accessory sexual organs They atrophy if androgen is withdrawn by castration

 The bulbourethral glands are a pair of small glands along the urethra below the prostate. Prior to ejaculation they secrete a clear mucus that neutralizes any acidic urine remaining in the urethra. Bulbourethral fluid also carries some sperm released before ejaculation. This is one of the reasons why the withdrawal method of birth control has a high failure rate.

 Ejaculation propels sperm from the epididymis to the vas deferens. The vas deferens run from the scrotum and behind the urinary bladder. Here each vas deferens joins with a duct from the seminal vesicle to form an ejaculatory duct. The ejaculatory ducts open into the urethra. The urethra drains both the excretory and reproductive systems. A male usually ejaculates about 2 5 mL of semen each milliliter containing about 50 130 million sperm.

 In the female reproductive tract:

Prostaglandins in semen thin the mucus at the opening of the uterus and stimulate uterine contractions When ejaculated semen coagulates:
This makes it easier for uterine contractions to move it along. Anticoagulants liquefy the semen and the sperm begin swimming.

The alkalinity of semen helps neutralize the acidic environment of the vagina.

Male Infertility
Infertility; no conception after 1 year of unprotected, regular intercourse 40 % of infertility is associated with a male factor
20 % male alone; 20 % both male and female

Majority of male infertility associated with abnormal semen parameters

Semen Analysis
Volume (2-4 ml) Viscosity Sperm density
Greater than 20 million/ml Average is 100 million/ml

Sperm motility
Greater than 40 %

Sperm morphology
Less than 60 % abnormal considered normal

Male Infertility Treatment

Life style changes
Marijuana, cigarettes, work environment

Medical therapies Fertility enhancement procedures

Intrauterine insemination of concentrated sperm In vitro fertilization (IVF)
Ovarian stimulation, oocyte collection, fertilization in vitro, in vitro embryo development for 2-4 days, embryo transferred into uterus

Intracytoplasmic sperm injection (ICSE) combined with IVF

Aksi Seksual Pria

Rangsang

Saraf Pudendus

Plexus Sacralis
Medula Spinalis Pars Sacralis Saraf Simpatis (N.Pelvikus) Sekresi Nitogen Oksida K..Urethra+K..Bulbouretralis

Arteri Jaringan Erektil Melebar,

Ereksi

Lubrikasi

Rangsang Kuat Saraf Simpatis L1 dan L2 Plexus Hipogastrik, Plexus Pelvikus Kontraksi Vesika Seminalis Kontraksi Vas deferens Prostat+semen Emisi

Sensasi penuh
Kontraksi otot Iskiokavernosus Dan otot Bulbokavernosus

Ejakulasi
Resolusi

Penis
Erected during copulation for insertion into vagina
Dilation of arterioles causes the erectile tissue of penis become turgid Muscles of epididymis contract Semen is squeezed from the penis to the top of vagina

Ejaculation

 The penis is composed of three layers of spongy erectile tissue. During sexual arousal the erectile tissue fills with blood from arteries. The resultant increased pressure seals off the veins that drain the penis. The engorgement of the penis with blood causes an erection. An erection is essential to the insertion of the penis into the vagina.

Penis Anatomy

 Impotence can result from the consumption of alcohol and other drugs, and emotional, nervous system, or circulatory problems. Treatment includes drugs and penile implant devices.
Viagra acts by promoting the action of nitric oxide.

 External structure of the penis: The shaft of the penis is covered by relatively thick skin. The sensitive glans penis is covered by thinner skin. The glans is covered by the prepuce which may be removed by circumcision.

Testosteron
An adult man produces 6 to7 mg testosteron per day ( 4mg / day in the seventh decade of life) there fore men do not undergo a sudden cessation of sex steroid upon aging, as women do during their postmenopausal period when the ova are completely depleted. Testosteron circulates bound to plasma proteins with only 2 to 3 % present as the free hormone

 About 30 to 40% is bound to albumin and the remainder to sex hormone binding globulin ( SHBG) produced by the liver. SHBG serves as a reservoir for testosteron In most target tissues, testosteron functions as prohormone and is converted to biological active derivatives DHT by 5 reductase or estradiol by aromatase DHT has high affinity for androgen receptor and is 2 to3 times more potent than testosteron Drugs that inhibit 5 reductase are currently used to reduce prostatic hypertrophy because DHT induces hyperplasia of prostatic epithelial cells.

 Aromatization of some androgens to esterogens occurs in fat , liver, skin and brain cells. Total esterogen in men can approach those of women in the early follicular phase Androgens are metabolized by 17 in the liver to biologically inactive water soluble derivatives ( 17 ketosteroid androsterone) suitable for excretion by kidneys. Testosteron are conjugated by conjugating enzymes to form sulfate and glucoronides which are water soluble and excreted into the urine

Effect on reproductive organs

Stimulate formation of male reproduction duct, glands, and exernal genitalia Promotes descent of the testes Stimulates growth and maturation of the internal and external genitalia at puberty. Maintains adult size and function Required for normal spermatogenesis via effects promoted by its binding to ABP on spermatogenesis Suppresses mamary gland development

Secundary sex characteristic and somatic effects of testosteron

Testosteron stimulate hair growth especially on the face , axillae, genital region and chest The growth and secretory activity of the sebaceous gland on the face, upper back, and chest are stimulated by androgen,primarily DHT, and inhibited by esterogen. Increased sensitivity of target cells to androgenic action especially during puberty , is the cause of acne vulgaris in both male and female

Secundary sex characteristic and somatic effects of testosteron

Stimulates the growth spurt at puberty : promotes increased bone mass (includes growth of vertebrae, long bones, shoulders) and skeletal mass At the end of adolescence testosteron accelerate closure of the epiphyses in the long bones Promotes growth of the larynx and thickening of the vocal cords and deepening of the voice

Metabolic effects of testosteron

Generally anabolic effects Increase red blood cell mass by stimulating erythropoetin production and by increasing stem cell proliferation in the bone marrow Enhance the basal metabolic rate

Neural effects of testosteron

Many site in the brain contain testosteron receptors, enzyme 5 alpha reductase Responsible for sex drive ( libido) Masculinizes brain Promotes aggressiveness

Effects of testosteron administration

Exogenous testosteron given to men would normally inhibit endogenous LH release through a negative feed back effect on the hypothalamic pituitary axis and lead to a suppression of testosteron production by leydig cells and a further decrease in testicular testosteron concentration High level of testosteron have an anbolic effect on muscle tissues, leading to increased muscle mass, strength, and performance, a desire result for body builders and athletes. Androgen abuse has been associated with abnormally aggressive behavior and potential incidence to increase of liver and brain tumors.

Hypogonadisme
The most common disorder of the HPT axis Classified as two types: 1. Testicular dysfunction is due to a decrease in testosterone production from the testes. LH and FSH increase because of a loss of negative feed back. Therefore, this is called HYPERGONADOTROPIC Hypogonadism and is analogous to primary adrenal insufficiency. The most common disorder is klinefelterssyndrome

2. Hypogonadotropic Hypogonadisme can be congenital ,idiopathic, or acquired. The most common congenital from is kallmannssyndrome which results from decrease or absent GnRH secretion. It is often associated with anosmia or hyposmia and is transmitted as autosomal dominan trait. Patient ddo not undergo pubertal development and have eunuchoidal features. Another cause is panhypopituitarism 3. another cause of Hypogonadotropic Hypogonadisme is hyperprolactinemia, which is ussualy due to a prolactin secreting pituitary adenoma. Elevated prolactin levels inhibit gonadotropin secretion and induce Hypogonadisme in male ( and amenorrhea in females).

 Gonadal failure before puberty resullts infantile appearance of external genitalia, poor or absent development of secondary sex characteristic creating a distinctive clinical presentation called eunuchoidism. Even though there is no androgen mediated pubertal growth spurt, there is also failure to close the epiphyseal plates and the long bones continue to grow Androgen deficiency after puberty usually results, changes in sexual performance, decreased libido , impotence( inability to achieve or maintain erection) and decreased in facial and body hair

Reproductive Cancers
Testicular Prostate

Testicular Cancer
Most common tumor in young men Primarily in men 15 35 yo Metastasize to lymph nodes, lungs, liver and bone

Testicular cancer etiology

Familial component Increased in undescended testis Connection with infection or trauma is not supported

Testicular Cancer

Signs & Symptoms

Hard painless unilateral mass Picked up on self exam Diagnostic test
CT scan, tumor markers (hCG, AFP)

Testicular Ca Treatment
Ochiectomy Radiation Chemotherapy with cytotoxic drugs Cure rate is excellent

Prostate Pathophysiology
Benign prostatic hyperplasia (BPH)
Enlargement of the prostate (central area) Formation of nodules around the urethra Does not progress to cancer

Prostate cancer
Adenocarcinoma surface epithelia Metastasis to lymph nodes, liver, bone, adrenal, lung in advanced stage

BPH
Symptoms
Hesitancy and reduced urinary stream due to compression of urethra Urinary retention can lead to cystitis

Treatment
Surgical (infrequent) Medical
Anti-androgen Alpha adrenergic blocker

Prostate Cancer
Etiology unknown
Genetic, environmental, hormonal?

Early detection is vital

Prostate specific antigen (PSA)
Also elevated with BPH and infection

Rectal examination Diagnosis confirmed by ultrasound and biopsy

Treatment of Prostate Ca
Surgery (prostatectomy) and radiation
Implants Anti-androgen (flutamide) if tumor is androgen sensitive

Indifferent gonads
Testes Testosterone Degenerates
MIF

Ovaries MIF No Testosterone

(No MIF)

No MIF Uterus, Uterine tubes Degenerates

Paramesonephric duct Mesonephric duct Other embryonic structures

Epididymides. Ductus deferentiaTestosterone Ejaculatory ducts

(No Testosterone)

Prostate Penis, scrotum

Testosterone

(No Testosterone)

Vagina, labia clitoris

Type I: Acute bacterial prostatitis E. coli; N. gonorrheae High fever, chills, pain (back/perineal), UTI syndroms Complications: (micro)abscesses, bacteremia Type II: Chronic bacterial prostatitis E. Coli (80 %); Klebsiella, Enterobacter, Proteus, Enterococci, CoNS (?) Asymptomatic vague complaints; relapsing UTI Very difficult to treat

Type III: Prostatitis/Chronic pelvic pain syndrome nonbacterial

Therapy: acute prosatitis: many agents FQ and co-trimoxazole are superior