Male & Female Reproductive System PDF
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This document is lecture notes on male and female reproductive systems. It covers topics such as the conversion of testosterone, genital development, puberty, and various disorders. The notes are well-organized and detailed, providing a comprehensive overview of the subject.
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Lecture 3: Male Reproductive System In males, the conversion of testosterone todihydrotestosterone, via the enzyme5α- reductasewithin these target tissues, is necessary for the formation of theprostate glandand themale external genitalia ...
Lecture 3: Male Reproductive System In males, the conversion of testosterone todihydrotestosterone, via the enzyme5α- reductasewithin these target tissues, is necessary for the formation of theprostate glandand themale external genitalia Genital foldsfuse to formpenis Labioscrotal swellingsform thescrotum Descentof thefetal testesinto the scrotumrequiresthesecretion of the fetal gonadotropinsand occurs during the last trimester of pregnancy ↑adrenarche = axillary and pubic hair growth Pubertybegins with the activation ofGnRH pulse generatorwithin the hypothalamus ○ KisspeptinstimulatesGnRH neurons ○ LeptinstimulatesKisspeptin(esp. In females) ○ ↑LH and FSH Complete androgen insensitivity syndrome (CAIS)results from thelack of functional androgen receptors ○ 46 XY DSD→ gonads become testes since Y chromie appears (testes remain undescended) ○ Müllerian-inhibiting substancecontinues to besecreted from theSertoli cells, resulting in the absence of the female internal genitalia. Patients have a short, blind-ended vagina without a cervix, uterus, or ovaries ○ Dihydrotestosteroneis made but cannot direct theWolffian ductto develop into male genitalia due to lack of androgen receptors; individuals have female external genitalia. ○ Masculinization does not occur during pubertybecause of the lack of testosterone action. Conversion of testosterone toestrogen causes breast development at puberty instead, but there is only a small amount of pubic hair.Diagnosis is often determined following failure of the onset of the menstrual cycle ○ Deficiency of 5α-reductaseis another example of 46 XY DSD and causesambiguous genitaliabecause it interferes with the conversion of testosterone to dihydrotestosterone Most common reason for ambiguous genitalia → congenital adrenal hyperplasia (CAH) Deficiency in 21-hydroxylase→excessive production of adrenal androgens The fluid of thevas deferensis relativelyacidicowing to the presence of citric acid and metabolic end products of the sperm and, consequently helps inhibit sperm fertility. ○ Sperm become optimally motile at ~pH 6-6.5 Slightly alkaline prostatic fluidhelps neutralize the acidity of the other seminal fluids during ejaculation and thus enhances the motility and fertility of the sperm Peripheral zone (PZ)= most carcinomas arise from here (palpable) Transitional zone (TZ)= BPH DHTisproducedfromtestosteronevia5α-reductase activity(which increases with age) → 5α-reductase inhibitors, such asfinasteride, are effective in management of BPH. Most of these sperm arestoredin theepididymis, although a small quantity is stored in thevas deferens. In males, the primordial germ cells give rise to precursors of male gametes calledspermatogonia. ○ The germinal epithelium that will later produce male gametes is formed by spermatogonia plus support cells calledSertoli cells. ○ The surrounding mesenchyme becomesLeydig cells, whichsecrete testosterone. At puberty, tight junctions develop between adjacentSertoli cells, creating an impermeable lining called theblood–testis barrier. ○ This barrier divides the seminiferous tubules into a basal compartment and an adluminal compartment,separatingmore advanced germ cellsfrom theimmune system. ○ The separation is necessary becausemature sperm are potentially antigenicsince they are not present at the prepubertal interval when much of the immune tolerance is established. Leydig cellssecretetestosterone LHsecretedby theanterior pituitary gland→stimulatesLeydig cellstosecretetestosterone LH & FSHsecretedby theanterior pituitary gland FSHstimulatesSertoli cells FSHalso stimulates the production ofinhibinin response toactive spermatogenesisandandrogen-binding globulin (ABP) Duringfetal life, the testes arestimulatedbychorionic gonadotropinfrom theplacentato produce moderate quantities oftestosterone throughout the entire period of fetal development and for 10 or more weeks after birth In the mature sperm, thehyaluronidaseandproteolytic enzymesare stored in theacrosome Capacitationcauses sperm to becomehyperactiveand prepared to undergo the acrosome reaction, allowing it to bind to and fuse with an oocyte Antisperm Antibodies (ASA):should be suspected withsperm agglutinationorisolated asthenozoospermiawith normal sperm concentrations. Normal testosteroneandLH with high FSH→primary spermatogenic failure(esp. Azoospermia or severe oligozoospermia) Normal LH→ proper Leydig cell function High FHS→ damage to seminiferous tubules Azoospermia+normal testicle size→ obstructive azoospermia Bilateral absent vas→CFTR gene mutation Low testosterone + high FSH and LH→ primary hypergonadotropic hypogonadism Kleinfelter syndrome (47XXY) ○Additional X chromie ○Most common chromosomal disorder associated with infertility ○Small testes and low testoterone levels ○Puberty is often delayed or incomplete ○Labs:increased serum FSH,normal or increased serum estradiol, andnormal or low serum testosterone ○Leydig cellfunction is commonlyimpairedin men. Kallman syndrome ○Gene defect →lack of GnRH neurons ○X-linked inheritance ○Hypogonadotropic hypogonadism- decreased or absent sense of smell (anosmia) Epididymitis ○< 35 yo = Chlamydia/Gonorrnea ○> 35 yo = E. coli Often associated with UTI and BPH ○Sx: tenderness and swelling of theposterior sideof theaffected testicle ○+ Prehn sign / intact cremasteric reflex Orchitis ○Mumps infection Testicular Torsion ○Cremasteric reflex is absent /- Prehn sign ○Bell clapper deformity → a tender, enlarged, high-riding testis, with its long axis oriented transversely due to the shortening of the spermatic cord Varicocele ○Most common cause of subfertility in men ○Possible pathogenic mechanisms in varicocele formation include the anatomical configuration of the left internal spermatic vein, incompetent or absent valves, and the potential for partial left renal vein compression between the aorta and the superior mesenteric artery An acute varicocele can also be caused by retroperitoneal malignancies compressing the venous system Cryptorchidism ○Associated with testicular malignancy, infertility, inguinal hernia, and torsion ○Unilateral = risk of impaired sperm production or of becoming malignant Benign prostatic hyperplasia (BHP) ○↑5α-reductaseage = ↑dihydrotestosteronelevels ○↑ PSA ○Patho:DHTbinds to and activatesandrogen receptors (ARs)found in both stromal and epithelialprostate cells ○Nodular hyperplasia of stromal and epithelial cells in the periurethral zone of the prostate gland ○Sx:chronic lower UT symptoms,symmetricallyenlarged, smooth, firm,non-tender prostatewith arubberytexture ○Complication:acute urinary retention(↑ withdiphenhydraminedrug) Male infertility Congenital bilateral absence of the vas deferens (CBAVD) ○Although most patients with classic CF carry severe mutations on both CFTR gene loci, patients with CBAVD can have a severe mutation in only one CFTR gene,coupled with a minor mutation in the other, or minor mutations on both loci. Lecture 4: Female Reproductive System abia minoraforms from thegenital folds L Clitorisforms anterior to theurethral opening Labia majoraformed from thelabioscotal swellings LeptinstimulatesKisspeptin Estrogensformedfrom testosterone by theSertoli cellswhenstimulatedbyFSH Theabsence of the Müllerian-inhibiting substancein the female fetus allows theMüllerian duct system(instead of the Wolffian duct) to develop, leading to the formation of the fallopian tubes, the uterus, and the upper vagina. LH surgeinitiatesovulation Ovariansteroidsecretionoccurs inresponse to FSH and LH Damage to the uterine ligaments(e.g., during childbirth) may result inprolapseof the uterus downward into the vagina Squamocolumnar junction→cervical cancercommonly occur The epithelium surrounding the oogonia differentiates intogranulosa cells, and the surrounding ovarian mesenchyme becomesthecal cells. The corpus luteum is a temporary endocrine structure in female ovaries involved in the production of relativelyhigh levels of progesterone,moderate levels of estradiol, andinhibin A First half of the menstrual cycle → follicular phase (1-14 days) Granulosa cellssecreteestrogen ○Inhibinunder the influence of FSH ○Rely on a supply ofandrogensfromthecal cellsas a substrate forestrogen production Continued progesterone secretionby the corpus luteumis essential toearly pregnancy Theproliferative phaseoccurs in the first half of the cycle prior to ovulation and is under theinfluence ofhigh estrogen levels The secretory phaseoccurs after ovulation, during the second half of the monthly cycle when thereisprogesterone dominance Placenta ○After the invasion by thesyncytiotrophoblast, the entire endometrium undergoes further biochemicaland morphologic change, calleddecidualization (decidual reaction), and forms the “membranes of pregnancy” calledthedecidua. Decidualizationbegins at the site of implantation and spreads in a concentric wave around the entire endometrium ○Thesyncytiotrophoblastdevelops spaces within it calledlacunae, as it invades deeper into the endometrium Chorionic villigrow from the cytotrophoblast into the syncytiotrophoblast to make contact with lacunae ○The two majorplacental peptides, which are onlysecretedduringpregnancy, arehuman chorionic gonadotropin (hCG)andhuman chorionic somatomammotropin (hCS) hCGrescues the corpus luteum from degeneration and allows continuedprogesterone secretionto support the early pregnancy Placental hCG secretion iscontrolledin aparacrine manner, by locally produced GnRH Proteinsmake up about 1% of milk; the proteinscaseinandlactalbuminareonly found in milk Colostrumis the thin, yellowish fluid produced within thefirst few days after parturition, before the main milk production begins ○contains more protein than milk, includingantibodiesand immune cells, and provides the neonatewith some immunologic protection Prolactinandoxytocinare thetwo key hormonesinvolved in the control oflactation ○Prolactin → milk production ○Oxytocin → milk ejection Infertility ○Most common factor is anovulatory menstrual cycles Common causes: polycystic ovarian syndrome, thyroid dysfunction, and stress Infection, endometriosis, and endometrial and cervical structural abnormalities Turner syndrome (45 XO) ○Lack one of the X chromie ○Rudimentary “streak” ovaries ○Inability to undergo puberty without hormone therapy Pelvic inflammatory disease (PID) ○STD → chlamydia or gonorrhea ○Complications: ectopic tubal pregnancy Dysmenorrhea ○Painful menstruation → excess prostaglandin and leukotriene levels → painful uterine cramping, n/v/d Amenorrhea ○Primary: Absence of spontaneous menstruation by age 16 years with secondary sex characteristics or age 14 years in the absence of secondary sex characteristics ○Secondary: (previously menstruated) absence of menses for 3 months if previous cycles were normal (irregular menses) the absence of menses for 6 months Ectopic pregnancy ○Common site of implantation of ectopic pregnancy =ampulla of the fallopian tube ○Common cause → occlusion of the tube secondary to adhesions ○Common risk factors → hx of previous ectopic pregnancy, previous salpingitis (caused by PID), previous abdominal, or tubal surgery The use of an intrauterine device and assisted reproduction Polycystic ovary syndrome (PCOS) ○Most common cause of androgen excessandhirsutism(male-patterned hair growth) in females ○Sx: bilaterally enlarged polycystic ovaries, amenorrhea or oligomenorrhea, and infertility Normal menses during adolescence → progressively longer episodes of amenorrhea ○Complications: endometrial hyperplasia and carcinoma Preeclampsia-eclampsia ○Most common causes of maternal death ○Hypertensioncan develop during pregnancy as an isolated finding(pregnancy-induced hypertension [PIH])or as a component of a dangerous syndrome(preeclampsia-eclampsia). ○Labs: proteinuria and edema ○Sx:tonic-clonic seizuresonpregnancy-induced hypertension ○HELLP syndrome Severe preeclampsia with hemolysis, elevated liver enzymes, low platelets ○Risk factor:nulliparity
