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Abnormal uterinebleeding can also be caused by a variety of uterine or adnexal dis-orders as well as systemic disorders in nonpregnant, reproductiveage women. In pregnant women, bleeding may be caused byrupture of a placental blood vessel or may foreshadow an impending miscarriage. Placenta previa, in which the placenta extendsover the cervix, is often associated with bleeding after the firsttrimester of pregnancy. Various causes of abnormal uterine bleeding are illustrated.EstrogenEstrogenEstrogen deficiency (ovarianprogesteroneexcessfailure) or excess progestinimbalanceHyperplastic(medications)Abnormaland anaplasticNormal secretoryendometrium Hypoplasticmenstru- endometriumationendometriumCancer (or sarcoma)of uterine bodyTubal or pelvicinflammationTuberculosisFibroid(submucous)CystsEndometrial polypsAdenomyosisEndocervical polypsCancer of cervixor endocervixEndometriosisErosion/ectropionTraumaTumors—granulosacell, theca cell, cancerLocal ovarianor adnexal disordersChancreLocal uterine disordersChoriocarcinomaHypothalamic(anorexia, weightloss, stress)Hypothyroidism, hyperthyroidismDefective enzymaticsteroid metabolismEctopicpregnancyAbortionor prematureseparation ofplacentaPlacenta previaBlood dyscrasiasHydatidiform molePregnancy disordersSystemic conditionsCauses of Abnormal Uterine Bleeding Abnormal uterine bleeding is associated with a variety ofdisease processes and disorders.361362Endocrine PhysiologyA.
Late follicular andovulatory phasesHypothalamusGnRHPituitaryLHThecacellFSHGranulosacellAndrogensEstrogensB. Luteal phaseHypothalamusGnRHPituitaryFSHLHLHThecacellFSHAndrogensProgestinsInhibinGranulosacellEstrogensFigure 31.5 Hormonal Regulation of the Menstrual Cycle The hypothalamic-pituitary-ovarianaxis is characterized by both positive and negative feedback over the course of a menstrual cycle. Initially,GnRH stimulates release of LH and FSH by the pituitary; estrogen synthesized by developing ovarian follicleshas negative feedback effects on the axis.
However, in the late follicular phase (A), blood estradiol reachesa high level that initiates positive feedback and a surge in LH and FSH release, provoking ovulation. In theluteal phase, the system is characterized by negative feedback (B). Estradiol, progesterone, and inhibinproduced by the corpus luteum have negative feedback actions on gonadotropin release. FSH, folliclestimulating hormone; GnRH, gonadotropin-releasing hormone; LH, luteinizing hormone.IMPLANTATION AND PREGNANCYAs discussed, fertilization of the ovum takes place within thefallopian tube.
Once the sperm penetrates the ovum, thesecond meiotic division is completed (all oocytes are arrestedin the first meiotic division until a woman reaches puberty;the “mature ovum” released during each cycle has undergonefurther development and is arrested in the second meioticdivision until sperm penetration). Subsequently, mitotic division of the fertilized egg begins and a blastocyst is formed.About 5 days after ovulation, the blastocyst begins to implantin the endometrial lining of the uterus. The sequence of eventsfrom follicular maturation to implantation of the blastocystis illustrated in Figure 31.6.The placenta is formed from trophoblast cells of the blastocyst and decidual cells of the endometrial lining.
Trophoblasts secrete a hormone known as human chorionicgonadotropin (HCG), which has LH-like actions. HCG“rescues” the corpus luteum from the regression that wouldotherwise occur at the end of the menstrual cycle, such thatsynthesis of estradiol and progesterone continues, and thus,the proliferated, secretory state of the endometrium is maintained to support the pregnancy. HCG is important in thisregard for the first trimester of pregnancy. By the second trimester, the placenta itself secretes large quantities of progesterone and estrogens (primarily estriol) to support theuterus.CLINICAL CORRELATEMeasurement of HCGMost pregnancy tests, including the widely available self-administered tests, are based on measurement of HCG.
Althoughblood tests are more sensitive and may detect pregnancy earlier,urine tests are capable of detecting HCG within a few days ofimplantation of the blastocyst. Serial measurement of HCG alsocan be useful in monitoring early progress of a pregnancy whenrisk of ectopic pregnancy or miscarriage is an issue, becauseHCG normally rises rapidly following successful implantation.Hormones of the Reproductive SystemMyometriumEarly morula(approx.
80 hr)Four-cell stage(approx. 40 hr)363ZygoteTwo-cell stage(approx. 30 hr)EndometriumAdvanced morula(4 days)OvaryBlastocyst(approx. 5 days)Early implantation(approx. 6 1/2 days)Fertilization(12 to 24 hr)DevelopingfolliclesEmbryoblast(inner cell mass)MaturefollicleDischargedovumFigure 31.6 Fertilization and Implantation Upon rupture of the graafian follicle, the ovum entersthe fallopian tube.
If fertilization occurs, it takes place within the fallopian tube, which transports the ovumor zygote to the uterus. A zygote will have reached the blastocyst stage by day 5 and will implant in theendometrial lining at that time.SpermatidLeydigcellsSecondaryspermatocytePrimaryspermatocyteSpermatogoniumSeminiferous tubuleSertoli cellFigure 31.7 The Testes and Spermatogenesis The testes contain convoluted seminiferoustubules, where spermatogenesis takes place, and, between the tubules, Leydig cells, which synthesize testosterone in the mature male (left panel). Sertoli cells constitute the epithelium of the tubules (right panel).Differentiation of primary spermatocytes to sperm cells begins between the Sertoli cells and is completedin the epididymis.MALE REPRODUCTIVE ENDOCRINOLOGYThe testes are the site of gametogenesis and steroidogenesisin males.
Spermatogenesis takes place within the convolutedseminiferous tubules of the testes, whereas the Leydig cellslocated between tubules produce testosterone (Fig. 31.7).The hormone inhibin is synthesized and released by Sertolicells in the lining of the seminiferous tubules. Sertolicells provide the structure upon which male germ cellsdevelop and secrete fluid that supports flow of sperm throughthe seminiferous tubules to the epididymis, where furthersperm maturation takes place, and sperm are stored until364Endocrine PhysiologySpermatogenesis is a complex process that begins withmitotic division of spermatogonia to form primary spermatocytes, along with additional spermatogonia (unlikewomen, in whom there are a fixed number of primary oocytes bythe time of birth, the number of germ cells in men is not fixed).Meiosis of primary spermatocytes produces secondary spermato-HeadNeckcytes, and subsequently, haploid spermatids, which undergofurther differentiation to become spermatozoa.
The final product,the mature spermatozoon, includes a head piece, a mitochondriarich middle section for energy production, and a motile tailsection. The head piece has a prominent acrosome containingproteolytic enzymes necessary for penetration of an ovum.Middle pieceTailPlasmamembraneAnnulusSide viewCentriolesAcrosomeMitochondrialsheathOuterdensefiberNucleusAxonemeTop viewDorsal and ventrallongitudinal columnsEnd pieceRibs offibrous sheathTailMature Spermatozoon The morphology of mature spermatozoa reflect their motility and ovumpenetrating functions.ejaculation.
Sertoli cell processes form tight junctions thatprovide a “blood-testis” barrier, sheltering the developingspermatocytes from potential damage by blood-bornesubstances.Endocrine Regulation of Testicular FunctionTesticular function (both gametogenesis and steroidogenesis) is regulated by the hypothalamus and pituitary gland(Fig. 31.8). GnRH is secreted by hypothalamic nuclei into thehypophyseal portal circulation (as in females, GnRH releaseis pulsatile in males), and subsequently stimulates the releaseof LH and FSH by anterior pituitary gonadotrophs. LH stimulates the first step in testosterone synthesis (conversion ofcholesterol to Δ5-pregnenolone by CYP11A10, whereas FSHacts on Sertoli cells, stimulating the synthesis of androgenbinding protein, which subsequently binds testosterone,promoting spermatogenesis in the seminiferous tubules(see Fig. 31.7).
Negative feedback in the hypothalamicpituitary-testis axis is effected by inhibition of GnRH and LHrelease by testosterone and by inhibition of FSH secretion viainhibin produced by Sertoli cells.Nonreproductive Actions of TestosteroneIn addition to the nonreproductive actions of testosteroneat puberty discussed, increased muscle mass, development ofthe male pattern of hair distribution and baldness, and deep-Hormones of the Reproductive SystemCLINCIAL CORRELATEKlinefelter’s SyndromeMale infertility has a large number of causes, including blockageof the vas deferens due to infection or injury; low sperm count(oligospermia) due to infections such as mumps and some sexually transmitted diseases; lack of sperm production as a result ofchronic disease, hormonal problems, or injury to the testes; impotence; and exposure to toxins.
In some cases, infertility may havePituitary gonadotropinsFSHLHa genetic basis. For example, Klinefelter’s syndrome is characterized by the genotype 47, XXY. Patients with this syndrome arephenotypic males but have some identifiable physical characteristics including gynecomastia (breast enlargement) and are nearlyalways infertile (see illustration). They are hypogonadal, meaningthat gonadal hormone levels are low, and as a result, gonadotropinlevels are elevated and testicular size is reduced. Klinefelter’s syndrome affects one to two men per 1000.Pituitary anterior lobeEnlarged breasts(gynecomastia)TubulecontainingSertoli cellsTestisSection of breastAndrogenLate pubertal testicularfailure (Klinefelter,noneunuchoidal variant)365Dense stromaSclerosedtubulesXXYNuclear chromatin often positive (female);usually XXY chromosomal patternbut XXXY, XXXXY, XXYY, and mosaicpatterns have been describedTesticular Failure in Klinefelter’s Syndrome The presence of two X chromosomes (47, XXY genotype) results in seminiferous tubular dysgenesis and infertility, as well as primary hypogonadism (low testicular hormone levels, and as a result, high gonadotropin levels).366Endocrine PhysiologyHypothalamusGnRHPituitaryLHFSHFSHInhibinLHLeydigcellSertolicellTestosteroneAndrogen-bindingproteinSpermatogenesisFigure 31.8 Control of Testicular Function GnRH secreted by the hypothalamus stimulates LHand FSH secretion by the anterior pituitary.
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