Uterus Anatomy

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The anatomy of the uterus consists of the following 3 tissue layers (see the following image):

The inner layer, called the endometrium, is the most active layer and responds to cyclic ovarian hormone changes; the endometrium is highly specialized and is essential to menstrual and reproductive function

The middle layer, or myometrium, makes up most of the uterine volume and is the muscular layer, composed primarily of smooth muscle cells

The outer layer of the uterus, the serosa or perimetrium, is a thin layer of tissue made of epithelial cells that envelop the uterus

The uterus is a dynamic female reproductive organ that is responsible for several reproductive functions, including menses, implantation, gestation, labor, and delivery. It is responsive to the hormonal milieu within the body, which allows adaptation to the different stages of a woman’s reproductive life. The uterus adjusts to reflect changes in ovarian steroid production during the menstrual cycle and displays rapid growth and specialized contractile activity during pregnancy and childbirth. It can also remain in a relatively quiescent state during the prepubertal and postmenopausal years. ^{[1, 2]}

The embryonic origin and development of the uterus is relatively complex. Until approximately 8 weeks’ gestation, primordia for both male and female internal genitalia—the mesonephric (Wolffian) and paramesonephric (Mullerian) ducts, respectively—coexist in the embryo. The sexual differentiation process involves multiple steps in which hormonal signals, growth factors, and specific genetic influences are required.

In the female embryo, due to the absence of a Y chromosome and lack of exposure to testosterone from functional testicular tissue, the normal developmental sequence of events results in fusion and canalization of the paramesonephric (Mullerian) ducts in the midline pelvis to form the female pelvic organs. Meanwhile, regression of the mesonephric (Wolffian) ducts occurs. Abnormalities in this process may occur during embryogenesis, which can result in the range of known paramesonephric anomalies.

The uterus is a pear-shaped organ located in the female pelvis between the urinary bladder anteriorly and the rectum posteriorly (see the image below). The average dimensions are approximately 8 cm long, 5 cm across, and 4 cm thick, with an average volume between 80 and 200 mL. The uterus is divided into 3 main parts: the fundus, body, and cervix.

Blood is provided to the uterus by the ovarian and uterine arteries, the latter of which arise from the anterior divisions of the internal iliac artery. The uterine artery occasionally gives off the vaginal artery (although this is usually a separate branch of the internal iliac around), which supplies the upper vagina, and the arcuate arteries, which surround the uterus. It then further branches into the radial arteries, which penetrate the myometrium to provide blood to all layers, including the endometrium (see the following image).

Once these vessels reach the endometrial level, they branch into the basal arteries and spiral arteries, which support the specialized functions of each layer. The basal arteries are not responsive to hormones; they support the basal endometrial layer, which provides the proliferative cells for endometrial growth. The spiral arteries supply the functionalis layer and are uniquely sensitive to steroid hormones. In ovulatory cycles in which pregnancy does not occur, menses results following constriction of these terminal arteries, causing endometrial breakdown with desquamation of the glands and stroma.

The uterus can be in various positions within the pelvis (see the image below). An anteverted uterus, which is normal, is tipped forward, whereas a retroverted uterus is tipped backward.

The uterine position can also be described based on the relative location of the fundus; that is, an anteflexed uterus, which is normal, is where the fundus tilts forward, and a retroflexed uterus is tilted backward.

The uterus can also exhibit normal variation in size and shape based on reproductive stage and exposure to ovarian steroid hormones. For example, the prepubertal uterus is generally small, but during the reproductive years, the uterus may be larger.

In addition, a nulliparous uterus, in which no previous pregnancy has occurred, can be smaller than a multiparous uterus, in which multiple pregnancies have occurred. Furthermore, the postmenopausal uterus may also appear small and atrophic to reflect the lack of hormonal stimulation and absent menstrual activity.

Paramesonephric (Mullerian) anomalies have been classified by Buttram and Gibbons based on the degree and type of fusion or canalization defect (see the following image).

The anomalies are as follows:

Segmental paramesonephric agenesis or hypoplasia (vaginal, cervical, fundal, combined)

Unicornuate uterus (with rudimentary horn, with endometrial cavity, communicating, noncommunicating, without endometrial cavity, without a rudimentary horn)

Uterine didelphys

Bicornuate uterus (complete [division to the internal os], partial, or arcuate) (see the image below)

Septate (complete [septum to the internal os], partial) (see the following image)

Diethylstilbestrol (exposure-related anomalies; eg, a T-shaped uterus)

Depending on the type and extent of paramesonephric anomaly, presenting signs and symptoms may include primary amenorrhea, cyclic pelvic pain, pelvic mass, or impaired reproductive function, including infertility, recurrent miscarriages, or preterm labor and delivery. ^[3]

Due to the common embryologic origin of the urogenital system and proximity of the primordial tissues, developmental defects of the internal genitalia often occur in conjunction with renal anomalies. Paramesonephric anomalies have a high correlation with urologic abnormalities, occurring in up to 30% of cases. Spinal defects are also associated with paramesonephric anomalies. This cluster of congenital anomalies is often referred to as Mayer-Rokitansky-Kuster-Hauser syndrome (MRKHS).

Several other genetic abnormalities lead to syndromes in which uterine anatomy can be affected. Rare genetic syndromes that involve paramesonephric defects include paramesonephric hypoplasia/aplasia – renal agenesis–cervicothoracic somite dysplasia (MURCS), Roberts syndrome, Bardet-Biedl syndrome (BBS), McKusick-Kaufman syndrome (MKS), Wolf-Hirschhorn syndrome, and thrombocytopenia absent radius syndrome (TARS).

Turner syndrome represents a chromosomal anomaly in which the second X chromosome is absent in an individual (46,X). Variants of Turner syndrome may exist, but affected individuals are generally phenotypic females, who may also have a spectrum of typical clinical characteristics. Depending on the degree of secondary X chromosome function, individuals with Turner syndrome may also have uterine variants, ranging from infantile anatomy to normal internal genitalia.

Beyond abnormalities in uterine development, many gynecologic disease processes may affect the uterus, some of which are discussed below.

Uterine fibroids, also known as leiomyomas or myomas, are benign smooth muscle tumors that arise in the myometrium of the uterus. These masses can grow within the endometrial cavity of the uterus (submucosal), in the myometrial layer (intramural), or in the outer wall of the uterus (subserosal), or they may extend off the outer layer of the uterus (pedunculated). See the following images.

Uterine polyps are benign growths on the inner surface of the uterus, derived from local overgrown endometrial tissue.

Adenomyosis is a benign condition in which endometrial tissue invades the myometrial layer of the uterus. It may be focal or diffuse. ^[4]

Endometrial hyperplasia is an overgrowth of the endometrial tissue within the uterus and may range from simple to complex (in which histology shows glands that are overcrowded and may show precancerous changes). ^[5]

Endometrial cancer is a malignancy arising from the inner layer of the uterus, the endometrium. Other forms of uterine cancer may involve different tissue layers, such as leiomyosarcoma.

Asherman syndrome is intrauterine scarring or adhesions (synechiae), commonly resulting from damage to endometrium from surgical procedures or infection.

Uterine prolapse is descent of the uterus into the vaginal canal and usually results from weakening of muscles and ligaments of the pelvic floor.

Strauss JF III, Lessey BA. The structure, function and evaluation of the female reproductive tract. Strauss JF III, Barbieri RL, eds. Yen and Jaffe’s Reproductive Endocrinology. 5th ed. Philadelphia, Pa: Saunders-Elsevier; 2004. Chapter 9.

Speroff L, Glass RH, Kase NG. The uterus. Clinical Gynecologic Endocrinology and Infertility. 6th ed. Baltimore, Md: Lippincott Williams & Wilkins; 1999. Chapter 4.

Behera M, Couchman G, Walmer D, Price TM. Mullerian agenesis and thrombocytopenia absent radius syndrome: a case report and review of syndromes associated with Mullerian agenesis. Obstet Gynecol Surv. 2005 Jul. 60(7):453-61. [Medline].

Ascher SM, Jha RC, Reinhold C. Benign myometrial conditions: leiomyomas and adenomyosis. Top Magn Reson Imaging. 2003 Aug. 14(4):281-304. [Medline].

Chaudhry S, Reinhold C, Guermazi A, Khalili I, Maheshwari S. Benign and malignant diseases of the endometrium. Top Magn Reson Imaging. 2003 Aug. 14(4):339-57. [Medline].

Millie A Behera, MD Assistant Professor (Adjunct), Division of Reproductive Endocrinology and Fertility, Department of Obstetrics and Gynecology, Duke University Medical Center; Medical Director, Bloom Reproductive Institute

Millie A Behera, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, American Society for Reproductive Medicine, AAGL

Disclosure: Nothing to disclose.

Thomas R Gest, PhD Professor of Anatomy, Department of Medical Education, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine

Disclosure: Nothing to disclose.

Uterus Anatomy

Research & References of Uterus Anatomy|A&C Accounting And Tax Services
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