NR 507 Final Exam Study Guide - Complete Study Document.

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Final Study Guide  Reproductive: o Endometrial cycle (menstrual cycle) and the occurrence of ovulation  During menstruation (menses), the functional layer if endometrium disintegrates and i ... s discharges through the vagina.  Follicular/proliferative phase - GnRH and a balance between activin and inhibin from the granulosa cells contribute to the rise of FSH levels, which stimulates a number of follicles. The pulsatile secretion of FSH from the anterior pituitary gland rescues a dominant ovarian follicle from apoptosis by days 5 to 7 days of the cycle. Together estrogen and FSH increase FSH receptors in the granulosa cells of the primary follicle, making them more sensitive to FSH. FSH and estrogen combine to induce production of LH receptors on the granulosa cells of the primary follicle, thus promoting LH stimulation to combine with FSH stimulation, causing more rapid secretion of follicular estrogen. As estrogen levels increase, FSH levels drop because of an increase in inhibin-B secreted by the granulosa cells in the dominant follicle. This drop in FSH level decreases the growth of the less-developed follicles. Estrogen causes cells of the endometrium to proliferate and stimulates production of LH.  Luteal/secretory phase – ovulation marks the beginning of this phase. The ovarian follicle begins its transformation into a corpus luteum. Pulsatile secretion of LH from the anterior pituitary stimulates the corpus luteum to secrete progesterone, which in turn initiates the secretory phase of endometrial development. Glands and blood vessels in the endometrium branch and curl throughout the functional layer, and the glands begin to secrete a thin glycogencontaining fluid, the secretory phase. If conception occurs, the nutrient-laden endometrium is ready for implantation. Human chorionic gonadotropin (HCG) is secreted 3 days after fertilization by blastocytes and maintains the corpus luteum once implantation occurs at about day 6 or 7. HCG can be detected in maternal blood and urine 8 to 10 days after ovulation.  Ischemic/menstrual phase  The production of estrogen and progesterone continues until the placenta can adequately maintain hormonal production. If conception and implantation do not occur, the corpus luteum degenerates and ceases production of progesterone and estrogen. Without progesterone or estrogen to maintain it, the endometrium becomes ischemic and disintegrates. Menstruation then occurs marking the beginning of another cycle.  Ovulatory cycles appear to have a minimum length of 24 to 26.5 days: the primary ovarian follicle requires 10 to 12.5 days to develop, and the luteal phase appears relatively fixed at 14 days (+/- 3 days). Menstrual blood flow usually lasts 3-7 days, but it may last as long as 8 days or stop after 1 to 2 days and still be considered within normal limits.  Ovulation – the release of an ovum from a mature follicle and marks the beginning of the luteal/secretory phase. o Uterine prolapse  Descent of the cervix or entire uterus into the vaginal canal.  In severe cases, the uterus falls completely through the vagina and protrudes from the introitus.  Symptoms of other pelvic floor disorders also may be present.  Urinary: sensation of incomplete emptying of the bladder, urinary incontinence, urinary frequency/urgency, bladder “splinting” to accomplish voiding  Bowel: constipation or feeling of rectal fullness or blockage, difficult defecation, stool or flatus incontinence  Urgency: manual “splinting” of posterior vaginal wall to accomplish defecation  Pain & Bulging: vaginal, bladder, rectum; pelvic pressure, bulging, pain, lower back pain  Sexual: dyspareunia, decreased sensation, lubrication, arousal  Tx:  Kegel exercises  Estrogen to improve tone and vascularity of fascial support  Pessary  Weight loss  Avoidance of constipation o Polycystic ovarian syndrome  Most common cause of anovulation and ovulatory dysfunction in women.  Defined as having at least two of the following three features: irregular ovulation, elevated levels of androgens (testosterone), and the appearance of polycystic ovaries on ultrasound.  Polycystic ovaries do not have to be present to diagnose PCOS, and conversely their presence alone does not establish the diagnosis.  Initial identification of genes involved in steroid biosynthesis, androgen biosynthesis, and insulin receptors within the ovary indicates genetic involvement.  A hyperandrogenic state is a cardinal feature in the pathogenesis of PCOS.  However, glucose intolerance/insulin resistance and hyperinsulinemia often run parallel to and markedly aggravate the hyperandrogenic state, thus contributing to the severity of signs and symptoms of PCOS.  Excessive androgens affect follicular growth, and insulin affects follicular decline by suppressing apoptosis and enabling follicles to persist.  Weight gain tends to aggravate symptoms, whereas weight loss may ameliorate some of the endocrine and metabolic events and thus decrease symptoms.  Women with PCOS tend to have increased leptin levels. Leptin influences the hypothalamic pulsatility of GnRH and consequent interaction along the entire HPO axis.  In PCOS there is dysfunction in ovarian follicle development. Inappropriate gonadotropin secretion triggers the beginning of a vicious cycle that perpetuates anovulation.  Typically, levels of FSH are low or below normal and LH levels and LH bioactivity are elevated. An increased frequency of GnRH pulses appears to cause increased frequency of LH pulses. Persistent LH elevation causes a increase in the levels of androgens. Androgens are converted to estrogen in peripheral tissues, and increased testosterone levels cause a significant reduction in SHBG, which in turn causes increased levels of free estradiol.  Elevated estrogen levels trigger a positive-feedback response in LH and a negative-feedback response in FSH.  The accumulation of follicular tissue is various stages of development allows an increased and relatively constant production of steroids in response to gonadotropin stimulation. Thus PCOS is characterized by excessive production of both androgen and estrogen.  In turn, persistent anovulation causes enlarged polycystic ovaries characterized by a smooth, pearly white capsule. This characteristic appearance is caused by an increase of surface area and increased volume of up to 2.8 times, doubling of growing and atretic follicles, thickening of the tunica by 50%, increasing cortical stromal thickening by one-third and a fivefold increase in subcortical stroma, and escalating hyperplasia.  Manifestations:  Usually appear within 2 years of puberty but may present after a variable period of normal menstrual function and possibly pregnancy.  Symptoms are related to anovulation, hyperandrogenism, and insulin resistance and include dysfunctional bleeding or amenorrhea, hirsutism, acne, acanthosis nigricans, and infertility.  Eval & Treatment:  Diagnosis is based on evidence of androgen excess, chronic anovulation, and sonographic evidence of polycystic ovaries with at least 2 of the 3 criteria present.  Tests for impaired glucose tolerance are recommended.  Evidence of hyperandrogenism must be present before PCOS is diagnosed in an adolescent female.  Goals of tx: reversing signs and symptoms of androgen excess, instituting cyclin menstruation, restoring fertility, and ameliorating any associated metabolic or endocrine, or both, disturbances.  First line: combined oral contraceptives for management of symptoms and to establish regular menses.  For those women with PCOS who are overweight or obese, lifestyle modifications including regular exercise and weight loss, also are considered firstline treatment. 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