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NR 507NR507 FINAL EXAM STUDY GUIDE (3) LATEST 2022.
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NR 507NR507 FINAL EXAM STUDY GUIDE (3) LATEST 2022.Endometrial cycle and occurrence of ovulation
Manifestation of female reproductive functioning is menstrual bleeding, which starts with menarche
(1st period) and ends with menopause (cessation of menstrual flow for 1 year). Average age of
menarche is 12 with a range of 9-17. Appears to be r/t body weight, especially body fat ratio. At first
cycles are anovulatory and vary from 10-60 days or >. Then in adulthood range form 25-35 days. Length
varies considerably.
Cycle and regular ovulation are dependent on
• The activity of gonadostat
• Initial pituitary secretion of gonadotropin FSH
• Estrogen positive feedback for the preovulatory FSH and LH surge, oocyte maturation,
and corpus luteum formation and production of progesterone.
The average menstrual cycle lasts 27 to 30 days and consists of three phases, which are named for ovarian
and endometrial changes: the follicular/proliferative phase, the luteal/secretory phase, and the
ischemic/menstrual phase.
Phase 1-is the follicular phase in which begins on day one of one’s menstrual cycle. It lasts
until about day 14.
-In phase 1 the endometrium grows to form a lush lining inside of the uterus.
Phase 2: Luteal phase-this is where the body secretes the hormones estrogen and progesterone.
-These hormones work together to prepare the lining of the uterus for implantation.
-This last for 12 days.
Phase 3: Menstrual phase-The estrogen and progesterone start to decline and the
endometrial lining begins to shed. This lasts for 3-5 days and the process restarts.
Ovulation
-Release of ovum
-Present at the beginning of the luteal/secretory phase.
-The ovarian follicle begins to transform into the corpus luteum.
-Pulsatile secretion of the LH from the anterior pituitary stimulates the corpus luteum to
secrete progesterone.
-This will initiate the secretory phase of endometrial development.
,NR 507NR507 FINAL EXAM STUDY GUIDE (3) LATEST 2022.
-Glands and blood vessels in the endometrium branch and curl through a functional layer, and
the glands begin to secrete a thin glycogen-containing fluid= the secretory phase.
*If conception occurs the nutrient-laden endometrium is ready for implantation.
*The HCG hormone is secreted 3 days after fertilization by blastocytes and maintains the
corpus luteum once implantation occurs at day 6 or 7.
*HCG can be detected in maternal blood or urine about 8-10 days after ovulation.
*Production of estrogen and progesterone continue until placenta can adequately maintain
hormonal production.
*Ovulatory cycles have a length of 24-26.5 days.
*The primary ovarian follicle requires 10-12.5 days to develop.
*The luteal phase appears at 14 days.
Ovarian events of the menstrual cycle are controlled by gonadotropins. High FSH levels stimulate follicle and
ovum maturation (follicular phase), then a surge of LH causes ovulation, which is followed by development of the
corpus luteum (luteal phase).
Ovarian hormones control the uterine (endometrial) events of the menstrual cycle. During the
follicular/proliferative phase of the ovarian cycle, estrogen produced by the follicle causes the endometrium to
proliferate (proliferative phase) and induces the LH surge and progesterone production in the granulosa layer.
During the luteal/secretory phase, estrogen maintains the thickened endometrium, and progesterone
causes it to develop blood vessels and secretory glands (secretory phase). As the corpus luteum degenerates,
production of both hormones drops sharply, and the “starved” endometrium degenerates and sloughs off,
causing menstruation, the ischemic/menstrual phase.
Cyclic changes in hormone levels also cause thinning and thickening of the vaginal epithelium, thinning and
thickening of cervical secretions, and changes in basal body temperature.
Uterine Prolapse
descent of cervix or entire uterus into vaginal canal. In severe cases the uterus falls completely through
the vagina and protrudes from the introitus. Symptoms of other pelvic floor disorders may also be
present. Tx depends on severity of symptoms and physical condition of woman. First line treatment is
often a pessary- removable mechanical device that holds uterus in position. The pelvic fascia may be
strengthened through kegels or by estrogen therapy in menopausal women. Healthy BMI, preventing
constipation, and treating chronic cough may also help. Surgical repair with or without hysterectomy is
the last resort.
Page-771 fig 25.11
-Dropping of the cervix or the entire uterus into the vaginal canal.
,NR 507NR507 FINAL EXAM STUDY GUIDE (3) LATEST 2022.
-In severe cases the uterus completely through the vagina and protrudes from the introitus.
-Symptoms of other pelvic floor disorders may also be present.
Symptoms: urinary-sensation of incomplete emptying of bladder,
incontinence,frequency,bladder splinting to accomplish voiding.
Bowel-constipation or feeling of rectal fullness, difficult defecation, stool or flatus incontinence.
*Pain or bulging includes pelvic pressure, low back pain, and vagina, bladder or rectum bulging.
*Sexual-decreased sensation, lubrication or arousal.
-Dyspareunia
Treatment:
-Depends on age and severity.
-Isometric exercise-strengthen the pubococcygeal muscle. KEGELS*
-Estrogen-to improve tone and vascularity of fascial support POSTMENOPAUSAL*
-Pessary—a removable device to hold pelvic organs in place.
-Weight loss
-Stool softeners to avoid constipation
-tx of lung and cough conditions
PCOS
Polycystic ovary syndrome (PCOS) is a difficult syndrome to diagnose because several factors are
involved. It is a syndrome in which at least two of the following are present: oligo-ovulation or
anovulation, elevated levels of androgens, or clinical signs of hyperandrogenism and polycystic ovaries.
Prolonged anovulation leads to infertility, menstrual bleeding disorders, hirsutism, acne, endometrial
hyperplasia, cardiovascular disease, and diabetes mellitus in women with hyperinsulinemia.
Presenting s/s: obesity, menstrual disturbance, oligomenorrhea, amenorrhea, regular menstruation,
hyperandrogenism, infertility or they could be asymptomatic.
Diagnosis of PCOS is based on evidence of androgen excess, chronic anovulation, and inappropriate gonadotropin secretion.
Tests for impaired glucose tolerance are recommended. As stated, polycystic ovaries do noT have to be present and,
conversely, their presence alone does not establish the diagnosis. Goals of treatment include reversing signs and symptoms of
androgen excess, instituting cyclic menstruation, restoring fertility, and ameliorating any associated metabolic or endocrine, or
both, disturbances.
, NR 507NR507 FINAL EXAM STUDY GUIDE (3) LATEST 2022.
*Most common cause of anovulation and ovulatory dysfunction in women.
*Leading cause of infertility and most common endocrine disturbance.
*Mostly common in younger women
*Usually has two/three of the following: irregular ovulation, elevated levels of androgens (testosterone), and the appearance of
polycystic ovaries on ultrasound.
*Polycystic ovaries do not need to be present to dx POS.
*Thyroid dysfunction, hyperprolactinemia, and congenital adrenal hyperplasia must be ruled out first.
*Associated with metabolic dysfunction, dyslipidemia, insulin resistance, and obesity.
*Strong genetic component and possibly differentially inherited.
*Difficult to diagnose as symptoms may change over time.
*80% of women have one or more of the symptoms with normal ovaries.
*More prominent sx as we age.
*May be associated with Cushing’s syndrome, acromegaly, premature ovarian failure, obesity, congenital adrenal hyperplasia,
thyroid disease and androgen producing adrenal tumors.
Pathophysiology:
*Underlying cause is unknown
*Genetic involvement suggested because of steroid and androgen biosynthesis.
*No single factor accounts for abnormalities of pcos.
***A HYPERANDROGENIC STATE IS A CARDINAL GEATURE IN THE PATHOGENSIS OF PCOS***
-3 X LIKELY TO HAVE INSULIN RESISTENCE.
*Insulin stimulates androgen secretion by the ovarian stroma and reduces the serum sex hormone-binding globulin.
* Free testosterone levels increase
*Excessive androgens affect follicular growth and insulin affects follicular decline by suppressing apoptosis
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