1
FINAL EXAM STUDY GUIDE
Reproductive
Endometrial cycle and the occurrence of ovulation
-menstrual cycle starts with menarche (first menstruation) ends with
menopause (cessation of menstrual flow for 1 year)
-Cycles -anovulatory at first may vary in length from 10 to 60 days or
more.
-As adolescence proceeds into adulthood, regular patterns of
menstruation and ovulation are established at intervals ranging from 21
to 45 days.
-
Menstruation continues to recur in a recognizable and characteristic
pattern during adulthood, with the length of the menstrual cycle
varying considerably among women.
- commonly accepted cycle average is 28 (27 to 30) days, with rhythmic
intervals of 21 to 35 days considered normal.
-Approximately 2 to 8 years before menopause, cycles begin to lengthen
again with variation related to changing hormone levels
-2 phases:
1) follicular/proliferative phase (postmenstrual)
-lasts until about day 14.
- endometrium grows to form a lush lining inside of the uterus.
2) luteal/secretory phase (premenstrual)
- this is where the body secretes the hormones estrogen and
progesterone. -These hormones work together to prepare the
lining of the uterus for implantation.
-lasts for 12 days
-During menstruation (menses), the functional layer of the endometrium
disintegrates and is discharged through the vagina.
● The estrogen and progesterone start to decline and the
endometrial lining begins to shed. This lasts for 3-5 days and the
process restarts.
Menstruation is followed by the follicular/proliferative phase.
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-Ovulation is the release of an ovum from a mature follicle and marks the
beginning of the luteal/secretory phase of the menstrual cycle. The
ovarian follicle begins its transformation into a corpus luteum hence the
name luteal phase.
● 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.
● 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.
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.
-due to weakness of the pelvic musculature, ligaments, and fascia or
obstetric trauma and lacerations sustained during labor and delivery.
- Pregnancy, obesity, prolonged standing, and chronic constipation
are associated with stretching of the fascia and prolapse over time.
- Women with connective tissue disorders are also at risk, so there is a
strong genetic/familial component. In addition, risk of prolapse increases
with age because of cumulative effects of stress on the pelvic floor.
-Because estrogen improves vascularity of the pelvic area,
postmenopausal women are at risk since their fascia and pelvis
musculature lose resilience with diminished estrogen levels
- Treatment is often progressive with less aggressive treatments
tried first.
P a g e 2 | 92
, 3
-The pelvic fascia may be strengthened through Kegel exercises (repetitive
isometric tightening and relaxing of the pubococcygeal muscles) or by
estrogen therapy in menopausal women.
-Maintaining a healthy body mass index (BMI), preventing constipation,
and treating chronic cough or constipation may help as well.
-A common treatment is a pessary, which is a removable device that,
when placed in the vagina, holds the uterus in position.
-
Surgical repair with or without hysterectomy is the
treatment of last resort.
Symptoms:
● Urinary
o Sensation of incomplete emptying of bladder
o Urinary incontinence
o Urinary frequency/urgency
o Bladder “splinting” to accomplish voiding
● Bowel
o Constipation or feeling of rectal fullness or
blockage
o Difficult defecation
o Stool or flatus incontinence
● Urgency
o Manual “splinting” of posterior vaginal wall to
accomplish defecation
● Pain and Bulging
o Vaginal, bladder, rectum
o Pelvic pressure, bulging, pain
o Lower back pain
● Sexual
o Dyspareunia
o Decreased sensation, lubrication, arousal
Polycystic ovarian syndrome
-most common cause of anovulation and ovulatory dysfunction in
women.
P a g e 3 | 92
, 4
- defined as having at least two of the following three features:
o irregular ovulation,
o elevated levels of androgens (e.g., testosterone)
o and the appearance of polycystic ovaries on ultrasound
-Polycystic ovaries do not have to be present to diagnose PCOS--
presence alone does not establish the diagnosis.
-The diagnosis is one of exclusion, and all other disorders potentially
responsible for the clinical findings also must be ruled out, including
thyroid dysfunction, hyperprolactinemia, and congenital adrenal
hyperplasia.
- associated with metabolic dysfunction, including
dyslipidemia, insulin resistance, and obesity
- Insulin stimulates androgen secretion by the ovarian stroma and reduces
serum sex hormone–binding globulin (SHBG) directly and independently.
The net effect is an increase in free testosterone levels. Excessive
androgens affect follicular growth, and insulin affects follicular decline by
suppressing apoptosis and enabling follicles to persist
- there appears to be a genetic ovarian defect in PCOS, which makes the
ovary either more susceptible to or sensitive to insulin's stimulation of
androgen production
-A HYPERANDROGENIC STATE IS A CARDINAL GEATURE IN THE
PATHOGENSIS OF PCOS
-3 X LIKELY TO HAVE INSULIN RESISTENCE.
- *FSH is low and LH are high.
-**Women with PCOS 3 x greater of developing uterine cancer.
Clinical Manifestations: *Appear within 2 years of puberty.
*May not present until normal menstrual function or pregnancy.
o anovulation, hyperandrogenism, and insulin resistance
dysfunctional bleeding or amenorrhea, hirsutism, acne,
acanthosis nigricans, and infertility.
Management:
*Goals are to suppress androgen, instituting menstruation, restore
fertility, and reduce endocrine disturbance.
P a g e 4 | 92
FINAL EXAM STUDY GUIDE
Reproductive
Endometrial cycle and the occurrence of ovulation
-menstrual cycle starts with menarche (first menstruation) ends with
menopause (cessation of menstrual flow for 1 year)
-Cycles -anovulatory at first may vary in length from 10 to 60 days or
more.
-As adolescence proceeds into adulthood, regular patterns of
menstruation and ovulation are established at intervals ranging from 21
to 45 days.
-
Menstruation continues to recur in a recognizable and characteristic
pattern during adulthood, with the length of the menstrual cycle
varying considerably among women.
- commonly accepted cycle average is 28 (27 to 30) days, with rhythmic
intervals of 21 to 35 days considered normal.
-Approximately 2 to 8 years before menopause, cycles begin to lengthen
again with variation related to changing hormone levels
-2 phases:
1) follicular/proliferative phase (postmenstrual)
-lasts until about day 14.
- endometrium grows to form a lush lining inside of the uterus.
2) luteal/secretory phase (premenstrual)
- this is where the body secretes the hormones estrogen and
progesterone. -These hormones work together to prepare the
lining of the uterus for implantation.
-lasts for 12 days
-During menstruation (menses), the functional layer of the endometrium
disintegrates and is discharged through the vagina.
● The estrogen and progesterone start to decline and the
endometrial lining begins to shed. This lasts for 3-5 days and the
process restarts.
Menstruation is followed by the follicular/proliferative phase.
P a g e 1 | 92
, 2
-Ovulation is the release of an ovum from a mature follicle and marks the
beginning of the luteal/secretory phase of the menstrual cycle. The
ovarian follicle begins its transformation into a corpus luteum hence the
name luteal phase.
● 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.
● 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.
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.
-due to weakness of the pelvic musculature, ligaments, and fascia or
obstetric trauma and lacerations sustained during labor and delivery.
- Pregnancy, obesity, prolonged standing, and chronic constipation
are associated with stretching of the fascia and prolapse over time.
- Women with connective tissue disorders are also at risk, so there is a
strong genetic/familial component. In addition, risk of prolapse increases
with age because of cumulative effects of stress on the pelvic floor.
-Because estrogen improves vascularity of the pelvic area,
postmenopausal women are at risk since their fascia and pelvis
musculature lose resilience with diminished estrogen levels
- Treatment is often progressive with less aggressive treatments
tried first.
P a g e 2 | 92
, 3
-The pelvic fascia may be strengthened through Kegel exercises (repetitive
isometric tightening and relaxing of the pubococcygeal muscles) or by
estrogen therapy in menopausal women.
-Maintaining a healthy body mass index (BMI), preventing constipation,
and treating chronic cough or constipation may help as well.
-A common treatment is a pessary, which is a removable device that,
when placed in the vagina, holds the uterus in position.
-
Surgical repair with or without hysterectomy is the
treatment of last resort.
Symptoms:
● Urinary
o Sensation of incomplete emptying of bladder
o Urinary incontinence
o Urinary frequency/urgency
o Bladder “splinting” to accomplish voiding
● Bowel
o Constipation or feeling of rectal fullness or
blockage
o Difficult defecation
o Stool or flatus incontinence
● Urgency
o Manual “splinting” of posterior vaginal wall to
accomplish defecation
● Pain and Bulging
o Vaginal, bladder, rectum
o Pelvic pressure, bulging, pain
o Lower back pain
● Sexual
o Dyspareunia
o Decreased sensation, lubrication, arousal
Polycystic ovarian syndrome
-most common cause of anovulation and ovulatory dysfunction in
women.
P a g e 3 | 92
, 4
- defined as having at least two of the following three features:
o irregular ovulation,
o elevated levels of androgens (e.g., testosterone)
o and the appearance of polycystic ovaries on ultrasound
-Polycystic ovaries do not have to be present to diagnose PCOS--
presence alone does not establish the diagnosis.
-The diagnosis is one of exclusion, and all other disorders potentially
responsible for the clinical findings also must be ruled out, including
thyroid dysfunction, hyperprolactinemia, and congenital adrenal
hyperplasia.
- associated with metabolic dysfunction, including
dyslipidemia, insulin resistance, and obesity
- Insulin stimulates androgen secretion by the ovarian stroma and reduces
serum sex hormone–binding globulin (SHBG) directly and independently.
The net effect is an increase in free testosterone levels. Excessive
androgens affect follicular growth, and insulin affects follicular decline by
suppressing apoptosis and enabling follicles to persist
- there appears to be a genetic ovarian defect in PCOS, which makes the
ovary either more susceptible to or sensitive to insulin's stimulation of
androgen production
-A HYPERANDROGENIC STATE IS A CARDINAL GEATURE IN THE
PATHOGENSIS OF PCOS
-3 X LIKELY TO HAVE INSULIN RESISTENCE.
- *FSH is low and LH are high.
-**Women with PCOS 3 x greater of developing uterine cancer.
Clinical Manifestations: *Appear within 2 years of puberty.
*May not present until normal menstrual function or pregnancy.
o anovulation, hyperandrogenism, and insulin resistance
dysfunctional bleeding or amenorrhea, hirsutism, acne,
acanthosis nigricans, and infertility.
Management:
*Goals are to suppress androgen, instituting menstruation, restore
fertility, and reduce endocrine disturbance.
P a g e 4 | 92
