03. Menstruation Flashcards
Two general phases of Menstrual & Ovulatory Cycles
Follicular phase & Luteal phase
Hormone surges during Follicular Phase (in order)
FSH & LH (minor surge); Estrogen surge; LH surge; FSH surge
Hormone surges during Luteal Phase (in order)
Progesterone (major) & Estrogen (minor surge)
Follicular Phase Characteristics
Begins at onset of menses; Ovarian follicle recruitment & maturation; Ends with pre-ovulatory surge of LH stimulating ovulation (24-36 hr at end)
Luteal Phase Characteristics
Begins with ovulation; Ends at onset of menses; Endometrium thickens in preparation for pregnancy; Ends in pregnancy or luteolysis
Estimated blood loss during menses
~30 cc
Excessive blood loss during menses
~80 cc
Period of heaviest blood loss during menses
First 2 days
FSH effects
Causes 15-20 eggs to begin maturing in each ovary; Follicles produce estrogen
Estrogen effects
Released by maturing follicles; when threshold is reached, follicle is mature and triggers LH surge
LH Effects
Triggered by high estrogen levels; Causes egg to burst from follicle; Stimulates ovary to produce progesterone after ovulation. Also stimulates follicles to produce androgens, which are converted to estrogen
Progesterone Effects
Produced by corpus luteum; Prevents release of all other eggs for that cycle; Causes thickening of endometrium & sustains life until corpus luteum distintegrates (12-16 days later); Causes changes in 3 fertility signs
What are the 3 fertility signs?
Change in temperature, cervical fluid, and cervical position
3 Major Components that Regulate the Menstrual Cycle
Hypothalamic/Pituitary Axis; Ovaries; Endometrium/Uterus
5 Small Peptides/Amines From Hypothalamus that affect Reproductive Cycle
GnRH; TRH; SRIF; CRF; PIF (Prolactin release-inhibitin factor)
GnRH Effects
Pulsatile release from hypothalamus; Increased during follicular phase; Decreased during luteal phase; Pulses q90min; To the ANTERIOR PITUITARY via portal circulation;
Negative Estrogen Feedback Mechanism
During early follicular phases, estrogen levels low
Positive Estrogen Feedback Mechanism
High concentrations at end of follicular phase trigger FSH & LH, which trigger increased estrogen release; Ensuring LH surge triggers ovulation
Follicle count of 20 week fetus
6 million
Follicle count of newborn
600,000
Follicle count at menarche
300,000
Follicle count at menopause
10,000
FSH & LH negative feedback
High levels of estrogen and progesterone during luteal phase suppress FSH & LH
What is the time span between the LH surge and ovulation?
24-36 hr
Days 1-4 of menstrual cycle
“Bleeding phase”; Estradiol & progesterone levels low; FSH begins to rise; LH begins rising days after FSH starts rising
Causes of uterine sx during menstruation
Corpus luteum involutes; Prog & est fall rapidly; Prostaglandins increase in myometrium to stimulate contraction
Days 4-14 of menstrual cycle
Follicular phase; Estradiol increases & peaks just before LH surge & ovulation; Progesterone stays low; FSH peak mid-cycle with LH, but in lesser surge; LH rapidly peaks mid-cycle & triggers ovulation
Day 12-14
Ovulation; mid-cycle between follicular & luteal phases
Uterine changes during luteal (secretory) phase
Progesterone stimulates glands to secrete mucus & glycogen; Glands become tortuous & dilated; Convoluted spiral arteries extend to superficial layer of endometrium;
Corpus luteum
Forms from the granulosa cells of the ruptured follicle; maintains pregnancy until placental progesterone production is adequate
What happens to the corpus luteum if pregnancy doesn’t occur?
It degenerates intoa corpus albicans, which causes regression of progesterone and estradiol levels.
Estrone
Hormone secreted by ovary & adrenal glands; converted to estrogen in peripheral fat to maintain vaginal tissue, minimize hot flashes/night sweats/mood swings
Which hormone remains elevated if pregnancy occurs?
Progesterone
What are negative effects of high prolactin levels?
Interfere with FSH/LH and may cause anovulation. This is why people think they can’t get pregnant while breast feeding.
How can hyperthyroidism cause infertility?
High TSH levels stimulate Prolactin production. High prolactin levels lead to anovulation, which results in infertility.
How can adrenal dysfunction lead to infertility?
High ACTH inhibits FSH & stimulates androgen production. In combo, this inhibits ovulation.
What hormonal dysfunctions occur in PCOS?
Ovary doesnﾒt make all hormones needed for fully mature egg. Follicles start to grow but ovulation doesn’t occur because ovaries make androgens instead. Progesterone isn’t made, which results in irregular or absent menstrual cycle.
Functional zones of endometrium
Functionalis (outer); Basalis (inner)
Functionalis
Outer portion of endometrium; Undergoes cyclic changes during menstrual cycle; Sloughed off with menstruation
Basalis
Inner portion of endometrium; relatively UNCHANGED during cycle; Provides stem cells and blood supply for renewal of functionalis
Endometrium - Menstrual phase
Day 1-4. Disruption & disintegration of endometrial gland & stroma; Leukocyte infiltration; RBC extravasation
Endometrium - Proliferative phase
Days 5-14. Endometrial growth secondary to estrogen surge. High estrogen causes proliferation of epithelial lining, endometrial gland, and connective tissue of stroma
Endometrium - Secretory phase
Days 15-28. Lining becomes stable & ready for implantation. Progesterone stimulates secretion of glycogen & mucus. Glands & vessels become tortuous. Lumens dilate and fill.
Premenstrual syndrome
Cyclic recurrence of physical, psychological and behavioral changes that cause distress and interfere with normal ADLs or relationships
APA diagnostic criteria for PMS
Must have one or more of the following: Affect lability (mood swings); Persistant/marked anger/irritability; Marked anxiety/tension; Markedly depressed/hopeless; AND
Must have a total of 5 symptoms (not all listed)
Dietary mods that may help PMS
Increase protein. Decrease carbs & salt. Limit caffeine & EtOH. Eat 4-6 small meals/day.
PMS pharmacologic tx
Serotonins (SSRIs) - Fluoxetine (Prozac) and Venlafaxine (Effexor)
Primary dysmenorrhea
Painful menstruation without associated pelvic disease; Caused by increased PG release from endometrial cells at time of menstruation. This causes uterine contractions, pressure, and some degree of ischemia. Lasts 12-72 hr.
Primary dysmenorrhea tx
NSAIDs- inhibition of PG production. Ibuprofen, naproxen, and ketoprofen preferred. Hormonal contraceptives 2nd line.
Secondary Dysmenorrhea
Pelvic pain present at non-menstruating times d/t identifiable pelvic pathology; unrelated to actual onset of menses each month; May or may not have normal pelvic exam.
Causes of Secondary Dysmenorrhea
Chronic PID; Endometriosis; Adhesions; Mullerian duct abnormalities; Adenomyosis; IUD; Tumor
What is endometriosis?
Presence of endometrial-like cells appearing and flourishing outside the uterine cavity. Influenced and respond to hormonal changes. Worsens with menstrual cycle.
What are common sites of endometriosis?
Ovaries (MC); Posterior cul-de-sace; Anterior cul-de-sac; Uterosacral ligaments; Broad ligament
Dyschezia
Constipation d/t defective defecation reflex; sign of endometriosis
Definitive endometriosis diagnosis
Requires direct visualization of endometriotic lesions via laparoscopy, laparotomy, or tissue bx.
Endometriosis Pathophysiology/Etiology
Retrograde menstruation;
Peritoneal coelomic metaplasia (metaplastic tissue assumes characteristics of endometrial tissue);
Hematogenous/lymphatic spread (Spread by vascular and lymphatic pathways to various structures)
Chocolate cysts
Invasive endometriotic lesions on the ovary filled with chocolate-colored blood. Can cause extensive pelvic adhesions, esp. peri-ovarian
Endometriosis Tx - Medical
Estrogen-progestin OCPs (inhibit ovulation)
Mini-pills (suppress endometrial stimulation)
Danazol ("anti-estrogen" to suppress endometrial growth)
GnRH AGONISTS (MOST DEFINITIVE MEDICAL MANAGEMENT; RESULTS IN MEDICAL MENOPAUSE!!! Eliminates ovarian estrogen)Endometriosis Tx - Surgical
Destruction of endometrial lesions; lysis of adhesions; Uterosacral ligament ablation or presacral neurectomy (relieve pelvic pain)
Oligomenorrhea
Infrequent, irregular bleeding with intervals >40 days
Polymenorrhea
Frequent, regular bleeding with intervals
Hypomenorrhea
Regular bleeding that is very light
Cryptomenorrhea
Outflow obstruction
Menorrhagia (hypermenorrhea)
Excessive amount or duration with regular intervals
Metrorrhagia
Regular periods with intermenstrual bleeding
Menometrorrhagia
Heavy periods with intermenstrual bleeding
2 Basic Etiologies of Abnormal Uterine Bleeding
Anatomic & Hormonal
Anatomic causes of abnormal uterine bleeding
Uterine fibroids; Adenomyosis; Uterineor cervical polyps
4 Main Categories of Abnormal Bleeding d/t Hormonal Dysorder
Estrogen withdrawal bleeding (Mid-cycle spotting)
Estrogen breakthrough bleeding (Missed menses followed by heavy bleeding x 10d)
Progesterone withdrawal bleeding (menstrual bleeding)
Progesterone breakthrough bleeding (Atrophic endometrium)
DUB
Dysfunctional uterine bleeding; No longer a recommended term. Considered abnormal uterine bleeding in absence of an anatomic lesion)
AUB
Abnormal uterine bleeding; Newer, preferred term. Replaces DUB.
Most common times of DUB presentation
Shortly after menarche; Perimenopause
Physical exam findings of DUB
No significant findings; R/O pregnancy, systemic dz, and obvious pathology.
When performing a work up for a patient presenting with DUB, which imaging technique should be used?
Pelvic or trans-vaginal U/S
What are the five general categories causing DUB?
Endocrine d/o; Structural lesions; Infections; Medications; Pregnancy
3 Goals of DUB Tx
Prevent endometrial hyperplasia/CA; Treat/prevent anemia; Restore quality of life
Progesterone Challenge & DUB
Give the progesterone missing due to lack of ovulation; Medroxyprogesterone acetate 10mg x 10 d, or Micronized progesterone 200mg x 10d; or progesterone 100mg IM. This is diagnostic & therapeutic if patient has withdrawal bleeding; reboots menstrual cycle.
Advantages of Progesterone Tx of DUB
CAN beused in women who CANNOT take OCPs; Manages bleeding; Treats endometrial hyperplasia; Inexpensive; DepoMPA for contraception or menorrhagia (3-12 months to work)
Disadvantages of Progesterone Tx of DUB
MPA 10mg x 10d; or Micronized progesterone 200 mg x 10d; or Progesterone 100mg IM have no protection against ovarian CA, may not help dysmenorrhea; offerno contraceptive protection
High-dose Estrogen to Tx DUB
Stops bleeding but does not treat underlying cause; induces endometrial growth, stimulates productino of progesterone receptors; allows progestin to differentiate endometrium
Recommended high-dose estrogen for DUB Tx
OCP qid x 5 d and/or followed by 1 QD for a total of 21 days
AUB vs DUB
AUB (bleeding differs in quantity or timing from natural cycle; d/t various causes). DUB (related to hormonal changes directly affecting menstrual cycle; NL menstruation disrupted due to anovulation; UNRELATED TO ANOTHER ILLNESS)
Amenorrhea Adverse Effects
Infertility, osteoporosis
Primary Amenorrhea
No period by age 14 AND no growth or development of secondary sex characteristics; OR
No period by age 16 regardless of secondary sex traits
Secondary Amenorrhea
Cessation of regular menstruation for >3 cycle intervals or >6 months total.
MCC of Secondary Amenorrhea
Pregnancy
Classifications of Amenorrhea
1) Primary/Secondary; or 2) Axes
4 Axes of Amenorrhea
Disorders of outflow tract; Disorders of ovaries; Disorders of anterior pituitary; Disorders of CNS/Hypothalamus
Functional hypothalamic amenorrhea
Common in female athletes
Functional hypothalamic amenorrhea tx
Weight restoration through nutrition rehab and decreased exercise; OCPs do NOT improve bone density, and shouldn’t be used soley for this purpose
