Menstrual and Uterine Disorders Flashcards
1
Q
Amenorrhea
A
Absence of menstrual bleeding
* Can be transient, intermittent, or permanent.
* Caused by dysfunction of the hypothalamic-pituitary-ovarian axis, the
ovaries, uterus, or the vagina.
2
Q
Primary vs. secondary amenorrhea
A
- Primary: Menses and secondary sexual characteristics never begin.
- Secondary: Menses stops (for at least 3 mos) after it has already occurred.
3
Q
Primary Amenorrhea
A
- Absence of menses by age 15
or - Both menses and secondary sexual
characteristics missing by age 13
4
Q
Etiology of primary amenorrhea
A
- Ovarian (Gonadal) dysgenesis (impaired development of the ovaries)
- Turner Syndrome
- Müllerian agenesis (absence of vagina and sometimes uterus)
- Delay of puberty due to genetics or other illness
- Polycystic ovary syndrome (PCOS)
5
Q
Secondary Amenorrhea
A
- Absence of menses for > 3 months in females who previously had regular
cycles or > 6 months in females who had irregular cycles
6
Q
Oligomenorrhea
A
fewer than 9 menstrual cycles per year or > 35 day cycles
* Same etiology, workup, treatment as secondary amenorrhea
7
Q
Etiologies of secondary amenorrhea
A
- Pregnancy is the most common cause of secondary amenorrhea
- Ovarian causes: PCOS, ovarian insufficiency
- Hypothalamic causes: Functional GnRH deficiency, anorexia
- Pituitary causes: Hyperprolactinemia, Cushing syndrome
- Uterine causes: Intrauterine adhesions
- Hypothyroidism
8
Q
Amenorrhea pathophysiology
A
- Hypothalamic-pituitary dysfunction: A result of interference with GnRH transport, GnRH
discharge, or congenital absence of GnRH - Hyperprolactinemia (galactorrhea often present)
- Ovarian Dysfunction
- Dysgenesis: Ovaries fail to develop (often due to Turner Syndrome)
- Premature ovarian failure: Depletion of ova before age 40
- PCOS: Exact mechanism unknown, but related to androgen sensitivity
- Pituitary Dysfunction
- Radiation, Sheehan syndrome, pituitary adenomas/prolactinomas
9
Q
Dysgenesis of the ovaries
A
Ovaries fail to develop (often due to Turner Syndrome)
10
Q
Hypothalamic-pituitary dysfunction
A
- A result of interference with GnRH transport, GnRH
discharge, or congenital absence of GnRH - Hyperprolactinemia (galactorrhea often present)
11
Q
History taking for amenorrhea
A
- Determine if menstruation has occurred previously
- Cycle, duration, and flow of menses. Date of last menstrual period (LMP)
- Determine if sexually active, use of contraception
- Headaches and visual field deficit (tumors)
- Environmental factors, stress, exercise, nutrition status/eating disorders
- Symptoms of estrogen deficiency: hot flashes, vaginal dryness, poor sleep
- Galactorrhea (hyperprolactinemia)
- Current Medications: Birth control, metoclopramide, antipsychotics, opioids
12
Q
Amenorrhea PE
A
- Breast development, pubertal growth spurt are delayed or absent in girls
with hypothalamic-pituitary failure - Hirsutism
- BMI (elevated in >50% of PCOS)
- Yellow skin, dental erosion, reduced gag reflex (Eating Disorders)
- Short stature, webbed neck, low-set hairline and/or ears (Turner Syndrome)
- Examine the breasts and perform a pelvic exam
13
Q
Amenorrhea diagnosis and testing
A
- Urine or serum HCG (Always!)
- TSH, FSH, (+ or - LH), estradiol, prolactin
- Androgen testing (testosterone, dehydroepiandrosterone sulfate) if signs of
hyperandrogenism - Pelvic ultrasound for primary amenorrhea (if normal vagina/uterus are not
obviously present) - Pituitary MRI if prolactin high and no obvious cause.
- Progestin challenge: medroxyprogesterone acetate 10 mg daily for 10 days
14
Q
Amenorrhea treatment
A
- Based on the underlying cause
- PCOS, thyroid dysfunction, hypothalamic, hyperprolactinemia,
ovarian failure…
15
Q
Goals of Amenorrhea treatment
A
- Goals: Correct pathology, achieve fertility, prevent complications.
- Education
- Referral
- Outflow tract abnormalities may require surgery
- Hormone replacement therapy
- Cognitive behavioral therapy
16
Q
Dysmenorrhea
A
Defined as: Painful menstruation, usually crampy lower abdominal pain
* Common in the first few years of menstruation
* Up to 85% of adolescent girls
* Prevalence higher among smokers
17
Q
Dysmenorrhea etiology
A
- Primary: occurs in the absence of pelvic pathology
- Secondary: Occurs due pelvic pathology
- Causes include anatomic abnormalities (like fibroids), endometriosis, ovarian cysts, psychogenic contributors, infection (Pelvic inflammatory disease)
18
Q
Dysmenorrhea pathophysiology
A
- Prostaglandin F2⍺ (PF2⍺)
- Myometrial stimulant
- Causes dysrhythmic uterine contractions,
hypercontractility, and increased uterine
muscle tone leading to uterine ischemia. - Also stimulates GI tract, leading to
nausea, vomiting, and diarrhea - Elevated levels in the endometrium
correspond to degree of pain
19
Q
Clinical presentation of dysmenorrhea (primary)
A
- Begins once menstrual cycles establish as ovulatory. Usually first presents
within 4-5 years of menarche. - Symptoms begin several hours prior to the onset of menstruation
- Durations is 1-3 days
- Labor-like, lower abdominal cramping/pain
- Can include nausea, vomiting, diarrhea, back pain, dizziness, fatigue, and
headache - Physical exam usually normal,
20
Q
Clinical presentation of dysmenorrhea (secondary)
A
- Secondary: Potential symptoms and exam findings depend on etiology.
- Often begins between ages 20-40 years old
- Symptoms can include: Heavy irregular flow, Dyspareunia, Infertility,
Bloating, Back pain, Pelvic heaviness - Possible Exam Findings: cervical motion tenderness, palpable uterine
mass, adnexal tenderness
21
Q
Dysmenorrhea diagnosis
A
- No specific tests for primary dysmenorrhea
- Secondary
- CBC c diff, STIs, HCG, ESR, UA, stool guaiac
- Ultrasound
- CT
- Laparoscopy
22
Q
Dysmenorrhea treatment
A
- Primary dysmenorrhea tends to improve over time, and often improves
after childbirth - NSAIDs (Antiprostaglandins): started at the onset of menses and
continued for the first one to two days of the menstrual cycle - Direct Heat
- Exercise
- Hormonal Therapy: Oral contraceptive pills (OCPs), Estrogen-progestin or
Progestin-only contraceptives - Levonorgestrel IUD is associated with reductions in dysmenorrhea
23
Q
Premenstrual Syndrome (PMS)
A
Cyclical behavioral, psychological, and physical changes
during the luteal phase (second half of the menstrual cycle)
24
Q
PMS risk factors
A
genetic predisposition, smoking, obesity, history of
traumatic events, anxiety disorders
25
PMS pathophysiology
Not completely understood
* Triggered by changes in gonadal steroids during the luteal phase in
susceptible women
* These interact with the functioning of central neurotransmitters, like serotonin.
* Lower blood serotonin
26
Clinical presentation of PMS
* Symptoms begin before menses (usually around 3-4 day) and resolve within
2-3 days of menses. Average duration is 6 days.
* Affective/behavioral symptoms:
* #1 is mood swings
* Others: Irritability, anxiety, sad/depressed mood, increased
appetite/cravings, sensitivity to rejection, and anhedonia
* Physical Symptoms:
* Top are abdominal bloating and sense of fatigue
* Breast tenderness, headaches, hot flashes, and dizziness
27
PMS diagnosis
* No labs or imaging studies generally
indicated
* May need to rule out other causes
such as such as hyper- or
hypothyroidism or excess cortisol.
28
Premenstrual Dysphoric Disorder
(PMDD)
Severe premenstrual distress
* Interferes with occupational and social functioning
* Affects about 2% of women
* Ages 30-50 years
29
RFs for PMDD
* Sexual abuse and/or Domestic violence
* Personal or family history of mood disorders
30
Clinical presentation for PMDD
* Same symptoms as PMS, but more severe and disabling.
* Irritability, depression/hopelessness, self-critical thoughts, anxiety,
difficulty concentrating, easy fatigability
* Breast tenderness, bloating, weight gain, or joint/muscles aches,
sleeping too much or not sleeping enough
* Mental status exam may be abnormal during the luteal phase
31
Diagnosis of PMDD
* Rule out organic causes
* Anemia, thyroid disorders,
menopause
* TSH, CBC c diff, FSH
DSM 5 criteria
32
Treatment of PMDD
All Patients:
* Exercise, relaxation techniques
* Cognitive Behavioral Therapy (CBT)
Moderate to Severe Symptoms:
* SSRIs - Any SSRI can be effective
* Options of continuous, Luteal phase, or Symptom-onset therapies
* Can consider SNRIs like Venlafaxine as well
* Combined estrogen-progestin contraception
* Reduce LH and FSH from pituitary by decreasing GnRH
* Drospirenone/ethinyl estradiol (Yasmin, Yaz)
33
Treatment of PMS and PMDD if severe symptoms
* GnRH agonist - for ovarian suppression
* only for those who don’t respond to or can’t
tolerate SSRIs or OCPs
* Leuprolide (Lupron)
* Should include low-dose
estrogen-progesterone "add back" therapy
* Hysterectomy with bilat oophorectomy (Last
resort)
34
Alternative Treatments for PMS and PMDD
* Vitex agnus castus
* Acupuncture
* Benzodiazepines NOT recommended
PMS and PMDD generally resolve completely after menopause
35
Abnormal Uterine Bleeding (AUB)
Irregular uterine bleeding without pelvic pathology, pregnancy,
or other medical disease
* Usually associated with anovulatory cycles
* Diagnosis of exclusion
36
Abnormal Uterine Bleeding (AUB) etiology
* PALM-COEIN (polyp, adenomyosis, leiomyoma, malignancy and
hyperplasia, coagulopathy, ovulatory dysfunction, endometrial, iatrogenic,
and not yet classified)
* Structural uterine pathology (eg, fibroids, endometrial polyps,
adenomyosis, neoplasia)
* Infections (eg, endometritis)
* Ovulatory dysfunction
* Estrogen breakthrough bleeding
* Estrogen withdrawal bleeding
* Perimenopausal women
* Iatrogenic
37
Clinical presentation of AUB
* Frequency of menstruation: frequent (<24 days) or infrequent (>38 days)
* Duration of menstruation: Can be prolonged (>8 days)
* Regularity of menstruation: Irregular - variation can be ≥10 days
* Flow Volume: Heavy or light
* Intermenstrual bleeding: Can be random or predictable
38
Diagnosis and Testing for AUB
* Test for pregnancy
* R/o iatrogenic causes, bleeding disorders, endocrine disorders
* Assess hemodynamic stability (ie, look for low blood volume and anemia)
* Endometrial biopsy - may be needed based on symptoms
* Pelvic ultrasound may also be needed based on symptoms (patients with
intermenstrual bleeding, heavy menstrual bleeding)
39
Abnormal Uterine Bleeding (AUB) treatment
* Correct any underlying etiology (structural,
infections, endocrine, bleeding disorders)
* Estrogen-progestin contraceptives
* Levonorgestrel IUD
* Cyclic progestin therapy
* NSAIDs
* Endometrial ablation
* Hysterectomy
40
Endometriosis
The presence of endometrial tissue (glands and stroma)
abnormally implanted in locations other than the uterine cavity
* Adenomyosis= ectopic endometrial tissue grows into myometria
* Despite location, continues to act as it normally would (cyclical)
* Prevalence higher in infertile women
* First degree relative increases risk 10x
41
Hemorrhagic uterine bleeding requires
high-dose estrogen therapy
* If bleeding is not controlled within 12-24 hours, a D&C is indicated
42
Endometriosis risk factors
* Family history of endometriosis
* Early age of menarche
* Short menstrual cycles (< 27 d)
* Long duration of menstrual flow (>7 d)
* Heavy bleeding during menses
* Inverse relationship to parity
* Delayed childbearing
* Defects in the uterus or fallopian tubes
43
Most common locations for endometriosis
posterior and anterior cul-de-sac,
uterosacral ligaments, tubes, ovaries
44
Pathophysiology of endometriosis
* Most common locations are the posterior and anterior cul-de-sac,
uterosacral ligaments, tubes, ovaries
* Can occur in any organ system
* This tissue responds to cyclic hormonal fluctuations in
much the same way as intrauterine endometrial tissue
* Metabolic products, including cytokines and
prostaglandins, lead to an altered inflammatory
response
* Neovascularization and fibrosis formation = adhesions
45
Endometriosis clinical presentation
* 30% of patients are asymptomatic
* Pelvic pain
* Dyspareunia
* Heavy/irregular bleeding
* Lower back pain or abdominal pain
* Pain with urination or defecation
* Dysmenorrhea
* Bloating, nausea, vomiting
* Infertility
* Exam WNL except for tenderness at involved site
46
Endometriosis diagnosis
* Pelvic ultrasonography, CT, and MRI are only useful in advanced disease
* Laparoscopy is the procedure of choice
* Sensitivity 97% ,specificity 77%
* Powder-burned or black-blue lesions
47
Endometriosis treatment
* NSAIDs
* Combined OCPs
* 3 month trial, consider continuous use
* Progesterone: Oral, injection, IUD
* Gonadotropin-releasing hormone agonists - Leuprolide acetate (Lupron)
* Danazol - inhibits the luteinizing hormone surge. Caution of androgenic
side effects
* These treatments have similar clinical efficacy in terms of reduction in
pain-related symptoms and duration of relief
* Aromatase inhibitors (letrozole) - severe, refractory, endometriosis
48
Endometriosis surgical intervention
*Removal of lesions
*Conservative = maintain potential fertility
*Total hysterectomy with bilateral oophorectomy with
cytoreduction of visible endometriosis lesions
*Recurrence rate of 15%
49
Endometriosis and infertility
* Peritubal and periovarian adhesions interfere mechanically with ovum
transport
* Peritoneal endometriosis interferes with tubal motility, folliculogenesis,
and corpus luteum function
* May cause sperm to bind to the ampullary epithelium
* No evidence indicates that medical or surgical treatment of endometriosis
reduces the spontaneous abortion rate
* Increases risk of early pregnancy loss and later pregnancy complications
