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.

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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.
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3
Q

Primary Amenorrhea

A
  • Absence of menses by age 15
    or
  • Both menses and secondary sexual
    characteristics missing by age 13
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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)
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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
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6
Q

Oligomenorrhea

A

fewer than 9 menstrual cycles per year or > 35 day cycles
* Same etiology, workup, treatment as secondary amenorrhea

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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
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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
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9
Q

Dysgenesis of the ovaries

A

Ovaries fail to develop (often due to Turner Syndrome)

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10
Q

Hypothalamic-pituitary dysfunction

A
  • A result of interference with GnRH transport, GnRH
    discharge, or congenital absence of GnRH
  • Hyperprolactinemia (galactorrhea often present)
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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
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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
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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
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14
Q

Amenorrhea treatment

A
  • Based on the underlying cause
  • PCOS, thyroid dysfunction, hypothalamic, hyperprolactinemia,
    ovarian failure…
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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
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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

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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)
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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
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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,
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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
Q

PMS pathophysiology

A

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
Q

Clinical presentation of PMS

A
  • 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
Q

PMS diagnosis

A
  • 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
Q

Premenstrual Dysphoric Disorder
(PMDD)

A

Severe premenstrual distress
* Interferes with occupational and social functioning
* Affects about 2% of women
* Ages 30-50 years

29
Q

RFs for PMDD

A
  • Sexual abuse and/or Domestic violence
  • Personal or family history of mood disorders
30
Q

Clinical presentation for PMDD

A
  • 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
Q

Diagnosis of PMDD

A
  • Rule out organic causes
  • Anemia, thyroid disorders,
    menopause
  • TSH, CBC c diff, FSH
    DSM 5 criteria
32
Q

Treatment of PMDD

A

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
Q

Treatment of PMS and PMDD if severe symptoms

A
  • 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
Q

Alternative Treatments for PMS and PMDD

A
  • Vitex agnus castus
  • Acupuncture
  • Benzodiazepines NOT recommended
    PMS and PMDD generally resolve completely after menopause
35
Q

Abnormal Uterine Bleeding (AUB)

A

Irregular uterine bleeding without pelvic pathology, pregnancy,
or other medical disease
* Usually associated with anovulatory cycles
* Diagnosis of exclusion

36
Q

Abnormal Uterine Bleeding (AUB) etiology

A
  • 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
Q

Clinical presentation of AUB

A
  • 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
Q

Diagnosis and Testing for AUB

A
  • 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
Q

Abnormal Uterine Bleeding (AUB) treatment

A
  • Correct any underlying etiology (structural,
    infections, endocrine, bleeding disorders)
  • Estrogen-progestin contraceptives
  • Levonorgestrel IUD
  • Cyclic progestin therapy
  • NSAIDs
  • Endometrial ablation
  • Hysterectomy
40
Q

Endometriosis

A

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
Q

Hemorrhagic uterine bleeding requires

A

high-dose estrogen therapy
* If bleeding is not controlled within 12-24 hours, a D&C is indicated

42
Q

Endometriosis risk factors

A
  • 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
Q

Most common locations for endometriosis

A

posterior and anterior cul-de-sac,
uterosacral ligaments, tubes, ovaries

44
Q

Pathophysiology of endometriosis

A
  • 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
Q

Endometriosis clinical presentation

A
  • 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
Q

Endometriosis diagnosis

A
  • 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
Q

Endometriosis treatment

A
  • 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
Q

Endometriosis surgical intervention

A

*Removal of lesions
*Conservative = maintain potential fertility
*Total hysterectomy with bilateral oophorectomy with
cytoreduction of visible endometriosis lesions
*Recurrence rate of 15%

49
Q

Endometriosis and infertility

A
  • 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