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OBGYN Clerkship- Amboss Study Plan > Menstrual Cycle and associated Disorders > Flashcards

Menstrual Cycle and associated Disorders Flashcards

1
Q

Menstrual Cylcle

A
  • The cycle lasts 21–35 days on average.
  • The cycle consists of two phases:
    • Follicular phase : First day of menses to the day before the LH surge
    • Luteal phase : lasts 14–15 days. Day of the LH surge to the beginning of the next menses
    • Menses last an average of 3–7 days
  • First few years following menarche → irregular menstrual cycles (caused by immaturity of the hypothalamic-pituitary-gonadal axis)
  • Menstrual cycles are longest at 25–30 years of age, with younger and older women having shorter cycles
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2
Q

Primary Dysmenorrhea

A

recurrent lower abdominal pain shortly before or during menstruation (in the absence of pathologic findings that could account for those symptoms)

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3
Q

Primarry Dysmenorrhea

Etiology

A
  • Etiology: unknown;
  • Risk factors
    • early menarche
    • nulliparity
    • smoking
    • obesity
    • positive family history
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4
Q

Primary Dysmenorrhea

Pathophysiology

A
  1. increased endometrial prostaglandin (PGF2 alpha) production →
  2. vasoconstriction/ischemia and stronger, sustained uterine contractions
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5
Q

Primary dysmenorrhea

clinical features

A
  1. Spasmodic, crampy pain in the lower abdominal and/or pelvic midline
  2. radiating to the back or thighs
  3. Usually occurs during the first 1–3 days of menstruation
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6
Q

Primary Dysmenorrhea

Tx

A
  • Symptomatic treatment: pain relief (e.g., NSAIDs), topical application of heat
  • Hormonal contraceptives (e.g., combined oral contraceptive pill, IUD with progestogen)
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7
Q

Secondary Dysmenorrhea

A

recurrent lower abdominal pain shortly before or during menstruation that is due to an underlying condition

Most common cases:

  1. Endometriosis
  2. Pelvic inflammatory disease (PID)

Other causes:

  1. Intrauterine device (IUD)
  2. Uterine leiomyoma
  3. Adenomyosis
  4. Psychological factors
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8
Q

Primarry Amenorhea

A
  • the absence of menarche at age 15 years despite normal development of secondary sexual characteristics
  • bsence of menses in girls aged 13 yearswith no secondary sexual characteristics
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9
Q

Primary amenorrhea with normal puberty

Etiology

A
  • Anatomic anomalies:
    • hymenal atresia,
    • vaginal septum,
    • Mayer-Rokitansky-Küster-Hauser (MRKH) syndrome
  • Competitive sports (low body mass index suppress the hypothalamic-pituitary-gonadal axis)
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10
Q

Mayer-Rokitansky-Küster-Hauser (MRKH)

aka: Müllerian aplasia

A

are, congenital defect in which the Müllerian ducts fail to fuse, which results in an atretic uterus, cervix, and upper-third of the vagin

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11
Q

Hypergonadotropic Hypogonadism

A

insufficient sex steroid production in the gonads that leads to low serum concentrations of sex hormones and compensatory increase in the concentrations of pituitary gonadotropins

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12
Q

Hypogonadotropic hypogonadism

A

decreased gonadal function due to a disease that primarily affects the pituitary gland and/or hypothalamus. Characterized by low concentrations of pituitary gonadotropins

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13
Q

Primary amenorrhea with development retardation

Etiology

A

Hypogonadism

  • Hypergonadotropic hypogonadism
  • Hypogonadotropic hypogonadism
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14
Q

Seoncdary Amenorrhea

A

absence of menses for more than 3 months (in women with previously regular cycles) or 6 months (in women with previously irregular cycles)

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15
Q

Secondary amenorrhea

etiology

A
  1. pregnancy most common cause
  2. Ovarian disease (PCOS)
  3. Hypogandism
    1. hypergonadotropic hypogonadism
    2. hypogonadotropic hypohonadism
  4. Hypothyroidism
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16
Q

Functional Hypothalamic amenorrhea

A

Hypogonadotropic Hypogonadism

Etiology: excessive exercise, reduced calorie intake (e.g., in eating disorders like anorexia nervosa), stress

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17
Q

Functional hypothalamic amenorrhea

pathophysiology

A
  1. states of decreased energy availability →
  2. body regulates reproductive potential down by decreasing GnRH release from the hypothalamus →
  3. decreased secretion of FSH and LH →
  4. anovulation and secondary amenorrhea →
  5. infertility
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18
Q

Functional hypothalmic amenorrhea

Tx

A
  • Lifestyle changes: reduce stress, improve nutrition, increase body weight BMI > 19 kg/m2
  • Offer pulsatile GnRH therapy or gonadotropin therapy to induce ovulation
    • Should only be offered in patients with BMI> 18.5 kg/m2
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19
Q

Premensstrual Syndrome (PMS)

A
  • onset of severe discomfort or functional impairment prior to menstruation
  • 5 days before menstruation; symptoms end within 4 days of start of menstruation
  • occurs in ∼ 5–10% of women
  • majority of women (∼ 75%) of reproductive age experience discomfort for 1–2 days prior to menstruation. These symptoms are usually mild and not considered premenstrual syndrome (PMS).
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20
Q

PMS Clinical Features

A
  • Pain: dyspareunia, breast tenderness, headache, back pain, abdominal pain
  • Gastrointestinal: nausea, diarrhea, changes in appetite
  • Tendency to edema formation
  • Neurological: migraine, increased sensitivity to stimuli
  • Psychiatric: mood swings, drowsiness, lethargy, exhaustion, depression, anxiety, aggressiveness
  • Premenstrual dysphoric disorder (PMDD)
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21
Q

Premenstrual Dysphoric Disorder (PMDD)

A
  • Psychiatric symptoms in pms: mood swings, drowsiness, lethargy, exhaustion, depression, anxiety, aggressiveness
  • Premenstrual dysphoric disorder (PMDD): severe form of affective symptoms that interferes with daily life, including having abnormal disagreements with family, friends, and colleagues
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22
Q

PMS tx

A
  1. Lifestyle changes can be beneficial
    • exercise, healthy diet,
    • avoiding individual triggers like alcohol or nicotine
  2. NSAIDs
  3. Oral contraceptives
  4. If PMDD: SSRIs (e.g., fluoxetine)
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23
Q

MIttelschmerz

A
  • Recurrent, unilateral, lower abdominal pain in women of reproductive age caused by the transient peritoneal irritation following enlargement and rupture of the follicular cyst during ovulation
  • Mittelschmerz is benign and occurs midcycle (immediately before or at the time of ovulation)
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24
Q

Mittelschmerz

clincal features and Tx

A
  • Clinical features: recurrent, unilateral, lower abdominal pain
  • Management: symptomatic treatment with NSAIDs as needed
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25
Q

Abnormal Uterine Bleed

A

Abnormal uterine bleeding is defined as menstrual bleeding that is abnormal and/or irregular in frequency, duration, and/or intensity. It may or may not be accompanied by dysmenorrhea.

two types

  1. strauctural causes
  2. non structural causes
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26
Q

PALM- COEIN system

A
  • (PALM) Structural Causes: Polyps, Adenomyosis, Leiomyomas, Malignancy/Hyperplasia
  • (COEIN) Non-structural causes: Coagulaopathy, Ovulatory dysfunction, Endometrial, Iatrogenic, Not yet classified
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27
Q

Polymenorrhea

A

cycles with intervals <21 days

Causes:

  • Menarche, menopause
  • Psychological stress
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28
Q

Oligomenorrhea

A

cycles with intervals of 35-90 days

Causes:

  • Pregnancy (including ectopic pregnancy)
  • PCOS
  • Insufficient caloric intake
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29
Q

Hypermenorrhea

A

Heavy Menstruation with bleeding volume >150ml

Causes:

  • Endometrial cancer/hyperplasia
  • Endometriosis
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30
Q

Menorrhagia

A

Increased Bleeding; volume > 80 mL and/or length of menstruation > 7 days

Common Causes:

  • Endometrial cancer/hyperplasia
  • Endometriosis
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31
Q

Hypomenorrhea

A

Very low bleeding volume (< 25 ml)

Common Causes:

  • Endometrial atrophy
  • Eating disorders (e.g., anorexia nervosa)
  • Chronic endometritis
  • Oral contraceptive use
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32
Q

meTROrrahagia

A

Bleeding between perios

common causes:

  • Ovarian insufficiency
  • Myoma, endometrial cancer/hyperplasia, cervical cancer
  • Oral contraceptive use
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33
Q

menometrorrhagia

A

Heavy irregular bleeding

Common causes:

  • Ovarian insufficiency
  • Myoma, endometrial cancer/hyperplasia, cervical cancer
  • Oral contraceptive use
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34
Q

Spotting

A

minimal bleeding seen in sevral condittions

Common causes:

  • After ovulation
  • Breakthrough bleeding: mid-cycle bleeding caused by hormoneimbalances (usually after starting new OCP therapy)
  • Endometriosis
  • Myomas, polyps, carcinomas, contact bleeding
  • During pregnancy: may indicate imminent abortion
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35
Q

Types of estrogen

A

estradiol, estrone, estriol

  • Potency: estradiol > estrone > estriol
  • During pregnancy:
    • 100-fold increase in estradiol and estrone
    • 1000-fold increase in estriol
  • Estriol is secreted by the placenta as unconjugated estriol (free or uE3)
    • Decreased levels are associated with Down syndrome, Edward syndrome, molar pregnancy, and fetal demise.
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36
Q

Estrogen Synthesis in the Ovaries

A

Primarily takes place in the ovarian granulosa cells

  1. LH stimulates androgen synthesis in ovarian theca cells
  2. FSH stimulates conversion of androgens to estrogens
    • catalyzed by the aromatase enzyme
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37
Q

Exogenous Estrogen synthesis

A

Aromatase containing tissues:

  • Adrenal glands
  • Fatty tissue
  • Placenta
  • Testicles
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38
Q

Effects of Estrogen on sex characteristics

A
  1. Uterus: endometrial proliferation
  2. Cervix: increased production of cervical mucus → facilitates passage of sperm
  3. Vagina: proliferation of epithelium
  4. Pubis: hair growth
  5. Breast: breast growth
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39
Q

effects of estrogen on extragenital

A
  1. Bones: promotes bone formation by inhibiting bone resorption (induces osteoclast apoptosis)
  2. Blood vessels: protective effect against atherosclerosis
  3. Blood clotting: increased risk of thrombosis
  4. Kidneys: increased water and sodium retention → may contribute to edema
  5. Liver: decreased bilirubin excretion
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40
Q

Adverse effects of estrogen

A
  1. Weight gain (edema)
  2. Liver toxicity
  3. Breast hypertrophy, gynecomastia (in men)
  4. Thrombosis
  5. Spider nevi, gynecomastia, and testicular atrophy in individuals with cirrhosis
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41
Q

Estrogen and Cancer

A

Increased cancer risk

  • Endometrial cancer
  • Breast cancer

Reduces the risk

  • colon cancer
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42
Q

Hyperestrogenism

A

a condition of increases circulating estrogen

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43
Q

Hyperestrogenism Etiology

A
  1. Increased estrogen production (e.g., due to ovarian tumors, obesity)
  2. Excess estrogen supplementation (e.g., due to hormone replacement therapy)
  3. Decreased metabolism and excretion of estrogens (e.g., due to chronic liver disease)
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44
Q

Hyperestrogenism Clinical Features in WOMEN

A

Women:

  • menstrual irregularities
  • enlargement of the breast and uterus
  • infertility
  • increased cancer risk (e.g., endometrial cancer)

Both sexes:

  • palmar erythema, spider telangiectasias
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45
Q

Hyperestrogenism Clinical Features in MEN

A

Men:

  • gynecomastia
  • testicular atrophy,
  • reduced libido
  • erectile dysfunction
  • infertility
  • decreased body hair (e.g., loss of chest hair, female pattern of pubic hair distribution)

Both sexes:

  • palmar erythema
  • spider telangiectasias
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46
Q

Hypoestrogenism

A

a condition of decreased circulating estrogen

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47
Q

Hypoestrogenism Etiologies

A
  1. Menopause
  2. Ovarian insufficiency: idiopathic or secondary to an underlying conditions (e.g., Turner syndrome, polycystic ovary syndrome)
  3. Congenital aromatase deficiency (↓ aromatase → ↑ androgens and ↓ estrogen)
  4. Hyperprolactinemia (e.g., in pituitary adenomas, hypothyroidism)
  5. GnRH agonists
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48
Q

Hypoestrogenism Clinical Features

A
  1. Hot flashes
  2. Headaches
  3. Reduced libido
  4. Breast atrophy
  5. Decreased bone density and secondary osteoporosis
  6. Urogenital atrophy
  7. Dyspareunia
49
Q

Menopause

A
  1. Premenopause
    • The time period from the first occurrence of climacteric irregular menstruation cycles to the last menstrual period
    • Onset: usually 45–55 years of age
  2. Menopause
    • Confirmed after 12 months of amenorrhea
    • The average age at menopause is ∼ 49–52 years
  3. Postmenopause:
    • 12 months after the last menstrual period
50
Q

Perimenopause

(menopausal transition, MT)

A

The time period from the first instance of climacteric symptoms caused by fluctuating hormonal levels to one year after menopause: the average length of perimenopause is 4 years

51
Q

Menopause Pathophysiology

A
  1. ↓ Ovarian function →
  2. ↓ estrogen and progesterone levels →
  3. loss of negative feedback to the gonadotropic hormones →
  4. ↑ GnRH levels →
  5. ↑ levels of FSH and LH in blood (hypergonadotropic hypogonadism) →
  6. anovulatory cycles become more and more frequent →
  7. progressive follicular depletion
52
Q

Menopause Clinical Features

Systemic Symptoms

A
  1. Irregular menses (which gradually decrease in frequency) → complete amenorrhea
  2. Increased sweating, hot flashes, and heat intolerance
  3. Vertigo
  4. Headache
  5. Weight gain and bloating
  6. Increased risk of coronary artery disease
53
Q

Menopause Clinical Features

Mental Symptoms

A
  1. Impaired sleep (insomnia and/or night sweats)
  2. Depressed mood or mood swings
  3. Anxiety/irritability
  4. Loss of libido
54
Q

Menopause Clinical Features

Atrophic Features

A
  1. Breast tissue atrophy: breast tenderness and reduced breast size
  2. Vulvovaginal atrophy: atrophy of the vulva, cervix, vagina → atrophic vaginitis
  3. Urinary atrophy: atrophy of the urinary tract →
    • incontinence, dysuria, urinary frequency, urgency,
    • increased urinary tract infections
55
Q

Atrophic Vaginitis

A

Symptoms include vaginal dryness, irritation and discomfort, with loss of labial fat pads, and receding pubic hair.

Treated with estrogen creams or tablets.

56
Q

Menopause Labs

A
  1. ↓ Estrogen, ↓ progesterone, ↑↑ FSH
  2. FSH levels can fluctuate widely in perimenopause.
  3. Lipid profile: ↑ total cholesterol, ↓ HDL
  4. Check TSH (hypothyroidism precents similarly )
57
Q

Menopause Tx

A
  1. For atrophic vaginal symptoms:
    • vaginal estrogen creams, rings, or tablets
  2. For impaired sleep and/or hot flashes:
    • exercise, acupuncture, and relaxation techniques
  3. Hormone replacement therapy (HRT)
    • short term for severe symptoms that affect quality of life
  4. Non-Hormonal Therapy
    • vasomotor symptoms
  5. Prevention of osteoporosis
    • Smoking cessation, adequate vitamin D intake and regular weight-bearing exercise
58
Q

Menopause HRT

Types

A
  1. Estrogen therapy: for women who have had a hysterectomy
  2. Estrogen plus progestin therapy: for women with a uterus
59
Q

Menopause HRT Risks

A
  1. Cancer
    • Unopposed estrogen- endometrial hyperplasia → endometrial cancer
    • Estrogen plus progestin→ breast cancer
  2. Cardiovascular disease:
    • coronary heart disease,
    • DVT, PE, stroke
  3. Gallbladder disease
  4. Stress urinary incontinence
60
Q

Menopause HRT Contraindications

A
  1. Undiagnosed vaginal bleeding
  2. Pregnancy
  3. Breast cancer/endometrial cancer
  4. Chronic liver disease
  5. Hyperlipidemia
  6. Recent DVT/stroke
  7. Coronary artery disease
61
Q

Menopause Non-HRT

A
  1. Selective estrogen receptor modulators: tamoxifen, ospemifene , and raloxifene
    • (dyspareunia and vaginitis)
  2. Paroxetine:
    • for vasomotor symptoms (i.e., hot flashes)
  3. Clonidine and/or gabapentin
    • (frequency of hotflashes)
62
Q

Premature Menopause

Menopause Precox

A

cessation of periods before the age of 40

63
Q

Premature Menopause Etiology

A
  • Idiopathic
  • Surgical: bilateral oophorectomy
  • Primary (or premature) ovarian insufficiency

often associated with smoking

64
Q

Ovarian insufficiency

A
  • cessation of menses due to primary ovarian failure before age 40
  • (failure of the ovary to function adequately, both as an endocrine gland and a reproductive organ)
65
Q

Ovarian Insufficiency Etiology

A

Primary ovarian insufficiency (POI): idiopathic

Secondary ovarian insufficiency:

  1. ovarian endometriosis; polycystic ovary syndrome
  2. Turner syndrome; androgen insensitivity syndrome
  3. autoimmune lymphocytic oophoritis, Hashimoto’s thyroiditis
  4. Post-oophorectomy
  5. Radiation and/or chemotherapy
  6. Addisons’s Disease
66
Q

Ovarian Insufficiency Pathophysiology

A
  1. impaired follicular development →
  2. ↓ estrogen levels →
  3. loss of feedback inhibition of estrogen on FSH and LH →
  4. ↑ FSH and LH (usually FSH > LH)
67
Q

Ovarian Insufficiency Diagnostics

A
  1. Confirmed by ↑ FSH after > 3 months of amenorrhea in a woman under age 40
  2. tests to determine the underlying disorder
68
Q

Ovarian Insufficiency Tx

A
  1. Hormone replacement therapy
  2. In vitro fertilization for infertility (for women who wish to bear children)
  3. Treatment of underlying disorder if present
69
Q

Endometriosis

A

A chronic, benign condition in which endometrial tissue is found outside the uterus, commonly in the fallopian tubes, ovaries, bladder, or rectouterine pouch

70
Q

Endometriosis Etiology

A
  • Not fully understood;
  • Retrograde menstruation seems to play a major role in the pathogenesis of endometriosis.

Other contributing factors include:

  • Coelomic metaplasia
  • Iatrogenic implantation
  • Hematogenic and lymphogenic dissemination of endometrial cells
  • Hereditary component
71
Q

Retrograde Menstruation

A

Backflow of menstrual fluid containing endometrialcells

72
Q

Coelomic Metaplasia

A

The coelomic (peritoneum) contains pluripotent cells that were differentiated into endometrial cells during embryonic development.

73
Q

Iatrogenic Implantation

Endometriosis

A

Postsurgical scars through episiotomy or laparotomyare thought to be prime locations for implantation of endometrial cells that are spread from delivery or surgical procedures.

74
Q

Endometriosis Pathophysiology

A
  • Endometral tissue reacts to the hormone cycle

Endometriotic implants: including ovaries, fallopian tubes, cervix result in

  1. ↑ Production of inflammatory and pain mediators
  2. Nerve dysfunction
  3. Altered anatomy (e.g., pelvic adhesions) → infertility
75
Q

Endometriosis Clinical Features

A
  1. Chronic pelvic pain that worsens before the onset of menses
  2. Dysmenorrhea
  3. Pre- or postmenstrual bleeding
  4. Dyspareunia
  5. Infertility
  6. Dyschezia
76
Q

Dyschezia

A

A condition of difficult or painful defecation

77
Q

Endometriosis and Infertility

A

Endometriosis may change the pelvic anatomy through inflammation and adhesions, altering egg quality and impairing implantation.

78
Q

Endometriosis Diagnostics

A
  • Physical examination
    • Rectovaginal tenderness
    • Adnexal masses
  • Transvaginal ultrasound (best initial test)
    • The uterus is generally not enlarged
    • Evidence of ovarian cysts (chocolate cysts)
  • Laparoscopy (confirmatory test)
79
Q

Chocolate Cysts

A

A cyst-like ovarian structure that contains blood, fluid, and menstrual debris. Caused by proliferation of ectopic endometrial tissue

80
Q

Endometriosis Pathology

A
  1. Endometrial implants present macroscopically as yellow-brown (sometimes reddish-blue) blebs, islands, or pinpoint spots.
  2. Gunshot lesions or powder-burn lesions
  3. Ovarian endometriomas or chocolate cysts
81
Q

Gunshot Lesions

Powder Burn Lesions

A

black, brown, or bluish nodules or cystic structures seen on the serosal surfaces of the ovaries and peritoneum

82
Q

Adenomyosis

A
  • benign disease characterized by the occurrence of endometrial tissue within the uterine wall
  • Peak 35-50 years age
  • Common Cause
    • Endometriosis
    • Uterine fibroids
    • Parity
83
Q

Adenomyosis Clinical Features

A
  1. Dysmenorrhea
  2. Menorrhagia
  3. Chronic pelvic pain, aggravated during menses
  4. Uniformly enlarged uterus, tender on palpation
84
Q

Adenomyosis

Diagnostics

A
  • Diagnosis is clinical
  • Transvaginal ultrasound and MRI findings:
    • Myometrial wall thickening
    • Myometrial cysts
85
Q

Adenomyosis Tx

A
  • Conservative:
    • combined oral contraceptives , progestin-only contraception
    • NSAIDs for pain relief
  • Surgical:
    • Hysterectomy is the definitive treatment
86
Q

Endometriosis Tx

A

Medical therapy

  • Mild to moderate pelvic pain without complications
    • Empirical medical therapy with NSAIDs and continuous hormonal contraceptives
  • Severe symptoms
    • GnRH agonists (e.g., buserelin, goserelin) and estrogen-progestin OCPs

Surgical Threapy

  • First-line: laparoscopic excision and ablation of endometrial implants
  • Second-line: open surgery with hysterectomy with or without bilateral salpingo-oophorectomy
87
Q

Endometriosis Complications

A
  1. Anemia
  2. Endometriosis in the uterotubal junction inhibits implantation of the egg:
    • ↑ risk of ectopic pregnancy
  3. fibrous adhesions → strictures and entrapment of organs (intestins, ureters)
88
Q

Polycystic Ovary Syndrome (PCOS)

A

a heterogeneous disorder characterized by hyperandrogenism, oligoovulation/anovulation, and/or the presence of polycystic ovaries.

89
Q

Hyperandrogenism

A

A state of excess androgen levels that causes symptoms such as growth of facial hair, deepening of the voice, and male-pattern baldness.

90
Q

Oligoovulation

A
  • A condition of infrequent or irregular ovulation
  • (often defined as cycles ≥ 36 days or < 8 cycles per year)
91
Q

Anovulation

A
  • menstrual cycle characterized by the absence of ovulation and a luteal phase, resulting in menstrual irregularities
  • Can be pathological or physiological (early after menarchy)
92
Q

PCOS pathophys

A
  • The exact pathophysiology is unknown.
  • may be genetically predisposed to lifestyle and/or hyperinsulinemia-causingdisturbances to the hypothalamic-pituitary-gonadal axis.
  • Reduced insulin sensitivity (peripheral insulin resistance) is present in PCOS, as in metabolic syndrome → hyperinsulinemia
93
Q

PCOS and Hyperinsulinermia

A

Results in:

  1. Obesity
  2. Acanthosis nigricans
  3. Hyperandrogenism
94
Q

PCOS Hyperandrogenism

pathophys

A

Increased androgen production in ovarian theca cells → imbalance between androgen precursors and the resulting estrogen produced in granulosa cells

  1. Increased LH secretion disrupts the LH/FSH balance → impaired follicle maturation and anovulation/oligoovulation
  2. Increased androgen precursor release → virilization and a reactive increase in estrogen production in adipose tissue
  3. Inhibits the production of SHBG (sex hormone-binding globulin) in the liver → ↑ free androgens and estrogens

Hyperandrogenism in women is most commonly caused by PCOS

95
Q

PCOS Clinical Features

A
  1. Onset typically during adolescence
  2. Menstrual irregularities (primary or secondary amenorrhea, oligomenorrhea)
  3. Difficulties conceiving or infertility
  4. Obesity and possibly other signs of metabolic syndrome(50%)
  5. Hirsutism
  6. Androgenic alopecia
  7. Acne vulgaris and oily skin
  8. Acanthosis nigricans: hyperpigmented, velvety plaques (axilla, neck)
  9. Premature adrenarche
96
Q

Adrenarche

A

Maturation of the zona reticularis of the adrenal gland leading to the production of androgens and subsequent development of pubic and axillary hair (pubarche) and adult body odor.

97
Q

PCOS Diagnostic Criteria

A

At least 2 of 3 after excluding other causes of irregular bleeding and elevated androgen levels

  1. Hyperandrogenism (clinical or laboratory)
  2. Oligo- and/or anovulation
  3. Polycystic ovaries on ultrasound
98
Q

PCOS Diagnostics

A
  1. ↑ Testosterone (both total and free) or free androgen index
  2. ↑ LH (LH:FSH ratio > 2:1)
  3. Evaluate for metabolic disease
    • oral glucose tolerance test
    • measure serum lipids and cholesterol
  4. TV Ultrasound
    • Enlarged ovaries with numerous anechoic cysts (polycystic ovaries)
    • “String of pearls” appearance
99
Q

PCOS

Diagnoses to rule out

A
  1. Pregnancy
  2. Congenital adrenal hyperplasia
  3. Cushing’s disease
  4. Androgen-secreting tumors
  5. Exogenous androgen intake
  6. Exogenous steroid intake
100
Q

PCOS Tx

A

If treatment for infertility is not sought: therapy aimed at controlling menstrual, metabolic, and hormonal irregularities

  • If the patient is overweight (BMI ≥ 25 kg/m2)
    • First-line: weight loss via lifestyle changes
    • Second-line: combined oral contraceptive therapy
  • If the patient is not overweight: combined oral contraceptive therapy

If seeking treatment for infertility

  • Ovulation induction with clomiphene citrate or letrozole
  • If the patient is overweight: advise weight loss
101
Q

PCOS complications

A
  1. Cardiovascular events
  2. Type 2 diabetes mellitus
  3. Endometrial cancer
  4. Increased miscarriage rate
102
Q

Ovarian Cysts

A
  • fluid-filled sacs within the ovary
  • Two types:
    • Functional Cysts
    • Nonfunctional Cysts
103
Q

Functional Cysts

A

result from a disruption in the development of follicles or the corpus luteum; often resolve on their own

  • Follicular cyst of the ovary (most common ovarian mass in young women)
    • Graafian follicle does not rupture and release the egg (ovulation) but continues to grow
  • Corpus luteum cyst
    • Enlargement and buildup of fluid in the corpus luteum after failed regression following the release of an ovum
  • Theca lutein cysts
    • Multiple cysts that typically develop bilaterally due to excessive amounts of circulating gonadotropins such as β-hCG
104
Q

Nonfunctional Cysts

A
  1. Chocolate cysts: related to endometriosis
  2. Dermoid cysts
  3. Cystadenoma
  4. Malignant cysts (form of ovarian cancer)
105
Q

Ovarian Cysts Clinical Features

A

Most often asymptomatic unless complications occur

In some cases, there may be signs of the underlying cause (e.g., menorrhagia in endometriosis or hirsutism, acne, and infertility in PCOS).

106
Q

Ovarian Cysts

Diagnosis

A
  • Pelvic ultrasound
    • Smooth lining on all sides
    • Single (e.g., follicular cyst of the ovary, corpus luteum cyst)
    • multiple (e.g., polycystic ovary syndrome, multilocular theca lutein cysts)
107
Q

Ovarian Cysts Complication

A
  1. Ovarian torsion
  2. Ruptured ovarian cyst
108
Q

Ovarian Cysts Tx

A
  • In most patients with functional cysts, watchful waiting is recommended, as cysts often regress spontaneously.
  • Surgery in the case of complications, large cysts, or persistent cysts that are painful
109
Q

Rupture Ovarian Cysts Casue

A

Rupture is caused by an increase in intracystic pressure ue to intracystic hemorrhage and/or increased intra-abdominal pressure

110
Q

Rupture Ovarian Cyst Etiology

A
  • Most common type of ruptured cyst: corpus luteum cyst

Risk factors

  • Vigorous physical activity
  • Vaginal intercourse
  • Large cysts
  • Reproductive age
111
Q

Rupture Ovarian Cyst Clinical Features

A
  • Sudden-onset unilateral lower abdominal pain
  • Minimal vaginal bleeding (spotting)
  • In case of significant hemorrhage: hypovolemic shock
112
Q

Rupture Ovarian Cyst Diagnostics

A

Transabdominal/transvaginal pelvic ultrasound: imaging modality of choice

  • Free fluid, most commonly in the pouch of Douglas (rectouterine pouch)
113
Q

Rupture Ovarian Cyst Tx

A
  1. Hemodynamically unstable patients: emergency exploratory laparoscopy/laparotomy to obtain hemostasis
  2. Hemodynamically stable patients: conservative management with analgesics and observation
114
Q

Ovarian Torsion

A
  • Partial or complete twisting of the ovary and the fallopian tube around their supporting ligaments
  • Also known as adnexal torsion or tubo-ovarian torsion
115
Q

Ovarian Torsion Etiolgy

A
  • Ovarian enlargement is the most important risk factor:
    • Ovarian cysts
    • Ovarian tumors
    • Ovarian hyperstimulation syndrome
    • Pregnancy
  • Strenuous physical activity
116
Q

Ovarian Torsion Clinical Features

A
  1. Sudden-onset unilateral lower abdominal and/or pelvic pain
  2. Nausea and vomiting
  3. Adnexal mass may be palpable
117
Q

Ovarian Torsion Pathophys

A
  1. Twisting of the ovary and the fallopian tube around the infundibulopelvic ligament and ovarian ligament →
  2. compression of the ovarian veins and lymphatics →
  3. ↓ venous and lymphatic outflow →
  4. edema of the fallopian tube and ovary →
  5. compression of the ovarian artery →
  6. ovarian ischemia and necrosis
118
Q

Ovarian Torsion Diagnostics

A
  • TA/TV pelvic ultrasound with Doppler: imaging modality of choice
    • Enlarged, edematous ovary with decreased blood flow
  • MRI abdomen and pelvis with contrast
    • Twisted vascular pedicle (whirlpool sign)
119
Q

Ovarian Torsion Tx

A

Emergency exploratory laparoscopy: indicated in all patients with suspected ovarian torsion

  1. Premenopausal women: adnexal detorsion and preservation of ovarian function
  2. Postmenopausal women: salpingo-oophorectomy

OBGYN Clerkship- Amboss Study Plan (9 decks)

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