USMLE Step 3 (Fach) / Gynecology (Lektion)

First Aid Step 3

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• Primary amenorrhea Absence of menses (onset of menarche) at the age of 15 or older Etiology:- Patients with normal puberty→ Anatomic anomalies: hymenal atresia, vaginal septum, Mayer-Rokitansky-Küster-Hauser (MRKH) syndrome→ Competitive sports  - Patients with growth delay and developmental retardation→ Hypergonadotropic hypogonadism→ Hypogonadotropic hypogonadism→ Patients with virilization: Congenital adrenal hyperplasia (CAH), Polycystic ovary syndrome (PCOS)
• Secondary amenorrhea Absence of menses for more than 3 months (in women with previously regular cycles) or 6 months (in women with previously irregular cycles) Etiology:- Pregnancy → most common cause of secondary amenorrhea- Ovarian disorders (e.g., polycystic ovary syndrome) - Hypergonadotropic hypogonadism- Hypogonadotropic hypogonadism: E.g., functional hypothalamic amenorrhea→ Etiology: excessive exercise, reduced calorie intake (e.g., in eating disorders like anorexia nervosa), stress→ Pathophysiology: states of decreased energy availability → body regulates reproductive potential down by decreasing GnRH release from the hypothalamus → decreased secretion of FSH and LH → anovulation and secondary amenorrhea → infertility→ Treatment:Lifestyle changes: reduce stress, improve nutrition, increase body weight BMI > 19 kg/m2→ Offer pulsatile GnRH therapy or gonadotropin therapy to induce ovulation  - Hypothyroidism (↓ T3/T4 → ↑ TRH → ↑ prolactin → ↓ GnRH → ↓ estrogens)
• Abnormal uterine bleeding Polymenorrhea: Cycles with intervals < 21 daysOligomenorrhea: Cycles with intervals of 35-90 days Hypermenorrhea: Heavy menstruation with bleeding volume > 150 mL (possibly visible blood clots)Menorrhagia: Bleeding volume > 80 mL and/or length of menstruation > 7 daysHypomenorrhea: Very low bleeding volume (< 25 ml) Metrorrhagia: Bleeding in between periodsMenometrorrhagia: Heavy and irregular bleeding Etiology:- Structural causes: polyps, adenomyosis, leiomyomas, malignancy/hyperplasia (PALM)- Non-structural causes: coagulopathy, ovulatory dysfunction, endometrial, iatrogenic, not yet classified (COEIN) Treatment:1. General measures: Immediate supportive measures in hemodynamically unstable patients: fluid resuscitation, blood transfusion, and intrauterine tamponade (e.g., intrauterine balloon or gauze packing)  2. Pharmacological - Acute AUB in hemodynamically stable patient → high-dose conjugated estrogen  → Alternatives: multi-dose regimens of OCs or oral progestins, as well as tranexamic acid (second-line)  - Menorrhagia→ Ovulatory bleeding: tranexamic acid, oral contraceptives, progestin (PO, IV, or as an IUD)→ Anovulatory bleeding: progestin PO for 10 days or as an IUD; oral contraceptives3. Surgical treatment 
• Abnormal uterine bleeding Polymenorrhea: Cycles with intervals < 21 daysOligomenorrhea: Cycles with intervals of 35-90 days Hypermenorrhea: Heavy menstruation with bleeding volume > 150 mL (possibly visible blood clots)Menorrhagia: Bleeding volume > 80 mL and/or length of menstruation > 7 daysHypomenorrhea: Very low bleeding volume (< 25 ml) Metrorrhagia: Bleeding in between periodsMenometrorrhagia: Heavy and irregular bleeding Etiology:- Structural causes: polyps, adenomyosis, leiomyomas, malignancy/hyperplasia (PALM)- Non-structural causes: coagulopathy, ovulatory dysfunction, endometrial, iatrogenic, not yet classified (COEIN) Treatment:1. General measures: Immediate supportive measures in hemodynamically unstable patients: fluid resuscitation, blood transfusion, and intrauterine tamponade (e.g., intrauterine balloon or gauze packing)  2. Pharmacological - Acute AUB in hemodynamically stable patient → high-dose conjugated estrogen  → Alternatives: multi-dose regimens of OCs or oral progestins, as well as tranexamic acid (second-line)  - Menorrhagia→ Ovulatory bleeding: tranexamic acid, oral contraceptives, progestin (PO, IV, or as an IUD)→ Anovulatory bleeding: progestin PO for 10 days or as an IUD; oral contraceptives3. Surgical treatment 
• Abnormal uterine bleeding Polymenorrhea: Cycles with intervals < 21 daysOligomenorrhea: Cycles with intervals of 35-90 days Hypermenorrhea: Heavy menstruation with bleeding volume > 150 mL (possibly visible blood clots)Menorrhagia: Bleeding volume > 80 mL and/or length of menstruation > 7 daysHypomenorrhea: Very low bleeding volume (< 25 ml) Metrorrhagia: Bleeding in between periodsMenometrorrhagia: Heavy and irregular bleeding Etiology:- Structural causes: polyps, adenomyosis, leiomyomas, malignancy/hyperplasia (PALM)- Non-structural causes: coagulopathy, ovulatory dysfunction, endometrial, iatrogenic, not yet classified (COEIN) Treatment:1. General measures: Immediate supportive measures in hemodynamically unstable patients: fluid resuscitation, blood transfusion, and intrauterine tamponade (e.g., intrauterine balloon or gauze packing)  2. Pharmacological - Acute AUB in hemodynamically stable patient → high-dose conjugated estrogen  → Alternatives: multi-dose regimens of OCs or oral progestins, as well as tranexamic acid (second-line)  - Menorrhagia→ Ovulatory bleeding: tranexamic acid, oral contraceptives, progestin (PO, IV, or as an IUD)→ Anovulatory bleeding: progestin PO for 10 days or as an IUD; oral contraceptives3. Surgical treatment 
• Primary dysmenorrhea Recurrent lower abdominal pain shortly before or during menstruation (in the absence of pathologic findings that could account for those symptoms) Epidemiology: prevalence up to 90% (most common gynecologic condition) Etiology: unknown; association with some risk factors (e.g., early menarche, nulliparity, smoking, obesity, positive family history) Pathophysiology: increased endometrial prostaglandin (PGF2 alpha) production → vasoconstriction/ischemia and stronger, sustained uterine contractions Clinical features:- Spasmodic, crampy pain in the lower abdominal and/or pelvic midline (often radiating to the back or thighs)  - Usually occurs during the first 1-3 days of menstruation- Headaches, diarrhea, fatigue, nausea, and flushing are common accompanying symptoms. Diagnostics: Primary dysmenorrhea is a diagnosis of exclusion; conditions causing secondary dysmenorrhea must be ruled out. Treatment:- Symptomatic treatment: pain relief (e.g., NSAIDs), topical application of heat- Hormonal contraceptives (e.g., combined oral contraceptive pill, IUD with progestogen)
• Secondary dysmenorrhea Recurrent lower abdominal pain shortly before or during menstruation that is due to an underlying condition Possible causes:- Endometriosis  - Pelvic inflammatory disease (PID)- Intrauterine device (IUD)- Uterine leiomyoma- Adenomyosis- Psychological factors Diagnostics, clinical features, and treatment depend on the primary cause.
• Secondary amenorrhea – Work-up 1. Progestin challenge- Withdrawal bleed → Hirsute → PCOS, rule out ovarian cancer, rule out adrenal tumor→ Non hirsute → Mild hypothalamic dysfunction- No withdrawal bleed→ Rule out Asherman's syndrome if necessary 2. FSH- Over 40 mIU/mL→ Ovarian failure- Under 40 mIU/mL→ Severe hypothalamic dysfunction
• Endometriosis Occurrence of endometrial tissue outside the uterus. Epidemiology:- Age of onset: 20-40 years- Incidence: 2-10% of all women- In the US, endometriosis is more common in white and Asian women than in black and Hispanic women. Clinical features:- Up to one-third of patients are asymptomatic.- Chronic pelvic pain that worsens before the onset of menses- Dysmenorrhea  - Pre- or postmenstrual bleeding- Dyspareunia- Infertility  - Dyschezia Diagnostics:- Patient history- Physical examination: Rectovaginal tenderness, Adnexal masses- Transvaginal ultrasound (best initial test)→ The uterus is generally not enlarged.  → Evidence of ovarian cysts (chocolate cysts)→ Nodules in bladder or rectovaginal septum- Laparoscopy (confirmatory test)  - MRI, colposcopy, cystoscopy, or other interventions are potentially indicated if endometrial cells are suspected.- Common locations of endometriotic implants: Ovaries, Rectouterine pouch, Fallopian tubes, Bladder Treatment1. Medical therapy  - Mild to moderate pelvic pain without complications: Empirical medical therapy with NSAIDs and continuous hormonal contraceptives  - NSAIDs alone if pregnancy is desired  - Severe symptoms: GnRH agonists (e.g., buserelin, goserelin) and estrogen-progestin OCPs  2. Surgical therapy- First-line: laparoscopic excision and ablation of endometrial implants
• Polycystic ovary syndrome (PCOS) Epidemiology:- Frequency: 6-10% of women in their reproductive years Clinical features:- Onset typically during adolescence- Menstrual irregularities (primary or secondary amenorrhea, oligomenorrhea)- Difficulties conceiving or infertility- Obesity and possibly other signs of metabolic syndrome- Hirsutism- Androgenic alopecia- Acne vulgaris and oily skin- Acanthosis nigricans: hyperpigmented, velvety plaques (axilla, neck)- Premature adrenarche Diagnostics: At least 2 out of 3 of the following- Hyperandrogenism (clinical or laboratory)- Oligo- and/or anovulation- Polycystic ovaries on ultrasound Blood hormone levels:- ↑ Testosterone (both total and free) or free androgen index - ↑ LH (LH:FSH ratio > 2:1)- Estrogen is normal or slightly elevated   Evaluate for metabolic disease:- Test for hypertension- Monitor BMI- Assess for insulin resistance or type 2 diabetes mellitus → oral glucose tolerance test- Assess for hyperlipidemia → measure serum lipids and cholesterol Transvaginal ultrasound:- Enlarged ovaries with numerous anechoic cysts (polycystic ovaries)- "String of pearls” appearance Treatment (not trying to become pregnant):- If the patient is overweight (BMI ≥ 25 kg/m2)→ First-line: weight loss via lifestyle changes (e.g., dietary modifications, exercise)  → Second-line (as an adjunct): combined oral contraceptive therapy- If the patient is not overweight: combined oral contraceptive therapy   Treatment (if trying to become pregnant):- First-line: → Ovulation induction with clomiphene citrate or letrozole  Clomiphene inhibits hypothalamic estrogen receptors, thereby blocking the normal negative feedback effect of estrogen → increased pulsatile secretion of GnRH → increased FSH and LH, which stimulates ovulation→ If the patient is overweight: advise weight loss- Second-line: ovulation induction with exogenous gonadotropins or laparoscopic ovarian drilling  
• Hydatidiform mole Definition:- Classified as complete or partial moles - Benign trophoblastic disease- Proliferates within the uterus without myometrial infiltration or hematogenic dissemination- May develop malignant traits and become an invasive mole Risk factors:- Prior molar pregnancy- History of miscarriage- Patients ≤ 15 and ≥ 35 years Complete mole:- Does not contain any fetal or embryonic parts- Caused by fertilization of an empty egg that does not carry any chromosomes → The (physiological) haploid chromosome set contributed by the sperm is subsequently duplicated.- In rare cases, the formation of a complete mole may also result from simultaneous fertilization of an empty egg by two sperms.- Fetal karyotypes→ 46XX: more common (∼ 90% of cases)→ 46XY: less common (∼ 10% of cases) Partial mole:- Contains fetal or embryonic parts in addition to trophoblastic tissue- Caused by fertilization of an egg containing a haploid set of chromosomes with two sperms (each of them containing a haploid set of chromosomes as well)- Fetal karyotypes: 69XXX, 69XXY, 69XYY Clinical features:- Vaginal bleeding during the first trimester- Uterus size greater than normal for gestational age- Passage of vesicles that may resemble a bunch of grapes through the vagina- Endocrine symptoms→ Preeclampsia (before the 20th week of gestation)→ Hyperemesis gravidarum→ Ovarian theca lutein cysts: bilateral, large, cystic, adnexal masses that are tender to the touch  → Hyperthyroidism  - Partial mole: Less severe symptoms due to β-HCG levels that are lower  Diagnostics:- Laboratory tests: β-HCG level measurement (initial test of choice), which should reveal β-HCG that is markedly elevated (usually > 100,000 mIU/dL)  - Transvaginal ultrasound: Complete hydatidiform mole: → Theca lutein cysts→ Echogenic mass interspersed with many hypoechogenic cystic spaces that represent hydropic villi (referred to as “swiss cheese,” “bunch of grapes,” or “snowstorm”)→ No amniotic fluid→ Lack of fetal heart tones- Transvaginal ultrasound: Partial hydatidiform mole→ Fetal parts may be visualized.→ Fetal heart tones may be detectable. → Amniotic fluid is present.→ Increased placental thickness- Uterine evacuation (for definite diagnosis and treatment): histopathological examination of evacuated uterine specimen- Chest x-ray: In case of dyspnea or chest pain Treatment:- Uterine evacuation by dilation and suction curettage: Complete moles have a 20% risk of becoming invasive and a 2% risk of developing into choriocarcinoma. Therefore, complete evacuation of the uterine cavity is the mainstay of treatment.- Monitor β-HCG levels until in reference range (usually 8-12 weeks)- Chemotherapy (usually methotrexate) if unresolved, as indicated by any of the following: → β-HCG values do not decrease.→ Histological features of malignant GTD are present.→ If metastases are present on chest x-ray.
• Vulvovaginitis Infectious vulvovaginitis:- Bacterial vaginosis- Vaginal yeast infection- Trichomoniasis- Gonorrhea- Chlamydial genitourinary infection- Enterobius vermicularis (especially in prepubescent girls)- Scabies (“seven-year itch”)- Pediculosis pubis (“crabs”, pubic lice)Partner therapy is recommended in most cases of STDs, particularly chlamydia, trichomoniasis, and gonorrhea. Bacterial vaginosis and vaginal yeast infection do not require treatment of the partner(s) according to the CDC! Noninfectious vulvovaginitis:- Atrophic vaginitis- Chemical irritants (e.g., soaps, shampoos)- Allergic (e.g., to detergents; see extra information)- Mechanical (e.g., clothing; see extra information)
• Atrophic vaginitis Etiology:- Low estrogen levels (e.g., after menopause, bilateral oophorectomy, radio-/chemotherapy, immunological disorders)- Atrophy of epithelium in vagina and vulva   Clinical features:- Decreasing labial fat pad- Vaginal soreness, dryness- Dyspareunia, burning sensation after sex- Discharge, occasional spotting  - Commonly associated with receding pubic hair Diagnostics: primarily a clinical diagnosis, additional tests (e.g., pH test, wet mount) are often nonspecific Treatment: estrogen cream (topical) or tablets (systemic)
• Vulvovaginitis in pediatric patients Etiology:- The most common cause is poor hygiene.- Use of perfumed soaps and bubble baths- Localized skin disorders- Foreign body in the genitourinary tract  - In some cases, sexual abuse   Pathophysiology: Estrogen levels are lower in prepubescent girls, making the vulvar skin and vaginal mucosa very thin. This makes them more susceptible to vulvovaginitis of any cause. Clinical features:- Vaginal discharge: often bloody, purulent, or foul-smelling- Pain in the lower abdomen and suprapubic region- Increased urinary frequency, burning on urination, and dysuria- In some cases, visible segment of a foreign body at the genital opening Diagnosis:- If an infectious etiology is suspected, then appropriate Gram stain, culture, prep, DNA PCR, etc. should be conducted.- Direct visualization of the foreign body, either on physical examination or by means of pelvic ultrasonography, plain pelvic radiography, vaginography, or MRI Treatment:- In case of foreign body: removal of foreign body→ First line of treatment: warm saline irrigation of the vagina in an outpatient setting  → If irrigation fails, removal under general anesthesia→ Antibiotics/antifungals are usually not needed if successful removal is achieved, as the vulvovaginitis would then spontaneously resolve.- Topical or oral antibiotics/antifungals- Conservative measures: improving hygiene, avoidance of tight clothing
• Bacterial vaginosis Epidemiology: most common vaginal infection in women (40-45% of all cases) Pathogen: Gardnerella vaginalis (a gram-variable rod)   Pathogenesis: Lower concentrations of Lactobacillus and overgrowth of Gardnerella vaginalis and other anaerobes, without vaginal epithelial inflammation due to absent immune response Risk factors:- Sexual intercourse - Intrauterine devices (IUDs)- Douching- Pregnancy Clinical features:- Commonly asymptomatic- Increased vaginal discharge, usually gray or milky with fishy odor  - Pruritus and pain are uncommon Diagnostics: vaginal discharge sample- Amsel's criteria: 3 of 4 must apply to confirm diagnosis→ Whiff test: add 1-2 drops of 10% KOH to vaginal fluid → intensification of the fishy odor→ Vaginal pH > 4.5→ No leukocytes visible on microscopy→ Clue cells: vaginal epithelial cells covered with bacteria identified on wet mount preparation. A sample of vaginal fluid/discharge is transferred to a slide and mixed with normal saline.  Treatment:- First-line: oral metronidazole- Alternative: topical metronidazole or clindamycin- Oral probiotics Complications: infection of mother results in higher risk of preterm delivery
• Vaginal yeast infection (Vulvovaginal candidiasis) Epidemiology: second most common cause of vulvovaginitis (20-25% of all cases) Pathogen: primarily Candida albicans   Risk factors:- Pregnancy  - Immunodeficiency, both systemic (e.g., diabetes mellitus, HIV, immunosuppression) and local (e.g., topical corticosteroids)- Antimicrobial treatment (e.g., after systemic antibiotic treatment)   Clinical features:- White, crumbly, and sticky vaginal discharge that may appear like cottage cheese and is typically odorless- Erythematous vulva and vagina- Vaginal burning sensation, strong pruritus, dysuria, dyspareunia Diagnostics:- Pseudohyphae on wet mount with potassium hydroxide (KOH)  - Vaginal pH within normal range (4-4.5) Treatment:- Topical azole (e.g., miconazole, clotrimazole)- Alternatively: nystatin pessary (where available) or single-dose oral fluconazole  
• Trichomoniasis Pathogen: Trichomonas vaginalis  Anaerobic, motile protozoan with flagella Transmission: sexual Clinical features:- Foul-smelling, frothy, yellow-green, purulent discharge- Vulvovaginal pruritus, burning sensation, dyspareunia, dysuria, strawberry cervix   Diagnosis:- Saline wet mount of vaginal smear: protozoa with multiple flagella  - If wet mount is inconclusive → culture  - pH of vaginal discharge > 4.5 Treatment: oral metronidazole or tinidazole for patient and sexual partner(s)
• Pelvic inflammatory disease (PID) Epidemiology:- Lifetime prevalence in the US (women aged 15-44): ∼ 6%- > 1 million women experience an episode of PID/year.- PID is one of the most common causes of infertility. Pathogen- Most common: Chlamydia trachomatis and Neisseria gonorrhoeae- Less common (consider coinfections): E. coli, Ureaplasma, and other anaerobes Risk factors:- Multiple sexual partners, unprotected sex- A history of prior STIs and/or adnexitis- Infrequently: IUD  - Risk is lower during pregnancy but if occurs PID increases the risk of maternal morbidity and preterm births. Possible sites of infection:- Cervix (cervicitis), or endometrium (endometritis)- Fallopian tubes (salpingitis), ovaries (oophoritis), or a combination of both (adnexitis)- Surrounding pelvic structures or even the peritoneum (peritonitis) Clinical features:- Lower abdominal pain (generally bilateral), which may progress to acute abdomen- Nausea, vomiting- Fever- Dysuria, urinary urgency- Menorrhagia and metrorrhagia- Dyspareunia- Abnormal vaginal discharge Important diagnostic criteria:- Patient history: most often a sexually active young woman- Lower abdominal pain- Vaginal examination→ Cervical motion tenderness (CMT) → Uterine and/or adnexal tenderness → Purulent, bloody cervical and/or vaginal discharge  - Blood tests: elevated ESR, leukocytosis- Pregnancy test: to rule out an (ectopic) pregnancy.- Cervical and urethral swab: gonococcal and chlamydial DNA (PCR) and cultures  → Giemsa stain of discharge can show cytoplasmic inclusions in C. trachomatis infections, but not N.- Ultrasound: free fluid, abscesses, pyosalpinx/hydrosalpinx  - Exploratory laparoscopy Treatment:- Empirical antibiotic therapy (also consider coinfections!)- Outpatient regimen: One single dose of IM ceftriaxone and oral therapy with doxycycline→ If signs of vaginitis or recent gynecological instrumentation → add oral metronidazole.- Inpatient regimen (parenteral antibiotics)→ Indications: no response to or unable to take outpatient oral regimen, non-compliance concerns (e.g., teenagers), high fever→ Cefoxitin or cefotetan plus doxycycline or→ Clindamycin plus gentamicin→ Switch to oral therapy with doxycycline after clinical improvement.
• Ectopic pregnancy Localization:1. Fallopian tube (96% of cases): ampulla >> isthmus > fimbriae > interstitial pregnancy: e.g., cornual pregnancy2. Ovary (3% of cases)3. Abdomen (1% of cases)4. Cervix (very rare) Risk factors:- Anatomic alteration of the fallopian tubes is the main cause of ectopic pregnancy. It may be due to:→ A history of PID→ Previous ectopic pregnancy→ Past surgeries involving the fallopian tubes→ Endometriosis→ Exposure to DES (diethylstilbestrol) in utero  → Bicornuate uterus  - Non‑anatomical risk factors→ Intrauterine device (IUD)  → History of infertility  → Hormone therapy   Clinical features:- Patients usually present with signs and symptoms 4-6 weeks after their last menstrual period.- Lower abdominal pain and guarding- Vaginal bleeding  - Signs of pregnancy: amenorrhea, nausea, breast tenderness, frequent urination- Tenderness in the area of the ectopic pregnancy- Cervical motion tenderness, closed cervix- Enlarged uterus- Interstitial pregnancies tend to present late, at 7-12 weeks of gestation, because of myometrial distensibility. Tubal rupture:- Acute course with sudden and severe lower abdominal pain (acute abdomen)  - Signs of hemorrhagic shock: e.g., tachycardia, hypotension, syncope- More common in interstitial pregnancy Diagnostics:- Positive pregnancy test: ↑ β-hCG→ Serum test: β-hCG verifiable from the 8th day after ovulation→ Follow-up measurements are required to monitor the increase of β‑hCG levels over time.  - Transvaginal ultrasound (TVUS): Best initial imaging test for determining the localization of the pregnancy and finding a heartbeat→ Empty uterine cavity in combination with a thickened endometrial lining→ Tubal ring sign: echogenic ring that surrounds an unruptured ectopic pregnancy.→ Possibly free fluid within the pouch of Douglas→ Interstitial pregnancy: Gestational sac appears separately, < 1 cm from the lateral edge of the uterine wall; Thin myometrial layer (< 5 mm) surrounding sac seen on ultrasound.- Endometrial biopsy: shows decidualization of the endometrium without chorionic villi or fetal parts Conservative management:- Indications: → Uncomplicated ectopic pregnancies→ Hemodynamic stability→ β-hCG ≤ 5000 mlU/mL→ No renal, hepatic, or hematologic diseases→ No fetal heartbeat and ectopic mass size < 4 cm- Treatment of choice: methotrexate (MTX)  - A decrease in β-hCG levels should occur within a week of MTX administration.- Anti-D immunoglobulin (RhoGAM)- Alternative: expectant management   Surgery:- Indications→ Hemodynamic instability, impending rupture→ Risk factors for rupture  → Contraindications for MTX treatment: e.g., renal insufficiency→ If conservative treatment is unsuccessful- Laparoscopic removal
• Oral contraceptive pill – Contraindications - Thromboembolism, coagulopathies- Coronary heart disease- Stroke- Arterial hypertension (> 160/95 mm Hg)- Metabolic disorders of the liver- Insulin-dependent diabetes mellitus- Hepatocellular carcinoma- Estrogen-dependent tumors- Lupus erythematodes- Smoking > 35 years of age  - Genital bleeding of unknown cause- Pregnancy
• Intrauterine devices (IUDs) Levonorgestrel IUD (Mirena): The progesterone in the IUD causes thickening of the cervical mucus and thinning of the endometrium, which can ↓ menstrual blood loss or cause amenorrhea.- Lasts 5 years- ↓ menstrual bleeding and dysmenorrhea; thus, a good choice or the treatment of heavy menstrual bleeding.- Side effects: Irregular menstrual bleeding or amenorrhea. Copper IUD (ParaGard): Causes a sterile inflammatory response that prevents pregnancy implantation.- Lasts 10 years.- Nonhormonal; a good choice or women who have contraindications to hormone treatment.- Side effects: Dysmenorrhea and ↑ menstrual bleeding.
• Emergency contraception Non-hormonal methods: Copper-containing intrauterine devices  - Added benefit of long-term contraception- Requires brief, clinical procedure Hormonal methods:- Most effective when taken within 3 days of intercourse- Typically administered as a single dose or as two doses over one day- Significantly less effective in patients who are obese or overweight  - Types:→ Levonorgestrel (over the counter)→ Antiprogestin (e.g., ulipristal acetate) (requires a prescription)→ Yuzpe regimen (combination of ethinyl estradiol and levonorgestrel)
• Infertility Inability of a couple to conceive despite 1 year of unprotected sex   Epidemiology: Infertility affects approx. 10-15% of couples of reproductive age. Etiology:Both sexes:- Systematic and endocrine diseases: diabetes mellitus, hypertension, thyroid disorders, obesity, Cushing's syndrome, celiac disease, chronic diseases (e.g., hepatic or renal)  - Infections (e.g., chronic chlamydia infection)  - Various prescription drugs, alcohol, nicotine, recreational drugs Female infertility:- Ovarian insufficiency (30%)- Impaired ovum transport in fallopian tubes (30%): fallopian tube adhesions and/or obstruction  - Sexual dysfunctions (10%): sexual arousal disorder, genito-pelvic pain disorder (pain and vaginal tightening during intercourse)- Diminished ovarian reserve (10%)- Uterine causes (5%): Anatomical anomalies, Uterine leiomyoma, Asherman's syndrome- Cervical anomalies (5%)  - Antisperm antibodies in the cervical mucus- Hypogonadotropic hypogonadism- Functional hypothalamic amenorrhea- PCOS- Hyperprolactinemia (e.g., pituitary adenoma) Male infertility:- Sperm disorders (e.g., reduced sperm count, impaired motility, reduced ejaculate volume)→ Can be caused by anabolic steroids  - Scrotal hyperthermia (varicocele)- Testicular damage (e.g., congenital anomalies, injuries, infections such as mumps)- Psychiatric and psychosomatic disorders (e.g., impaired libido, anejaculation)- Kallmann syndrome   Diagnostics:1. History of both partners, especially gynecological history2. Assess ovulatory function- Body temperature analysis to monitor menstrual cycle  - Hormone tests (between the 3rd and 5th day of the menstrual cycle)→ Mid-luteal serum progesterone level: progesterone should increase shortly after ovulation→ failure of progesterone levels to rise indicates anovulation→ Prolactin and androgen levels: elevated levels induce negative feedback to the hypothalamus → inhibits GnRH secretion → lowers estrogen levels and suppresses ovulation→ FSH levels: elevated in ovarian insufficiency and indicate reduced ovarian reserve→ TSH levels: elevated levels in hypothyroidism  → Prolactin levels: hyperprolactinemia- Endometrial biopsy: usually performed 1-3 days before menstruation to determine thickness of endometrium → flat endometrial lining indicates a defect in the luteal phase of the menstrual cycle  3. Assess patency of fallopian tubes and uterus: hysterosalpingography  or sonohysterosalpingography  - Screen for tubal occlusion and structural uterine abnormalities (e.g., septate uterus, submucous fibroids, intrauterine adhesions)- Can also be therapeutic since it removes small adhesions or mucous plugs obstructing the tubal lumen- If evidence of intrauterine abnormalities or tubal occlusion → hysteroscopy and/or laparoscopy indicated4. Examine cervix: Pap smear and physical exam; testing for antisperm antibodies in cervical mucus  Treatment:- Ovulation induction→ Clomiphene citrate  → GnRH (pulsatile): stimulates the release of FSH, LH → follicle maturation→ Gonadotropins (e.g., recombinant hCG, recombinant LH): stimulate final oocyte maturation → ovulation→ Tamoxifen (selective estrogen receptor modulator)→ GnRH-antagonists  - Oocyte donation- Surgical removal of tubal, cervical, or uterine adhesions, as well as myomas and scar tissue- Assisted reproductive technology→ In vitro fertilization (most common)  → Intracytoplasmic sperm injection  - Treatment of underlying causes: e.g., levothyroxine, bromocriptine (for hyperprolactinemia), metformin (for PCOS)
• Menopause 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.Menopause: Confirmed after 12 months of amenorrhea. The average age at menopause is ∼ 49-52 years. Postmenopause: the time period beginning 12 months after the last menstrual period. Clinical features:- Irregular menses (which gradually decrease in frequency) → complete amenorrhea- Autonomic symptoms  → Increased sweating, hot flashes, and heat intolerance→ Vertigo→ Headache- Mental symptoms→ Impaired sleep (insomnia and/or night sweats)→ Depressed mood or mood swings→ Anxiety/irritability→ Loss of libido- Atrophic features: result from an age-related drop in estrogen levels→ Breast tissue atrophy: breast tenderness and reduced breast size→ Vulvovaginal atrophy: atrophy of the vulva, cervix, vagina → vaginal dryness, pruritus, and dyspareunia→ Urinary atrophy: atrophy of the urinary tract → urinary incontinence, dysuria, urinary frequency, urgency, and increased urinary tract infections- Weight gain and bloating- Increased risk of coronary artery disease Diagnostics: Clinical- ↓ Estrogen, ↓ progesterone, ↑↑ FSH - FSH levels can fluctuate widely in perimenopause.- Testosterone and prolactin levels are within normal ranges.- Lipid profile: ↑ total cholesterol, ↓ HDL Treatment may be considered in the following cases:- Symptoms are severe enough to infringe significantly on functional capacity, and hence affect quality of life.- In premature menopause  - Surgical menopause (e.g., post-oophorectomy) General measures:- For hot flashes: avoidance of triggers (e.g., bright lights, predictable emotional triggers); environmental temperature regulation (e.g., using fans)- For atrophic vaginal symptoms: vaginal estrogen creams, rings, or tablets (estrogen therapy may reduce the incidence of UTIs and features of overactive bladder)- For impaired sleep and/or hot flashes: exercise, acupuncture, and relaxation techniques- Prevention of osteoporosis: Smoking cessation, adequate vitamin D intake and regular weight-bearing exercise   Hormone replacement therapy (HRT):- HRT is usually employed for the short-term treatment of menopausal symptoms.  - Types→ Estrogen therapy: for women who have had a hysterectomy→ Estrogen plus progestin therapy: for women with a uterus  - Routes: oral, transdermal- Risks→ Unopposed estrogen can result in endometrial hyperplasia → increased risk of endometrial cancer→ Estrogen plus progestin therapy → increased risk of breast cancer→ Cardiovascular disease: coronary heart disease, deep vein thrombosis, pulmonary embolism, stroke→ Gallbladder disease→ Stress urinary incontinence Non-hormonal therapy:- Non-hormonal therapy is used to treat menopausal vasomotor symptoms in women who do not want to use hormonal medications or who have contraindications for HRT.- Selective estrogen receptor modulators: tamoxifen, ospemifene, and raloxifene- Paroxetine: for vasomotor symptoms (i.e., hot flashes)- Clonidine and/or gabapentin  
• Urinary incontinence Etiology:- Neurological causes→ Multiple sclerosis→ Spinal injury→ Normal pressure hydrocephalus→ Dementia→ Delirium- Genitourinary causes→ Trauma to the pelvic floor  → Intrinsic sphincter deficiency→ Urethral hypermobility in women→ Impaired detrusor contractility→ Bladder outlet obstruction→ Pelvic floor weakness→ Urogenital fistula- General risk factors: Obesity, caffeine, alcohol, recurrent urinary tract infections- Potentially reversible causes: Drugs (e.g., diuretics), urinary tract infections, postmenopausal atrophic urethritis, psychiatric causes (especially depression, delirium/confused state), excessive urinary output (in conditions like hyperglycemia, hypercalcemia, CHF), impaired mobility, stool impaction Stress incontinence:- Increase in intra-abdominal pressure (e.g., from laughing, sneezing, coughing, exercising) → ↑ pressure within the bladder → bladder pressure > urethral sphincter resistance to urinary flow  - Urethral hypermobility in women secondary to poor pelvic support caused by pelvic postmenopausal estrogen loss, connective tissue disorders, or childbirth (i.e., damage of the pelvic floor muscle levator ani and/or the S2–S4 nerve roots)- Urinary leakage on activities that increase intra-abdominal pressure Urge incontinence:- Inflammatory conditions or neurogenic disorders → sphincter dysfunction, detrusor overactivity or overactive bladder → autonomous contractions of the detrusor muscle and premature initiation of a normal micturition reflex- Strong, sudden sense of urgency, followed by involuntary leakage- Treatment: Anticholinergic medication, surgery Mixed incontinence:- Combination of mechanisms of stress and urge incontinence- Treatment: Anticholinergics to treat aspects of urge incontinence Total incontinence:- Complete loss of sphincter function (due to previous surgery, nerve damage, metastasis) or abnormal anatomy (fistula between urinary tract and skin)- Urinary leakage occurs at all times, with no associated preceding symptoms or specific trigger activity- Treatment: Usually requires surgery Overflow incontinence (overflow bladder):- Impaired detrusor contractility and/or bladder outlet obstruction → chronically distended bladder with ↑ bladder pressure → dribbling of urine when intravesical pressure > outlet resistance- Frequent, involuntary intermittent/continuous dribbling of urine in the absence of an urge to urinate- Occurs only when the bladder is full- Often occurs with changes in position- Treatment:→ Acute settings: intermittent catheterization→ Timed voiding for day to day management Detrusor sphincter dyssynergia:- Commonly seen in multiple sclerosis or spinal cord injury  - Simultaneous contractions of the detrusor muscle and involuntary activation of the internal urethral sphincter → blockage of bladder outlet → small amounts of urineare pressed through the contracted sphincter muscle → high intravesical pressure along with inappropriate contraction of the urethral sphincter- Voiding and/or storage dysfunction, intermittent voiding, urinary retention- Irregular, small volume incontinence without an associated urge to void (sometimes referred to as reflex incontinence)- Treatment:→ Injection of botulinum toxininto the detrusor muscle  → Transurethral resection of external urinary sphincter (TURS)→ Alpha-blockers and/or anticholinergics Diagnostics:- Detailed medical history (including medication)- Voiding diary to assess frequency and volume of micturition- Neurological, vaginal, and rectal examination  - Laboratory tests:→ Urine dipsticks and urine culture to exclude urinary tract infections→ Creatinine and blood urea nitrogen (BUN)- Sonography:→ Quantification of residual urine after micturition→ Renal ultrasound- Quantification of leaked urine: pad test- Micturating cysto-urethrogram (MCU) to detect morphological abnormalities- Urodynamic examination to measure bladder pressure and urethral closure pressure- Cystoscopy to rule out tumors and vesicorectal or vesicovaginal fistulae- MRI to identify pelvic floor defects
• Fibroadenoma Benign breast tumor with fibrous and glandular tissue Etiology: unknown, but a hormonal relationship has been established (increased estrogen, e.g., during pregnancy or before menstruation, may stimulate growth)   Epidemiology:- The most common breast tumor in women < 35 years of age- Peak incidence: 15-35 years Clinical features: mostly solitary, well-defined, non-tender, rubbery, and mobile mass Diagnosis:- Ultrasound: well-defined mass- Mammogram: well-defined mass that may have popcorn-like calcifications- If imaging is inconclusive: fine-needle aspiration showing fibrous and glandular tissue Treatment: regular check-ups
• Phyllodes tumor Rare fibroepithelial tumor with histology similar to that of fibroadenoma Etiology: unknown Epidemiology:- 1% of all breast tumors- Most commonly benign  - Peak incidence: 40-50 years Clinical features:- Painless, smooth, multinodular lump in the breast- Variable growth rate: may grow slowly over many years, rapidly, or have a biphasic growth pattern- Average size 4-7 cm Diagnosis:- Ultrasound and mammogram findings are similar to fibroadenoma, but phyllodes tumors tend to be larger and grow faster than fibroadenomas.- Despite the fact that the lesion is typically benign, a suspected phyllodes tumor should be considered a suspicious mass until proven otherwise.- If a phyllodes tumor is suspected (based on clinical or imaging findings) → core biopsy  → Leaf-like architecture with papillary projection of epithelium-lined stroma and varying degrees of atypia and hyperplasia Treatment:- Surgical excision  - In case of recurrence: total mastectomy
• Intraductal papilloma Solitary or multiple benign lesions that arise from the epithelium of breast ducts Epidemiology:- Peak incidence: 40-50 years→ Solitary lesions: ∼ 48 years→ Multiple lesions: ∼ 41 years Clinical features:- Solitary lesions  → Most common cause of bloody nipple discharge→ Large, central lesion→ Palpable breast tumor close to or behind the nipple- Multiple lesions→ Usually asymptomatic but may cause nipple discharge in rare cases→ Peripheral lesions; smaller than solitary papilloma Diagnosis:- If lesion is palpable: Core needle biopsy is confirmatory and rules out malignancy. Shows papillary cells with fibrovascular core.- Otherwise: ductogram   Treatment: surgical excision of the affected duct Prognosis: generally excellent  
• Galactocele Milk retention cyst located in the mammary gland Epidemiology:- Most common benign breast lesion in lactating women- Frequently occurs during or after lactation   Pathophysiology: obstruction of lactiferous duct → distention of the duct due to collection of milk and epithelial cells → cyst formation Clinical features:- Soft, nontender mass; typically located in the sub-areolar region- Pain suggests secondary infection. Diagnosis:- Primarily a clinical diagnosis- Fine needle aspiration: milky substance (diagnostic and therapeutic)- Ultrasound: complex mass; findings depend on the fat and water content of the cyst- Mammography (rarely indicated): galactoceles may appear as an indeterminate mass or a mass with the classic fat-fluid level Treatment:- Usually not necessary (most cases resolve spontaneously)- Repeated needle aspiration or surgical excision for symptomatic cysts Prognosis: good; no increased risk of subsequent breast cancer
• Fibrocystic changes Benign changes characterized by the formation of fibrotic and/or cystic tissue Epidemiology:- Most common benign lesion of the breast- Up to 50% of women are affected during their lifetime.- Primarily in premenopausal women 20-50 years of age Clinical features:- Premenstrual bilateral breast pain- Tender or nontender breast nodules- Clear or slightly milky nipple discharge Diagnosis:- Physical exam- First-line: ultrasound and mammogram→ Ultrasound: Findings range from normal appearance to focal regions of thick parenchyma; cysts may be present.→ Mammogram (not recommended for women < 30 years): round or oval masses with clear borders; in some cases, dispersed calcifications- Fine-needle aspiration (after imaging confirms a cystic lesion): indicated if the patient is symptomatic and/or requests the procedure  - Biopsy: confirms diagnosis if imaging is inconclusive→ Cysts: dilated, fluid-filled ducts (blue dome cysts)  → Stromal fibrosis (no malignant potential)→ Sclerosing adenosis: proliferation of small ductules and acini in the lobules, calcifications (slightly increased risk of breast cancer)→ Ductal hyperplasia: Papillary proliferation (papillomatosis), apocrine metaplasia→ Epithelial hyperplasia of terminal duct cells and lobular epithelium; the presence of atypical cells is associated with an increased risk of breast cancer Treatment:- General approach: If symptoms are mild, treatment is not required. In case of severe symptoms: oral contraceptives, tamoxifen, or progesterone- Fine-needle aspiration or surgery→ If a cyst causes severe pain, discomfort, or disfiguration→ In case of proliferative lesions with atypical cells→ Reevaluate the cyst after 4-6 weeks. Prognosis: depends on the histologic subtype- Nonproliferative lesions do not increase the risk of cancer- Proliferative lesions with atypical cells (e.g., ductal epithelial hyperplasia) are associated with an increased risk of cancer
• Mastitis Inflammation of the breast parenchyma Incidence: up to 10% of nursing mothers (particularly 2-4 weeks postpartum) Etiology:- Staphylococcus aureus (most common)- Other pathogens (Streptococcus, Escherichia coli) are rare. Clinical features:- Tender, firm, swollen, erythematous breast (generally unilateral)- Pain during breastfeeding- Reduced milk secretion- Flu-like symptoms, malaise, fever, and chills- In some cases, reactive lymphadenopathy Diagnosis:- Clinical diagnosis- Breast milk cultures or imaging may be required if there is no response to initial treatment. Treatment:- In nursing mothers, frequent emptying of the breast: → Breastfeeding with alternate breasts is recommended every 2-3 hours.  → Analgesics (e.g., ibuprofen)→ Cold compresses→ Antibiotic treatment: Oral penicillinase-resistant penicillin or cephalosporin (e.g., dicloxacillin or cephalexin)→ In the case of methicillin-resistant Staphylococcus aureus (MRSA): clindamycin or trimethoprim-sulfamethoxazole (TMP-SMX)   Complications: Breast abscess - Clinical features:→ Breast pain, erythema, and edema→ Purulent discharge from the nipple of the affected breast→ Fever→ Nausea→ Fluctuating mass on palpation- Treatment:→ Incision and drainage→ Needle aspiration is possible for abscesses less than 5 cm in diameter
• Fat necrosis of the breast Nonsuppurative inflammatory lesion affecting breast adipose tissue Etiology: trauma Epidemiology:- Incidence: < 3% of all breast lesions- Peak incidence: 50 years Clinical features: irregularly defined and dense breast mass (generally periareolar) causing skin retraction, erythema, or ecchymosis   Diagnosis:- Mammogram and/or ultrasound: fluid-filled cyst- Also on mammogram: coarse rim calcification- If any suspicious or inconclusive imaging findings → perform biopsy→ Shows foam cells, multinucleated giant cells, hemosiderin deposition, and chronic inflammation Treatment: unnecessary
• Overrepresented health issues in women who have sex with women - Cardiovascular disease- Type 2 diabetes mellitus- Obesity- Cervical cancer- Breast cancer- Ovarian cancer- Depression, anxiety- Intimate partner violence- Bacterial vaginosis
• Pelvic organ prolapse Risk factors:- Multiple vaginal deliveries and/or traumatic births  - Low estrogen levels (e.g., during menopause)- Congenital connective tissue disorders- Previous pelvic surgery (e.g., hysterectomy)- Increase intraabdominal pressure (e.g., cough related to chronic lung disease and/or smoking, ascites, obesity, pelvic tumors, or constipation.)- Diabetes mellitus   Clinical features:- Feeling of pressure on or discomfort around the perineum (“sensation of vaginal fullness”)- Lower back and pelvic pain (may become worse with prolonged standing or walking)- Rectal fullness, constipation, incomplete rectal emptying- Prolapse of the anterior (in cystocele/urethrocele) or the posterior (in enterocele/rectocele) vaginal wall, possibly with excessive vaginal discharge on inspection, bimanual examination, and speculum examination of the patient in lithotomy position; occurs at rest and with increased abdominal pressure- Weakened pelvic floor muscle and anal sphincter tone   Diagnostics: Pelvic Organ Prolapse Quantitation system (POP-Q)Stage 0: no prolapseStage 1: The most distal portion of prolapse is more than 1 cm above the level of the hymen.Stage 2: The most distal portion of prolapse is 1 cm or less proximal or distal to the hymenal plane.Stage 3: The most distal portion of prolapse is more than 1 cm from the hymenal plane but no more than 2 cm less than the vaginal length.Stage 4: The vagina is completely everted or uterine procidentia has occurred. Conservative treatment:- First-line treatment for all cases of POP. - Insertion of a vaginal pessary to support the pelvic organs → Pessary insertion is not a long-term treatment!  - Reduction of modifiable risk factors (e.g., avoid smoking to prevent a chronic cough, weight loss, prevent constipation)- Kegel exercises: pelvic floor muscle training (also as a preventive measure) Surgery- Indicated for symptomatic prolapse if conservative treatment fails or the patient declines it.- Obliterative surgery: vagina is closed off or narrowed to provide more support for pelvic organs.- Reconstructive surgery (abdominal or vaginal approach): to restore the original position of the descended pelvic organs
• Imperforate hymen A hymen without an opening Etiology: congenital defect Incidence: 1/2000 females Pathophysiology: central cells of the Müllerian eminence in the urogenital sinus do not disintegrate → imperforate hymen → cryptomenorrhea at puberty (outflow tract obstruction leads to backup of menstrual blood) → hematocolpos Clinical features:- Asymptomatic before puberty- Primary amenorrhea with periodic lower abdominal pain- Possible urinary retention, frequency, dysuria  - Possible palpable lower abdominal mass  - Perineal examination: tense, bulging, bluish membrane in the vulva Diagnostics: primarily a clinical diagnosis- Imaging may be conducted to rule out transverse vaginal septum Treatment: excision of the imperforate hymen (hymenectomy)
• Breast discharge – Work-up Bilateral:- Pregnancy test- Galactorrhea evaluation Unilateral:- Age < 30: Ultrasound ± mammogram- Age > 30: Ultrasound ± mammogram
• Ovarian torsion Risk factors:- Ovarian mass- Women of reproductive age- Infertility treatment with ovulation induction Clinical features:- Sudden-onset unilateral pelvic pain- Nausea & vomiting± Palpable adnexal mass Diagnostics:- Ultrasound: Adnexal mass with absent Doppler flow to ovary Treatment:- Laparoscopy with detorsion- Ovarian cystectomy- Oophorectomy if necrosis or malignancy
• Ovarian hyperstimulation syndrome A potentially life-threatening complication of ovulation induction with human chorionic gonadotropin that is characterized by formation of multiple ovarian follicles, rapid ovarian enlargement, and occasionally ascites due to increased capillary permeability and leakage of fluid from the peritoneum. Clinical features:- Ascites- Respiratory distress- Hemoconcentration- Hypercoagulability- Electrolyte imbalances- Multiorgan failure (eg, renal failure)- Disseminated intravascular coagulation Evaluation:- Fluid balance monitoring- Serial CBC, electrolytes- Serum hCG- Pelvic ultrasound- Chest x-ray- Echocardiography Management:- Correct electrolyte imbalances- Paracentesis &/or thoracentesis- Thromboembolism prophylaxis
• Condylomata acuminata (anogenital warts) HPV types 6 and 11: responsible for ∼ 90% of genital warts Location♀: vulvar, cervix, urethra (rare), anal region♂: glans penis, foreskin, urethra, anal region Diagnosis:- Visual inspection- Application of 5% acetic acid turns lesions white (not a specific finding) Clinical findings:- Exophytic, cauliflower-like lesions  - Often asymptomatic; may cause pruritus, tenderness, or bleeding in rare cases Treatment:- Pharmacotherapy: local cytostatic treatment (e.g., 5-fluorouracil, trichloroacetic acid, podophyllin, or salicylic acid) or immune response modifiers (e.g., imiquimod and interferon alfa)- Cryotherapy: freezing external warts with CO2, N2O, or N2 - In case of numerous warts: curettage, laser surgery, or electrocoagulation
• Genetic testing for inherited breast cancer disorders - 2 1st-degree relatives with breast cancer (including 1 before age 50)- 3 1st- or 2nd-degree relatives with breast cancer- 1st- or 2nd-degree relative with breast and ovarian cancer- 1st-degree relative with bilateral breast cancer- Breast cancer in a male relative- Ashkenazi Jewish women with any 1st- or 2nd-degree relative with breast or ovarian cancer
• Contraception side effects Combined hormonal contraceptives (pills, patch, ring):- Breakthrough bleeding- Breast tenderness- Nausea Depot medroxyprogesterone acetate (DMPA):  - Initial irregular bleeding- Amenorrhea- Reversible bone loss- Delayed return to fertility± Weight gain Progestin subdermal implant: Irregular bleeding Progestin IUD:- Irregular bleeding- Amenorrhea Copper IUD:- Heavy menses- Dysmenorrhea
• Uterine sarcoma Risk factors:- Pelvic radiation- Tamoxifen use- Postmenopausal patients Presentation:- Abnormal/postmenopausal bleeding- Pelvic pain or pressure- Uterine mass Diagnosis:- Ultrasound ± additional imaging- Endometrial biopsy- Histopathology of surgical specimen Treatment:- Hysterectomy± Adjuvant chemotherapy, radiation therapy
• Vulvodynia Clinical manifestations:- Raw, burning vulvar pain ≥ 3 months- Positive Q-tip test- Pain with labial separation- Idiopathic Diagnosis of exclusion Treatment:- Behavior modification- Pelvic floor physical therapy- Cognitive-behavioral therapy

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