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USMLE Step 2 (Subject) / Gynecology (Lesson)

Step 2 CK

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  • Tubo-ovarian abscess Pathogenesis: Repeated acute PID causes inflammation and allows the vaginal flora to access the uterus, tubes, and ovary Clinical features:- Fever- Leukocytosis- Adnexal mass Diagnostics: Ultrasound Treatment:- Antibiotics x 72 hrs and continue if there is improvement- If not, the abscess needs to be drained- Indications to go to emergent surgery for TOA→ Patient is very ill→ Very large abscess (> 8 cm)TOA is one of the few abscess conditions that doesn’t require emergent drainage.
  • Abnormal uterine bleeding Etiology:- Structural causes: polyps, adenomyosis, leiomyomas, malignancy/hyperplasia (PALM)- Non-structural causes: coagulopathy, ovulatory dysfunction, endometrial, iatrogenic, not yet classified (COEIN) Diagnostics:1. Gynecological history: E.g., age at menarche, cycle length and regularity, pregnancies, family history, recent complaints2. Physical examination- If bleeding is acute, ensure the hemodynamic stability of the patient!- Assess the severity and source of bleeding → exclude structural abnormalities, neoplasms, and trauma- Pap smear → rules out cervical carcinoma- Swabs for microbiologic testing → rules out cervicitis due to gonorrhea/chlamydial infection3. Initial laboratory testing- CBC → rules out anemia- Platelet count, PT, PTT → rule out bleeding disorders- Beta-HCG → rules out pregnancy- Additional testing if required (e.g., thyroid function tests, prolactin, serum iron)4. Ultrasound: rules out structural anomalies (e.g., polycystic ovaries) and allows evaluation of endometrial thickness5. Endometrial biopsy indicated if:- Endometrial thickness is ≥ 4 mm in a postmenopausal patient OR- Patient is > 35 years of age and has risk factors for endometrial hyperplasia (e.g., obesity) Management: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- Dilation and uterine curettage (D&C)- Endometrial ablation- Transcatheter uterine artery embolization: First line in AVM- Hysterectomy
  • Precocious puberty Definition: the appearance of secondary sexual characteristics before the age of 8 years in girls and 9 years in boys Work-up:1. Wrist X-ray- If > 2 years age difference between bone age and chronological age → positive2. GnRH stimulation test- ↑ LH → Central precocious puberty- ↓ LH → Peripheral precocious puberty Central precocious puberty- MRI ⊕ → Tumor → Resect- MRI ⊝ → Constitutional → Continuous leuprolide Peripheral precocious puberty- Get an ultrasound of the ovaries and adrenals while getting estradiol, DHEAS, and 17-OH-progesterone
  • Delayed onset of puberty Absent or incomplete development of secondary sex characteristics by the age of 14 in boys or 13 in girls Work-up:1. Wrist x-ray, basal FSH and LH- ↑ FSH, ↑ LH → Hypergonadotrophic→ Problem with the ovaries: PCOS, Turner syndrome, primary ovarian failure→ Karyotpye- Normal FSH, normal LH → Hypogonadotrophic→ Order prolactin, TSH, T4, CBC, ESR, LFTs, MRI If negative → constitutional
  • Anomalies of Müllerian duct fusion Pathophysiology:- Defective fusion of the Müllerian ducts during embryonal development- Normally functioning gonads and female karyotype → normal development of secondary sexual characteristics (e.g., breast, pubic hair development) Müllerian agenesis: Both the Müllerian ducts fail to develop → absent or hypoplastic uterus, absent cervix, and vaginal atresiaUnicornuate uterus: One of the Müllerian ducts fails to developBicornuate uterus: Incomplete fusion of the Müllerian ducts to various degrees- Uterus bicornis unicollis: double uterus, single cervix, and single vagina- Uterus bicornis bicollis: double uterus and double cervix with/without a vaginal septumSeptate uterus: The Müllerian ducts fuse, but the septa between the two ducts persists either partially (subseptate uterus) or completely (septate uterus). Clinical features:- Asymptomatic before puberty- Infertility and dyspareunia- In some cases, periodic lower abdominal pain- Müllerian agenesis: primary amenorrhea- Increased risk of the following obstetric complications: Ectopic pregnancy, cervical incompetence, preterm labor- Associated urological (25-50% of cases) and skeletal malformations (10-15% of cases) Diagnostics:- Transvaginal or abdominal ultrasound- Hysterosalpingography- Confirmatory test: MRI The mere presence of a Müllerian duct anomaly is not an indication for surgical therapy. In a patient with infertility and congenital uterine anomalies, it is important to rule out other causes of infertility before surgical therapy is considered!
  • Androgen insensitivity syndrome (testicular feminization) X-linked recessive mutation of the gene locus encoding the androgen receptor → varying degrees of end-organ insensitivity to androgensKaryotype: 46,XY Complete androgen insensitivity:- Female external genitalia (testicular feminization) and physique- Blind-ended vaginal pouch, uterine agenesis- Scant or missing pubic hair- Primary amenorrhea, infertility (no menarche) Partial androgen insensitivity: - Variations in phenotype, depending on the degree of androgen insensitivity- Male internal genitalia- Detection of abdominal/inguinal masses in newborns → intra-abdominal localization of undescended testicles Diagnostics:- Before puberty: ↑↑ testosterone- After puberty: high levels of LH and borderline/elevated levels of testosterone (with lack of virilization)- Genetic testing Therapy:- Management depends on receptor status and, especially, on the phenotype and gender identity of the affected patient.- Hormone treatment→ Female phenotype (complete androgen insensitivity): estrogen replacement→ Male phenotype (partial androgen insensitivity): high-dose androgen therapy- Gonadectomy for intra-abdominal testicles typically performed after puberty (high risk of malignancy)- Psychological support
  • Asherman syndrome (intrauterine adhesions) Etiology:- Following uterine curettage (most common cause)- Postinflammatory (e.g., chlamydia) Clinical features:- Usually asymptomatic- Secondary amenorrhea- Infertility- Recurrent pregnancy loss- Periodic abdominal pain Diagnostics:- Progesterone withdrawal test: bleeding does not occur following progestin withdrawal given block of outflow track- Confirmatory test: hysteroscopy to directly visualize adhesions Treatment:- Hysteroscopic resection of the adhesions- Treatment is only indicated if patients are symptomatic
  • Secondary amenorrhea Work-up:1. Is it the common stuff?→ UPT, TSH, prolactin, meds 2. Is the endometrium ready to bleed?→ Progestin challenge 3. Is the endometrium capable of bleeding?→ Estrogen and Progesterone challenge 4. Is there a signal coming from the pituitary? → FSH and LH 5a. Is there a problem with the anterior pituitary? → MRI5b. Are there follicles? → U/S 6. All has been negative - Hypothalamus
  • Urethral diverticulum Localized urethral mucosa herniated into surrounding tissue Etiology: Recurrent periurethral gland infections along the anterior vaginal wall Clinical features:- Dysuria- Postvoid dribbling- Dyspareunia- Tender anterior vaginal wall mass- Purulent or bloody urethral discharge Diagnostic testing:- Urinalysis- Urine culture- MRI of the pelvis- Transvaginal ultrasound Treatment: Surgical excision
  • Vesicovaginal fistula Risk factors:- Pelvic surgery- Pelvic irradiation- Prolonged labor/childbirth trauma- Genitourinary malignany Clinical features:- Painless, continuous urine leakage from the vagina Diagnotics:- Physical examination- Dye test- Cystourethroscopy
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  • Mature cystic teratoma Pathology:- Benign ovarian germ cell tumor- Endoderm, mesoderm, ectoderm tissue Clinical features:- Most asymptomatic- Ovarian torsion- Struma ovarii subtype: hyperthyroidism- Unilateral adnexal mass- Ultrasound: Complex, cystic, calcifications- Gross appearance: sebaceous fluid, hair, teeth Management: Ovarian cystectomy or oophorectomy
  • Skene glands Bilateral paraurethral glands in the anterior vaginal vestible.Located lateral to the urethral meatus. May form with duct obstruction.
  • Prepubertal vaginal bleeding Withdrawal of estrogen:- Presents in neonatal period- Lasts < 1 week- Examination otherwise normal Trauma:- Usually unintentional from fall- Can be sign of sexual abuse- Genital examination may show laceration/abrasion Malignancy (eg, rhabdomyosarcoma):- Rare- Presents age < 3- May visualize protruding vaginal nodules
  • 5-alpha-reductase deficiency Etiology: rare autosomal recessive loss-of-function mutation of chromosome 2 Karyotype: 46,XY Pathophysiology:- Normal testosterone production- Defective 5-alpha-reductase: testosterone not converted into dihydrotestosterone (DHT) → DHT-dependent virilization of genitalia does not occur Clinical features:- Female external genitalia at birth, sometimes with pseudovaginal perineoscrotal hypospadias- Internal urogenital organs are male- In puberty, increasing synthesis of testosterone leads to virilization (phallic growth, testicular descent, development of male gender identity). Diagnostics:- Hormone levels: n/↑ testosterone, ↓ DHT (elevated testosterone-to-DHT ratio) - Genetic testing for definitive diagnosis Therapy:- Female gender identity: gonadectomy; estrogen substitution therapy upon completion of longitudinal growth- Male gender identity: testosterone substitution
  • HPV vaccination HPV immunization preferably before first sexual intercourse. Indications:- 2 doses should be administered 6 months apart to all individuals between the ages of 11 and 12 years- Immunization can be started as early as 9 years of age.- 3 doses of nine-valent HPV vaccine should be administered for all unvaccinated individuals between the ages of 27 and 45 years.
  • Ovarian hyperstimulation syndrome A potentially life-threatening complication of ovulation induction with human chorionic gonadotropin that is characterized by the formation of multiple ovarian follicles, rapid ovarian enlargement, and occasionally ascites due to increased capillary permeability and leakage of fluid. Pathophysiology:- ↑ hCG enhances ovarian vascular permeability- Acute fluid shift to extravascular space Clinical features:- Ascites- Respiratory distress- Hemoconcentration- Hypercoagulability- Electrolyte imbalances- Multiorgan failure (e.g., 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 thoracocentesis- Thromboembolism prophylaxis
  • 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, mobile, 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:- Asymptomatic cysts: None- Symptomatic cysts: Repeated needle aspiration or surgical excision

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