Obstetrics and Gynecology

1046 soru

Soru 1001Soru →

Match each classic clinical presentation of an obstetric complication with its most likely underlying etiology.

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Öğeler

Placental abruption
Placenta previa
Vasa previa
Uterine rupture

Eşleşmeler

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Cevap

Placental abruption is characterized by painful bleeding and a rigid uterus. Placenta previa presents with painless bleeding and a soft uterus. Vasa previa features painless bleeding directly tied to membrane rupture with rapid fetal distress. Uterine rupture presents with sudden severe pain, loss of fetal station, and abrupt cessation of uterine contractions.
Each obstetric complication has a highly specific clinical hallmark: abruption features pain and hypertonus; previa features painless bleeding; vasa previa is tied to membrane rupture and fetal distress; and uterine rupture features loss of station and contraction cessation.

Adım Adım Çözüm

1
Analyze the presentation for the presence or absence of maternal pain and uterine tenderness.
Painful bleeding suggests placental abruption or uterine rupture; painless bleeding suggests placenta previa or vasa previa.
Pain is a key initial differentiating factor in evaluating antepartum hemorrhage.
2
Evaluate the timing of bleeding relative to membrane rupture and fetal heart rate changes.
Bleeding immediately after rupture of membranes with rapid, severe fetal bradycardia points directly to vasa previa.
The bleeding in vasa previa is purely fetal, leading to rapid fetal exsanguination before maternal hemodynamic changes occur.
3
Assess labor progress and the uterine contraction pattern.
Loss of fetal station and sudden cessation of contractions are classic, life-threatening signs of uterine rupture.
When the myometrium completely tears, the uterus can no longer generate contractions, and the fetus may be extruded into the maternal abdomen.

Anahtar Kavram

Differentiating etiologies of antepartum hemorrhage and acute intrapartum emergencies based on classic clinical presentation features.
Soru 1002Soru →

A 28-year-old nulligravid woman comes to the office due to an inability to conceive over the past 14 months despite regular, unprotected intercourse. Her menstrual periods were previously regular every 28 days but became increasingly spaced apart starting 8 months ago. She has had no menses for the last 4 months. The patient also reports a recent onset of constipation, generalized fatigue, and a 4.5-kg (10-lb) weight gain. She takes no medications. Vital signs are temperature 36.4°C (97.5°F), blood pressure 110/70 mm Hg, and pulse 58/min. BMI is 27 kg/m227\ kg/m^2. Physical examination reveals a moderately enlarged, non-tender thyroid gland and bilateral milky nipple discharge expressible on palpation. Neurologic examination shows delayed relaxation of the deep tendon reflexes. A urine pregnancy test is negative.

Laboratory studies show:
- Prolactin: 58 ng/mL (normal: <25 ng/mL)
- Thyroid-stimulating hormone (TSH): 18.2 µU/mL (normal: 0.4-4.0 µU/mL)
- Free thyroxine (T4): 0.5 ng/dL (normal: 0.8-1.8 ng/dL)

Which of the following is the most appropriate next step in management for this patient?

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Cevap: Initiation of levothyroxine

Cevap

Initiation of levothyroxine
The correct answer is initiation of levothyroxine. This patient presents with secondary amenorrhea, galactorrhea, and infertility in the setting of primary hypothyroidism (elevated TSH, low free T4). In primary hypothyroidism, the lack of negative feedback from thyroid hormones leads to increased hypothalamic production of Thyrotropin-Releasing Hormone (TRH). TRH stimulates not only thyrotrophs (increasing TSH) but also lactotrophs in the anterior pituitary, leading to hyperprolactinemia. Elevated serum prolactin inhibits the pulsatile secretion of Gonadotropin-Releasing Hormone (GnRH), resulting in decreased FSH and LH, anovulation, and secondary amenorrhea. Treating the root cause with levothyroxine will normalize free T4 and TSH levels, thereby decreasing TRH, resolving the hyperprolactinemia, and restoring normal ovulatory cycles without the need for further fertility treatments.

Adım Adım Çözüm

1
Identify the primary diagnosis based on clinical presentation and laboratory results.
The patient has weight gain, fatigue, bradycardia, delayed reflexes, elevated TSH, and low free T4, confirming overt primary hypothyroidism.
Establishing the root cause of the endocrine disturbance is necessary before treating downstream effects.
2
Connect the primary diagnosis to the secondary reproductive symptoms.
Primary hypothyroidism causes increased Thyrotropin-Releasing Hormone (TRH). TRH directly stimulates lactotrophs in the anterior pituitary, leading to mild hyperprolactinemia and galactorrhea. Elevated prolactin inhibits GnRH secretion, causing amenorrhea and infertility.
Understanding the physiological axis explains why multiple endocrine abnormalities are present.
3
Determine the next best step in management.
Treat the root cause by initiating thyroid hormone replacement (levothyroxine).
Correcting the hypothyroidism will normalize TRH levels, resolve the hyperprolactinemia, and restore normal ovulatory cycles.

Anahtar Kavram

Primary hypothyroidism can cause secondary hyperprolactinemia due to TRH-mediated stimulation of pituitary lactotrophs, leading to anovulation and infertility that resolves with levothyroxine therapy.
Soru 1003Soru →

A 24-year-old G1P0 woman at 39 weeks of gestation is evaluated in the labor suite. She was admitted 4 hours ago in spontaneous active labor and is currently not receiving any medications. Her temperature is 37.1°C (98.8°F), blood pressure is 118/72 mm Hg, pulse is 88/min, and respirations are 16/min. Physical examination reveals mild bilateral lower extremity pitting edema and a grade 2/6 systolic ejection murmur at the left sternal border. The cervix is 6 cm dilated and 90% effaced, with the fetal vertex at 0 station. Fetal heart rate monitoring demonstrates a baseline of 140/min with moderate variability. Over the last 30 minutes, there are recurrent, symmetric decreases in the fetal heart rate that begin gradually with the onset of each uterine contraction, reach their nadir of 120/min exactly at the peak of the contraction, and return to the baseline as the contraction ends. Which of the following is the most appropriate next step in management?

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Cevap: Continue routine expectant management of labor

Cevap

The correct answer is to continue routine expectant management of labor, as the patient has normal physiologic changes of pregnancy and a reassuring fetal heart rate tracing.
This patient has a reassuring Category I fetal heart rate (FHR) tracing characterized by a normal baseline, moderate variability, and early decelerations. Early decelerations are symmetrical, gradual decreases in the FHR that perfectly mirror uterine contractions—meaning the nadir of the deceleration occurs simultaneously with the peak of the contraction. They are caused by physiologic fetal head compression during contractions, which alters cerebral blood flow and triggers a benign vagal response. Because this is a normal finding in active labor, no acute intervention is required, and continuing routine expectant management is the correct next step. Furthermore, her mild peripheral edema and grade 2/6 systolic ejection murmur are normal physiologic adaptations to pregnancy (arising from increased plasma volume and decreased systemic vascular resistance) and do not represent a pathological complication.

Adım Adım Çözüm

1
Evaluate the maternal vital signs and physical examination findings.
The blood pressure is normal (118/72 mm Hg). The mild lower extremity edema and systolic ejection murmur are identified as benign, physiologic adaptations to pregnancy.
Differentiating normal physiologic changes of pregnancy from pathological states (like preeclampsia or heart failure) prevents unnecessary and potentially harmful interventions.
2
Interpret the fetal heart rate (FHR) tracing.
The baseline is 140/min, variability is moderate, and decelerations exactly mirror the uterine contractions (the nadir aligns with the peak of the contraction).
Accurate interpretation of the FHR tracing is required to classify it into a specific category and determine fetal well-being.
3
Identify the etiology of the FHR decelerations based on the timing relative to contractions.
The pattern describes early decelerations, which are caused by physiologic fetal head compression altering cerebral blood flow and triggering a benign vagal response.
Understanding the pathophysiology of decelerations dictates the clinical response. Early decelerations are normal and part of a Category I tracing.
4
Determine the appropriate clinical intervention.
Because both the maternal clinical status and the fetal tracing are reassuring, no acute intervention is required.
A Category I tracing indicates normal fetal acid-base status and warrants routine expectant management.

Anahtar Kavram

Early fetal heart rate decelerations (symmetrical decreases mirroring contractions) are a benign finding caused by fetal head compression and require no intervention.
Soru 1004Soru →

A 35-year-old nulligravid woman with a history of severe endometriosis is undergoing her first in vitro fertilization (IVF) cycle using a standard gonadotropin-releasing hormone (GnRH) antagonist protocol. Arrange the following pharmacological interventions and clinical steps of the IVF cycle in the correct chronological sequence, starting from the beginning of ovarian stimulation to the post-retrieval phase.

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Cevap

The correct chronological sequence for a standard GnRH antagonist IVF cycle is: 1) Exogenous FSH, 2) GnRH antagonist, 3) hCG trigger, 4) Oocyte retrieval, 5) Supplemental progesterone.
In a GnRH antagonist IVF cycle, the treatment begins with exogenous FSH to stimulate multifollicular growth. As follicles enlarge and estradiol levels rise, a GnRH antagonist is introduced (usually on stimulation day 5 or 6) to immediately block pituitary GnRH receptors, preventing a premature LH surge and spontaneous ovulation. Once ultrasound confirms the leading follicles have reached a mature diameter (18-20 mm), an hCG injection is given to mimic the natural LH surge, which induces final oocyte maturation and the resumption of meiosis. Transvaginal oocyte retrieval is strictly scheduled 34-36 hours post-hCG, just prior to expected follicular rupture. Finally, because the physical retrieval process depletes granulosa cells and the patient's endogenous pituitary function was suppressed, the resulting corpus luteum is inadequate; therefore, exogenous progesterone is mandatory for luteal phase support to allow for successful embryo implantation.

Adım Adım Çözüm

1
Identify the goal of the initial phase of the IVF cycle.
The first step is to stimulate multiple follicles using exogenous FSH.
Natural cycles typically yield one dominant follicle; IVF requires multi-follicular development to maximize oocyte yield.
2
Determine the necessary intervention as follicles mature and estrogen levels rise.
A GnRH antagonist must be initiated.
Rising estrogen from multiple developing follicles would normally trigger an LH surge, causing premature ovulation and cycle cancellation. The GnRH antagonist prevents this.
3
Identify the step required for final oocyte maturation once follicles are large enough.
An hCG 'trigger' is administered.
Oocytes must resume meiosis I and detach from the follicular wall, which is naturally driven by the LH surge and mimicked here by hCG.
4
Determine the timing of the procedural harvesting of the oocytes.
Transvaginal oocyte retrieval is performed.
This must be precisely timed (34-36 hours post-trigger) to capture mature oocytes just before they are naturally ovulated into the pelvis.
5
Identify the final required pharmacological support.
Initiation of supplemental progesterone.
The natural luteal phase is defective in IVF cycles due to the aspiration of hormone-producing granulosa cells and previous pituitary suppression, requiring exogenous support for endometrial preparation.

Anahtar Kavram

Pharmacological sequence and endocrinological rationale of controlled ovarian hyperstimulation in In Vitro Fertilization (IVF)
Tahmini Süre:1m 30s
Soru 1005Soru →

Match each underlying etiology of male factor infertility with its characteristic clinical and serum laboratory profile.

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Öğeler

Klinefelter syndrome (47,XXY)
Kallmann syndrome
Exogenous androgen abuse
Cystic fibrosis (CFTR gene mutation)

Eşleşmeler

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Cevap

Klinefelter syndrome matches with elevated FSH/LH and decreased testosterone. Kallmann syndrome matches with decreased FSH/LH and decreased testosterone. Exogenous androgen abuse matches with decreased FSH/LH and elevated testosterone. Cystic fibrosis matches with normal hormone levels.
Male factor infertility can be classified based on the corresponding hormonal profile. Primary testicular failure (e.g., Klinefelter syndrome) results in hypergonadotropic hypogonadism due to loss of negative feedback on the pituitary. Central defects (e.g., Kallmann syndrome) result in hypogonadotropic hypogonadism due to lack of GnRH. Exogenous steroid use mimics central suppression through profound negative feedback, but is uniquely associated with elevated serum testosterone levels. Obstructive causes (e.g., bilateral absence of the vas deferens in cystic fibrosis) do not affect the HPG axis, resulting in completely normal reproductive hormone levels.

Adım Adım Çözüm

1
Identify the primary site of the defect within the hypothalamic-pituitary-gonadal (HPG) axis for each condition.
Categorized conditions into primary hypogonadism, secondary hypogonadism, external suppression, and obstructive processes.
Understanding the HPG axis is crucial for interpreting male reproductive hormone profiles.
2
Evaluate the primary hypogonadism and obstructive etiologies.
Matched Klinefelter syndrome with hypergonadotropic hypogonadism (elevated FSH/LH, low testosterone). Matched CFTR mutation with a normal hormonal profile (obstructive azoospermia).
Testicular failure eliminates negative feedback, whereas obstructive azoospermia leaves the endocrine axis entirely unaffected.
3
Differentiate between central causes and exogenous suppression.
Matched Kallmann syndrome with hypogonadotropic hypogonadism (low FSH/LH, low testosterone). Matched exogenous androgens with suppressed gonadotropins but elevated serum testosterone.
Both central defects and exogenous steroid abuse suppress the pituitary, but exogenous androgens present with high circulating testosterone levels.

Anahtar Kavram

Endocrine evaluation of male factor infertility
Soru 1006Soru →

Identify the most likely underlying etiology for each of the following distinct clinical presentations of postpartum hemorrhage.

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Öğeler

Uterine atony
Genital tract laceration
Retained products of conception
Uterine inversion

Eşleşmeler

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Cevap

Uterine atony matches with a soft, boggy uterus. Genital tract laceration matches with a firm uterus and persistent bleeding. Retained products of conception match with an echogenic mass on ultrasound. Uterine inversion matches with an absent fundus and a vaginal mass.
Each etiology of postpartum hemorrhage possesses distinct clinical hallmarks. Uterine atony fails to compress spiral arteries, leaving the uterus soft and boggy. Lacerations bleed from vaginal or cervical tears despite a properly contracted, firm uterus. Retained products represent physical tissue remnants visible as echogenic masses on ultrasound. Uterine inversion involves the fundus prolapsing through the cervix, creating a palpable vaginal mass and an absent abdominal fundus.

Adım Adım Çözüm

1
Evaluate the clinical presentation for uterine tone and position.
A soft, boggy uterus indicates atony, whereas a firm uterus suggests an alternative source of bleeding such as a laceration.
Uterine tone is the critical initial branch point in the diagnostic algorithm for postpartum hemorrhage.
2
Identify characteristic distinguishing physical and imaging findings for non-atony etiologies.
An absent fundus with a vaginal mass identifies uterine inversion, while an echogenic mass on ultrasound confirms retained products.
Pathognomonic signs allow for rapid differentiation and targeted treatment of less common but critical etiologies of postpartum hemorrhage.

Anahtar Kavram

The clinical differentiation of postpartum hemorrhage etiologies relies primarily on uterine tone, uterine position, and specific physical or sonographic findings.
Soru 1007Soru →

A 31-year-old woman comes to the physician because she has not had a menstrual period since giving birth 13 months ago. Her pregnancy was complicated by placental abruption and severe postpartum hemorrhage requiring the transfusion of 4 units of packed red blood cells. She reports that after delivery, her "milk never came in" despite frequent attempts to breastfeed. Over the past 6 months, she has experienced progressive fatigue, cold intolerance, and occasional dizzy spells when standing up. Physical examination shows a blood pressure of 90/60 mm Hg. There is thinning of the lateral eyebrows and an absence of axillary and pubic hair. Pelvic examination shows vaginal mucosal atrophy. Which of the following is the most likely underlying mechanism for this patient's current symptoms?

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Cevap: Ischemic necrosis of the anterior pituitary gland

Cevap

Ischemic necrosis of the anterior pituitary gland
The correct answer is ischemic necrosis of the anterior pituitary gland (Sheehan syndrome). During pregnancy, the anterior pituitary gland enlarges and becomes highly vascular, making it exquisitely sensitive to hypoperfusion. A massive postpartum hemorrhage (as seen in this patient with placental abruption requiring transfusions) can lead to ischemic necrosis of the gland. This results in panhypopituitarism. The lack of prolactin causes failure to lactate. The lack of gonadotropins (FSH, LH) causes secondary amenorrhea and vaginal atrophy. The lack of TSH causes secondary hypothyroidism (fatigue, cold intolerance, delayed reflexes). Finally, the lack of ACTH leads to secondary adrenal insufficiency, causing hypotension and the loss of axillary and pubic hair (which are dependent on adrenal androgens).

Adım Adım Çözüm

1
Analyze the patient's obstetric history.
The patient experienced placental abruption and massive postpartum hemorrhage requiring blood transfusions.
Identifying severe peripartum hypovolemia establishes the primary risk factor for pituitary ischemia.
2
Evaluate the patient's current symptoms and physical exam findings.
Failure to lactate (prolactin deficiency), secondary amenorrhea and vaginal atrophy (FSH/LH deficiency), fatigue and cold intolerance (TSH deficiency), and hypotension with loss of pubic hair (ACTH deficiency).
Connecting these symptoms reveals a pattern of multiple anterior pituitary hormone deficiencies (panhypopituitarism).
3
Correlate the risk factor with the clinical presentation.
Massive postpartum hemorrhage followed by panhypopituitarism indicates Sheehan syndrome.
The pituitary gland enlarges during pregnancy, making it highly susceptible to ischemic necrosis during episodes of profound hypotension.

Anahtar Kavram

Sheehan syndrome (postpartum pituitary necrosis) presents with panhypopituitarism following massive postpartum hemorrhage, characterized by failure to lactate, amenorrhea, and signs of secondary hypothyroidism and adrenal insufficiency.
Soru 1008Soru →

A 29-year-old G0P0 woman with a body mass index of 33 kg/m233 \text{ kg/m}^2 is evaluated for difficulty conceiving over the past 18 months. She reports menses occurring every 45 to 60 days. Physical examination reveals terminal hair growth on her chin and upper lip. Pelvic ultrasound displays bilaterally enlarged ovaries with multiple small peripheral follicles. Her partner's semen analysis and her hysterosalpingogram are both within normal limits.

Arrange the following management steps for this patient's infertility in the correct evidence-based sequential order, starting from the most appropriate initial step to the most advanced intervention.

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Cevap

The correct sequential order is: 1) Counseling on weight loss and lifestyle modifications, 2) Ovulation induction with oral letrozole, 3) Controlled ovarian hyperstimulation with exogenous gonadotropins, 4) In vitro fertilization (IVF) and embryo transfer.
The correct sequence for managing anovulatory infertility in Polycystic Ovary Syndrome (PCOS) follows an evidence-based, stepwise approach from the least to most invasive intervention. Weight loss and lifestyle modification represent the most appropriate initial step for overweight/obese patients, as losing even a small percentage of body weight can spontaneously restore normal ovulatory cycles. When pharmacologic therapy is required, oral letrozole is the preferred first-line agent. If multiple cycles of oral agents fail, the next progressive step is controlled ovarian hyperstimulation using exogenous gonadotropins. Finally, in vitro fertilization (IVF) is reserved as the most advanced, third-line intervention due to its high cost, invasiveness, and complexity.

Adım Adım Çözüm

1
Identify the patient's underlying diagnosis based on the clinical presentation.
The patient has irregular menses (oligo-ovulation), hyperandrogenism (hirsutism), and polycystic ovaries on ultrasound, confirming Polycystic Ovary Syndrome (PCOS).
Establishing the specific etiology of anovulatory infertility dictates the stepwise treatment algorithm.
2
Determine the most appropriate initial, non-pharmacologic intervention.
Counseling on weight loss and lifestyle modifications.
In overweight patients with PCOS, a minor reduction in body weight can restore spontaneous ovulation and improve baseline fertility.
3
Identify the primary first-line pharmacologic treatment for ovulation induction.
Ovulation induction with oral letrozole.
Current ACOG and ASRM guidelines recommend letrozole over clomiphene as the preferred first-line oral medication for PCOS infertility.
4
Select the appropriate second-line medical therapy if oral agents fail.
Ovulation induction with exogenous gonadotropins.
Gonadotropin injections directly stimulate the ovaries and are utilized when oral agents are unsuccessful.
5
Identify the definitive, most advanced fertility treatment.
In vitro fertilization (IVF).
IVF is reserved as a final option for isolated PCOS infertility due to its high cost and invasive nature.

Anahtar Kavram

Stepwise management of infertility in Polycystic Ovary Syndrome (PCOS)
Soru 1009Soru →

A primigravida at 41 weeks of gestation is in the second stage of labor. Following the delivery of the fetal head, it immediately retracts tightly against the maternal perineum. The attending physician attempts gentle downward traction, but the anterior shoulder fails to pass beneath the pubic symphysis. Arrange the following interventions in the correct chronological sequence of escalation for managing this obstetric emergency.

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Cevap

The correct sequence of management for shoulder dystocia progresses from immediately halting pushing and calling for help, to external positional maneuvers (McRoberts and suprapubic pressure), followed by internal vaginal maneuvers (delivering the posterior arm), and finally culminating in catastrophic interventions like cephalic replacement (Zavanelli maneuver) if all else fails.
The algorithm for shoulder dystocia is strictly sequential to minimize fetal and maternal morbidity. It begins with immediate recognition and halting of pushing (which worsens impaction), followed by external positional changes (McRoberts maneuver) and suprapubic pressure. If these fail, the physician must move to internal maneuvers, such as delivering the posterior arm or performing rotational maneuvers (Woods corkscrew, Rubin). Only when all vaginal delivery options have failed is the Zavanelli maneuver (cephalic replacement followed by cesarean delivery) indicated as a last resort.

Adım Adım Çözüm

1
Recognize the turtle sign and immediately call for help while instructing the mother to stop pushing.
Prevents further impaction of the anterior shoulder and ensures adequate personnel are present.
Pushing against an impacted shoulder stretches the brachial plexus and worsens the dystocia.
2
Perform the McRoberts maneuver simultaneously with suprapubic pressure.
Rotates the maternal symphysis pubis superiorly and attempts to push the fetal shoulder obliquely.
These are the most successful and least invasive first-line maneuvers to relieve the obstruction.
3
Perform internal maneuvers, such as delivery of the posterior arm or Woods corkscrew maneuver.
Reduces the biacromial diameter of the fetus by 2 to 3 centimeters, allowing the anterior shoulder to slide under the symphysis.
Required when external manipulation fails to alter the pelvic geometry enough to permit delivery.
4
Execute the Zavanelli maneuver (cephalic replacement).
Returns the fetus to the uterine cavity, allowing for an emergency cesarean delivery.
This is a salvage procedure of last resort associated with high morbidity, used only when all other methods have failed to prevent fetal asphyxia.

Anahtar Kavram

The sequential management of shoulder dystocia emphasizes progressing from the least invasive external maneuvers to internal manipulations, reserving highly morbid interventions for refractory cases.
Soru 1010Soru →

Secondary amenorrhea and anovulatory infertility can result from various distinct pathophysiologic processes affecting the hypothalamic-pituitary-ovarian (HPO) axis. Match each patient's clinical presentation with its most characteristic serum endocrine laboratory profile.

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Öğeler

A 22-year-old competitive cross-country runner with a body mass index of 17 kg/m²
A 33-year-old with severe hot flashes, vaginal dryness, and a history of FMR1 gene premutation
A 28-year-old with worsening facial acne, hirsutism, and a body mass index of 32 kg/m²
A 30-year-old with persistent bilateral galactorrhea and intermittent headaches

Eşleşmeler

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Cevap

The competitive runner matches with decreased FSH, LH, and estradiol (functional hypothalamic amenorrhea). The patient with the FMR1 premutation matches with elevated FSH/LH and decreased estradiol (primary ovarian insufficiency). The patient with hirsutism matches with normal/elevated LH and normal estradiol (polycystic ovary syndrome). The patient with galactorrhea matches with elevated prolactin and suppressed gonadotropins (prolactinoma).
Each condition affects the hypothalamic-pituitary-ovarian axis uniquely: functional hypothalamic amenorrhea suppresses central GnRH (leading to low FSH, LH, and estradiol); primary ovarian insufficiency represents primary end-organ failure without central negative feedback (leading to high FSH, high LH, and low estradiol); polycystic ovary syndrome is a normogonadotropic state with altered pulsatility (leading to high/normal LH, normal FSH, and normal estradiol); and prolactinomas suppress GnRH via elevated prolactin levels.

Adım Adım Çözüm

1
Analyze each clinical presentation to determine the underlying etiology of the amenorrhea and infertility.
Identify functional hypothalamic amenorrhea, primary ovarian insufficiency, polycystic ovary syndrome, and prolactinoma.
Accurate diagnosis of the underlying mechanism is required to predict the downstream laboratory profile.
2
Determine the state of the hypothalamic-pituitary-ovarian axis for each identified etiology.
Map each condition to its specific gonadotropin (FSH, LH) and sex steroid (estradiol) pattern based on the level of the defect.
Different etiologies disrupt the HPO axis at different anatomical levels (hypothalamus, pituitary, or ovary), resulting in distinct, recognizable endocrine signatures.

Anahtar Kavram

Endocrine evaluation of secondary amenorrhea and infertility localizes the physiological defect to the hypothalamus, pituitary, or ovaries based on the pattern of FSH, LH, and estradiol levels.
Soru 1011Soru →

A 2424-year-old nulliparous woman at 3939 weeks of gestation is evaluated in the labor unit. She was admitted 2020 hours ago following spontaneous rupture of membranes. She has been having irregular, mild contractions. Her temperature is 39.0∘C39.0^\circ\text{C} (102.2∘F102.2^\circ\text{F}), blood pressure is 112/72 mm Hg112/72\text{ mm Hg}, pulse is 118/min118/\text{min}, and respirations are 18/min18/\text{min}. Fetal heart rate monitoring demonstrates a baseline of 175/min175/\text{min} with moderate variability and no decelerations. The uterine fundus is tender to palpation. Cervical examination reveals 4 cm4\text{ cm} dilation and 80%80\% effacement. Purulent-appearing fluid is noted in the vaginal vault. When discussing possible interventions, the patient expresses severe anxiety about surgical procedures and states, 'I will absolutely not consent to a cesarean delivery under any circumstances, even if the baby is in distress.' She is fully conscious, competent, and understands the risks associated with her refusal. Which of the following is the most appropriate next step in management?

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Cevap: Intravenous administration of broad-spectrum antibiotics and oxytocin augmentation

Cevap

Intravenous administration of broad-spectrum antibiotics and oxytocin augmentation
The patient's clinical presentation—fever, maternal and fetal tachycardia, fundal tenderness, and purulent vaginal fluid following prolonged rupture of membranes—is diagnostic of intra-amniotic infection (chorioamnionitis). The standard of care for this obstetric complication is the prompt administration of intravenous broad-spectrum antibiotics (typically ampicillin and gentamicin) and the expedition of delivery. Because there are no absolute contraindications to vaginal delivery and the fetal heart tracing is reassuring despite the tachycardia (moderate variability is present), augmenting labor with oxytocin is medically appropriate. Crucially, this management plan also strictly respects the competent patient's fundamental right to refuse surgical intervention.

Adım Adım Çözüm

1
Diagnose the primary obstetric complication.
The patient has intra-amniotic infection (chorioamnionitis), indicated by maternal fever (>39.0∘C>39.0^\circ\text{C}), fetal tachycardia, prolonged rupture of membranes, purulent fluid, and uterine tenderness.
Accurate diagnosis dictates the need for urgent antibiotic therapy and expedition of delivery.
2
Determine the appropriate medical therapy.
Broad-spectrum intravenous antibiotics (e.g., ampicillin and gentamicin) must be administered.
Intra-amniotic infections are polymicrobial and require comprehensive coverage; narrow-spectrum monotherapy is inadequate.
3
Evaluate the route of delivery in the context of fetal status and ethical constraints.
Augmentation of labor with oxytocin is selected to expedite a vaginal delivery.
The fetal heart tracing shows moderate variability (reassuring), meaning immediate surgical rescue is not indicated. Furthermore, the patient is competent and has explicitly refused a cesarean delivery, an autonomous decision that must be legally and ethically respected.

Anahtar Kavram

Diagnosis and management of intra-amniotic infection combined with maternal autonomy
Tahmini Süre:1m 30s
Soru 1012Soru →

An obstetric patient at 39 weeks gestation is admitted to the labor suite for induction of labor due to chronic hypertension. A continuous oxytocin infusion is currently being administered to augment uterine contractions. The patient's blood pressure is 138/88 mmHg. The continuous electronic fetal monitor displays a baseline heart rate of 145/min with moderate variability. The tracing demonstrates recurrent, gradual decreases in the fetal heart rate, with each deceleration starting after the peak of a uterine contraction and returning to baseline only after the contraction has completely finished. The contractions are occurring every 2 to 3 minutes. Cervical examination shows 5 cm dilation and 90% effacement. Which of the following is the most appropriate initial step in the management of this patient?

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Cevap: Discontinue the continuous oxytocin infusion

Cevap

Discontinue the continuous oxytocin infusion
The patient is experiencing recurrent late decelerations, which are characterized by a gradual decrease in the fetal heart rate that begins after the peak of the uterine contraction. This pattern indicates uteroplacental insufficiency, resulting in transient fetal hypoxemia. The most appropriate initial step is intrauterine resuscitation aimed at maximizing uteroplacental blood flow and fetal oxygenation. Essential steps include maternal repositioning (typically left lateral decubitus), administering intravenous fluids, providing supplemental oxygen, and immediately discontinuing any uterotonic agents. Therefore, stopping the oxytocin infusion is a critical and necessary intervention.

Adım Adım Çözüm

1
Analyze the fetal heart rate tracing description.
The gradual decreases starting after the peak of a contraction and ending after the contraction finishes are defined as late decelerations.
Accurate identification of the deceleration type is required to determine the underlying pathophysiology.
2
Determine the etiology of the identified decelerations.
Late decelerations are caused by uteroplacental insufficiency, meaning the fetus is experiencing transient hypoxemia during contractions.
Understanding the cause guides the specific resuscitative interventions.
3
Select the most appropriate initial management step.
The immediate goal is to improve uteroplacental blood flow through intrauterine resuscitation. A key step is decreasing uterine work by stopping any uterotonic agents.
Oxytocin stimulates contractions which reduce blood flow to the placenta; stopping it allows the uterus to relax and restores fetal oxygenation.

Anahtar Kavram

Recurrent late decelerations indicate uteroplacental insufficiency. Initial management involves intrauterine resuscitation, which includes maternal repositioning, supplemental oxygen, intravenous fluids, and discontinuation of uterotonic agents like oxytocin.
Soru 1013Soru →

A 28-year-old G3P3 woman experiences sudden cardiovascular collapse and a large gush of vaginal bleeding immediately following the vaginal delivery of a healthy infant at 39 weeks of gestation. Physical examination reveals a beefy red, smooth mass protruding from the introitus. The uterine fundus cannot be palpated on abdominal examination. Her blood pressure is 75/40 mm Hg and pulse is 130/min. Intravenous fluids and blood products are rapidly initiated. Arrange the following steps in the correct escalation sequence for the definitive management of this patient's condition.

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Cevap

The correct sequence is: (1) Attempt immediate manual replacement, (2) administer a uterine relaxant if needed, (3) proceed to surgical repositioning if manual methods fail, and (4) administer uterotonic agents once the uterus is reverted.
The standard escalation protocol for acute uterine inversion begins with an immediate attempt at manual replacement. If unsuccessful, uterine relaxants are given to facilitate manual reduction. If pharmacological relaxation fails, surgical repositioning (laparotomy) is required. Once the uterus is successfully reverted by any method, uterotonic agents are administered to maintain uterine tone and prevent reinversion.

Adım Adım Çözüm

1
Identify the clinical diagnosis.
The presentation of a protruding vaginal mass, absent uterine fundus, and profound shock postpartum indicates acute uterine inversion.
Accurate diagnosis is required to initiate the specific management algorithm.
2
Determine the initial definitive intervention.
Attempt immediate manual replacement of the uterus.
Prompt manual reduction is often successful if performed immediately before a cervical contraction ring forms.
3
Determine the next step if initial reduction fails.
Administer a uterine relaxant (e.g., nitroglycerin).
Uterine relaxation resolves the cervical constriction ring, facilitating manual replacement.
4
Determine the surgical step if pharmacological relaxation fails.
Proceed to laparotomy for surgical repositioning.
Refractory cases require surgical intervention to physically revert the uterus.
5
Determine the final maintenance step.
Administer uterotonic agents.
Once reverted, the uterus must be kept firmly contracted to prevent recurrence and control bleeding.

Anahtar Kavram

Management algorithm for acute uterine inversion
Tahmini Süre:1m 0s
Soru 1014Soru →

A 31-year-old woman, gravida 2, para 1, is evaluated in the labor and delivery ward at 38 weeks of gestation. She reports regular, painful uterine contractions. Her prenatal course was notable for a second-trimester ultrasound showing a succenturiate placental lobe. On admission, her blood pressure is 116/74 mm Hg, and her heart rate is 84/min. The fetal heart rate tracing demonstrates a baseline of 145/min with moderate variability and no decelerations. Cervical examination reveals 5 cm dilation and 80% effacement with a bulging amniotic sac. The attending physician performs an artificial rupture of membranes to augment labor. Immediately following the procedure, the patient experiences a sudden gush of bright red vaginal bleeding. The patient reports no new abdominal pain. Simultaneously, the fetal heart rate drops abruptly to a baseline of 70/min and remains there for 4 minutes. The patient is awake, alert, and expresses concern about the baby's status. Which of the following is the most appropriate next step in management?

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Cevap: Emergency cesarean delivery

Cevap

The correct answer is to proceed with an emergency cesarean delivery.
The patient's presentation of sudden, painless vaginal bleeding and acute fetal bradycardia immediately after an amniotomy is the classic presentation of a ruptured vasa previa. A succenturiate placental lobe is a major risk factor, as fetal vessels often connect the lobes through the membranes. Because the bleeding originates from the fetus, exsanguination occurs rapidly, resulting in profound fetal distress. The only appropriate life-saving intervention is an immediate emergency cesarean delivery.

Adım Adım Çözüm

1
Analyze the clinical presentation and timing of symptoms.
The patient developed sudden, painless vaginal bleeding accompanied by acute fetal bradycardia immediately following artificial rupture of membranes.
Establishing the precise sequence of events (amniotomy followed by bleeding and fetal distress) is critical for diagnosis.
2
Identify relevant risk factors from the patient's prenatal history.
The patient has a known succenturiate placental lobe.
A succenturiate lobe significantly increases the risk of fetal blood vessels traversing the amniotic membranes (vasa previa).
3
Synthesize the findings to determine the most likely diagnosis.
The combination of a succenturiate lobe, amniotomy, sudden painless bleeding, and immediate fetal bradycardia strongly indicates a ruptured vasa previa.
Rupture of unprotected fetal vessels leads to rapid fetal exsanguination, which causes sudden and prolonged fetal heart rate decelerations or bradycardia.
4
Select the definitive management strategy based on the diagnosis.
Emergency cesarean delivery must be performed immediately.
Fetal blood volume is very small, and hemorrhage from ruptured vasa previa is rapidly fatal unless the fetus is delivered expeditiously.

Anahtar Kavram

Vasa previa classically presents with sudden, painless vaginal bleeding and acute fetal distress (e.g., bradycardia) immediately following the rupture of membranes, necessitating emergency cesarean delivery to prevent fetal exsanguination.
Soru 1015Soru →

Match the following clinical presentations of couples experiencing infertility with their most appropriate first-line targeted fertility treatment or management strategy.

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Öğeler

30-year-old female with BMI of 33 kg/m², oligoovulation, and clinical hyperandrogenism
28-year-old female with primary infertility and bilateral hydrosalpinges identified on hysterosalpingography
32-year-old female with secondary amenorrhea, galactorrhea, and a 6-mm pituitary adenoma on MRI
Couple whose male partner has a semen analysis showing a sperm concentration of 2 million/mL with 5% motility

Eşleşmeler

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Cevap

PCOS is treated first-line with Letrozole; bilateral tubal factor requires standard IVF; a prolactinoma is managed medically with Cabergoline; and severe male factor infertility (oligospermia/asthenospermia) necessitates ICSI.
Optimal management of infertility requires directing therapy at the underlying pathophysiologic defect. Endocrine abnormalities like PCOS and hyperprolactinemia are managed with targeted pharmacotherapy (letrozole and cabergoline, respectively), while anatomical barriers (tubal occlusion) and severe sperm deficits require specific assisted reproductive technologies (IVF and ICSI).

Adım Adım Çözüm

1
Analyze the clinical presentation to establish the primary mechanism of infertility (ovulatory, tubal, central/endocrine, or male factor).
Identified four distinct etiologies: PCOS (ovulatory), bilateral hydrosalpinges (tubal), prolactinoma (central endocrine), and severe oligospermia/asthenospermia (male factor).
Correctly identifying the anatomic or endocrine defect dictates the specific interventional pathway.
2
Select the standard-of-care, first-line intervention that directly addresses the identified defect.
Matched PCOS to letrozole for ovulation induction, and prolactinoma to cabergoline for medical suppression.
Evidence-based guidelines prioritize targeted medical therapies before invasive or broadly applied assisted reproductive technologies when specific, reversible endocrine issues are identified.
3
Differentiate between indications for standard in vitro fertilization versus those requiring intracytoplasmic sperm injection.
Assigned standard IVF to tubal factor and reserved ICSI for severe male factor infertility.
Tubal factor simply requires bypassing the fallopian tubes (IVF), while severe male factor requires bypassing the sperm's need to independently penetrate the zona pellucida (ICSI).

Anahtar Kavram

Etiology-specific management of infertility algorithms
Soru 1016Soru →

Match each distinctive clinical presentation or intrapartum event to the most appropriate obstetric complication.

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Öğeler

Sudden cessation of active labor contractions, acute tearing abdominal pain, and palpation of fetal parts outside the uterine contour.
Painless vaginal bleeding immediately following artificial rupture of membranes, accompanied by a rapid, sustained drop in fetal heart rate.
Sudden onset of severe, continuous abdominal pain, a board-like and tender uterus, and high-frequency, low-amplitude uterine contractions.
An episode of bright red, painless vaginal bleeding in the third trimester with a soft, non-tender uterus and a reactive fetal heart tracing.

Eşleşmeler

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Cevap

The presentations map to their respective etiologies based on the presence or absence of pain, uterine tone, and fetal heart rate changes: loss of contractions with palpable fetal parts indicates uterine rupture; painless bleeding post-amniotomy with fetal bradycardia indicates vasa previa; painful bleeding with a rigid uterus indicates placental abruption; and painless bleeding with a soft uterus indicates placenta previa.
Each clinical presentation contains classic pathognomonic features that reliably differentiate the four most critical etiologies of late pregnancy and intrapartum hemorrhage.

Adım Adım Çözüm

1
Evaluate the clinical presentation of sudden tearing pain, cessation of contractions, and palpable fetal parts.
Matches with Uterine rupture.
These findings are pathognomonic for a complete transmural tear of the uterus, allowing the fetus to extrude into the maternal abdomen.
2
Evaluate the presentation of painless bleeding immediately following amniotomy, paired with rapid fetal bradycardia.
Matches with Vasa previa.
The timing of bleeding (synchronous with membrane rupture) and rapid fetal decompensation strongly suggest torn fetal vessels crossing the internal os.
3
Evaluate the presentation of severe constant pain, a rigid uterus, and high-frequency contractions.
Matches with Placental abruption.
Concealed or revealed bleeding behind the placenta acts as a profound uterine irritant, causing constant pain and hypertonus.
4
Evaluate the presentation of third-trimester painless bleeding with a soft, non-tender uterus.
Matches with Placenta previa.
Bleeding is strictly maternal in origin from the lower uterine segment and does not typically irritate the myometrium or cause immediate fetal distress.

Anahtar Kavram

Differentiating third-trimester bleeding and intrapartum emergencies requires analyzing maternal pain, uterine tone, contraction patterns, and the timing of fetal distress.
Tahmini Süre:1m 30s
Soru 1017Soru →

A pregnant individual at 33 weeks of gestation presents to the obstetrical triage unit reporting a sudden gush of clear vaginal fluid that occurred two hours ago. She has not experienced any abdominal pain, uterine contractions, or vaginal bleeding. Her previous pregnancy resulted in an uncomplicated vaginal delivery at term. Vital signs show a temperature of 37.2°C (99.0°F), blood pressure of 112/72 mm Hg, pulse of 88/min, and respiratory rate of 16/min. A sterile speculum examination confirms a closed external cervical os with a pool of clear fluid in the posterior vaginal fornix that turns nitrazine paper blue. Laboratory evaluation demonstrates a leukocyte count of 14,500/mm³. Continuous fetal monitoring shows a baseline heart rate of 145/min with moderate variability and no decelerations. Tocodynamometry reveals no uterine activity. Which of the following is the most appropriate next step in the management of this patient?

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Cevap: Admit the patient, administer intramuscular betamethasone, and start ampicillin and azithromycin

Cevap

Admit the patient, administer intramuscular betamethasone, and start ampicillin and azithromycin
This patient presents with preterm premature rupture of membranes (PPROM) at 33 weeks of gestation without signs of intra-amniotic infection or fetal compromise. The most appropriate next step is expectant management. This includes admission for inpatient observation, administration of intramuscular corticosteroids (e.g., betamethasone) to accelerate fetal lung maturity, and targeted latency antibiotics (typically a macrolide such as azithromycin and a beta-lactam such as ampicillin) to prolong the pregnancy and reduce the risk of ascending infection.

Adım Adım Çözüm

1
Diagnose the primary condition
Preterm premature rupture of membranes (PPROM)
The patient presents with a gush of fluid, pooling in the vaginal vault, and a positive nitrazine test prior to the onset of labor.
2
Determine the gestational age and clinical stability
The patient is at 33 weeks of gestation and is clinically stable.
Vital signs are normal, FHR tracing is reassuring, and there are no signs of chorioamnionitis. The mild leukocytosis is a physiologic change of pregnancy.
3
Select the appropriate management algorithm based on gestational age
Expectant management with corticosteroids and latency antibiotics
For uncomplicated PPROM between 24 and 34 weeks, the goal is to prolong gestation to allow fetal lung maturity. Magnesium sulfate is only added if less than 32 weeks.

Anahtar Kavram

Management of preterm premature rupture of membranes (PPROM) relies heavily on gestational age, with expectant management and latency antibiotics favored between 24 and 34 weeks, and immediate delivery favored at or after 34 weeks or if intrauterine infection occurs.
Tahmini Süre:1m 0s
Soru 1018Soru →

Correlate the following clinical descriptions of late-pregnancy obstetric emergencies with their corresponding anatomical or pathophysiological etiology.

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Öğeler

Sudden-onset, painful dark red vaginal bleeding with a hypertonic, tender uterus in a patient with severe chronic hypertension.
Painless, bright red vaginal bleeding noted shortly after sexual intercourse in a patient with a history of two prior cesarean deliveries.
Acute vaginal bleeding accompanied by a rapid drop in fetal heart rate to 80/min occurring immediately following artificial rupture of membranes.
Sudden, tearing abdominal pain with an abrupt cessation of previously regular uterine contractions and a palpable fetal part in the maternal abdomen.

Eşleşmeler

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Cevap

The correct correlations link painful bleeding with hypertonia to premature placental separation (abruption); painless postcoital bleeding to placental implantation over the cervical os (previa); bleeding with fetal bradycardia after membrane rupture to unprotected fetal vessels (vasa previa); and tearing pain with contraction cessation to full-thickness uterine disruption (rupture).
Each clinical vignette provides the classic hallmark features of a specific obstetric emergency. Recognizing whether the bleeding is painful or painless, evaluating the timing of fetal distress relative to membrane rupture, and assessing uterine tone are critical diagnostic steps for distinguishing between these third-trimester and intrapartum complications.

Adım Adım Çözüm

1
Evaluate the patient presenting with painful, dark red bleeding and a hypertonic uterus.
This matches with premature separation of the placenta from the uterine decidua.
Hypertension is a major risk factor for placental abruption, which causes bleeding into the decidua basalis, leading to intense pain and sustained uterine irritability (hypertonia).
2
Analyze the case of painless, bright red bleeding following intercourse.
This matches with implantation of placental tissue extending over the internal cervical os.
Placenta previa presents painlessly and is often triggered by mechanical disruption of the highly vascular placental tissue near the cervix, such as during coitus or cervical exams.
3
Assess the scenario involving bleeding and fetal bradycardia immediately post-amniotomy.
This matches with fetal blood vessels traversing the amniotic membranes unprotected by Wharton jelly.
Artificial rupture of membranes can easily lacerate these unprotected vessels (vasa previa), causing rapid fetal exsanguination and an immediate fetal heart rate deceleration.
4
Evaluate the presentation of tearing abdominal pain, loss of contractions, and palpable fetal parts.
This matches with complete, full-thickness disruption of the uterine wall.
These catastrophic findings signify that the fetus has extruded into the maternal abdomen due to a uterine rupture, an acute emergency most common in patients undergoing a trial of labor after a prior cesarean delivery.

Anahtar Kavram

Differentiating etiologies of third-trimester bleeding and intrapartum emergencies based on maternal and fetal clinical signs.
Soru 1019Soru →

A 25-year-old nulligravid woman presents to the clinic reporting an inability to conceive for the past 16 months. She and her partner have regular unprotected intercourse. The patient has a history of unpredictable menstrual cycles since menarche at age 12, often going 3 to 4 months between menses. Over the past few years, she has noted progressive development of dark, coarse hair on her upper lip, chin, and chest. She takes a daily multivitamin. Her BMI is 31 kg/m231 \text{ kg/m}^2. Physical examination is notable for hirsutism, moderate facial acne, and thickened, velvety, hyperpigmented skin on the nape of her neck. Pelvic examination is normal. Transvaginal ultrasonography reveals bilaterally enlarged ovaries, each containing about 20 small peripheral follicles. A urine pregnancy test is negative. Serum thyroid-stimulating hormone and prolactin levels are within normal limits.

To formally confirm the most likely diagnosis, which of the following diagnostic tests is required to exclude a phenotypically similar mimicking condition?

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Cevap: Serum 17-hydroxyprogesterone

Cevap

Serum 17-hydroxyprogesterone
The correct answer is serum 17-hydroxyprogesterone. This patient presents with the classic triad of oligo-ovulation, clinical hyperandrogenism (hirsutism, acne), and polycystic ovaries, strongly suggesting Polycystic Ovary Syndrome (PCOS). However, PCOS is fundamentally a diagnosis of exclusion. Non-classic congenital adrenal hyperplasia (NCCAH), typically due to a partial 21-hydroxylase deficiency, can present identically with irregular menses, hirsutism, and even polycystic ovarian morphology on ultrasound. Therefore, clinical guidelines mandate measuring an early morning serum 17-hydroxyprogesterone level in all women with suspected PCOS to rule out NCCAH before a definitive diagnosis can be made.

Adım Adım Çözüm

1
Identify the patient's triad of symptoms
Oligomenorrhea, clinical hyperandrogenism (hirsutism, acne), and polycystic ovaries on ultrasound.
These findings fulfill all three components of the Rotterdam criteria for suspected Polycystic Ovary Syndrome (PCOS).
2
Recall the diagnostic prerequisites for PCOS
PCOS is a diagnosis of exclusion. Mimicking conditions must be ruled out.
Endocrine disorders such as thyroid disease, hyperprolactinemia, and congenital adrenal hyperplasia can present identically to PCOS.
3
Select the appropriate exclusionary laboratory test
Serum 17-hydroxyprogesterone must be ordered.
It specifically screens for non-classic congenital adrenal hyperplasia (21-hydroxylase deficiency), which is a common mimic of PCOS in young women.

Anahtar Kavram

The diagnosis of Polycystic Ovary Syndrome (PCOS) requires the exclusion of mimicking hyperandrogenic disorders. Serum 17-hydroxyprogesterone is routinely measured to rule out non-classic congenital adrenal hyperplasia.
Tahmini Süre:1m 15s
Soru 1020Soru →

Match the following structural imaging or procedural findings encountered during a female infertility evaluation with their most likely underlying diagnosis.

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Öğeler

Hysterosalpingogram demonstrates dilated, fluid-filled, sausage-shaped adnexal structures with an absence of free contrast spill into the peritoneal cavity.
Saline infusion sonohysterography shows a well-circumscribed, echogenic mass projecting directly into the endometrial cavity, distorting its contour.
Pelvic magnetic resonance imaging reveals a deep external fundal indentation (greater than 1 cm) with two distinct, widely separated endometrial cavities.
Hysteroscopy displays multiple dense, avascular fibrous bands bridging the anterior and posterior surfaces of the endometrium.

Eşleşmeler

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Cevap

The correct pairings identify structural causes of female infertility based on their classic diagnostic imaging or procedural appearances: hydrosalpinx (dilated tubes without spill), submucosal leiomyoma (intracavitary mass), bicornuate uterus (fundal indentation), and Asherman syndrome (intrauterine adhesions).
Each structural abnormality produces a distinct morphological signature on imaging or direct visualization. Hydrosalpinx involves the adnexa, submucosal leiomyoma distorts the internal endometrial cavity, bicornuate uterus alters the external fundal contour, and Asherman syndrome creates internal fibrous adhesions.

Adım Adım Çözüm

1
Evaluate the adnexal findings on hysterosalpingogram.
Dilated tubes with absent intraperitoneal spill indicate distal tubal obstruction, classically representing a hydrosalpinx.
Contrast must spill freely into the pelvis in normal patent fallopian tubes.
2
Assess the intracavitary mass seen on sonohysterography.
An echogenic mass distorting the endometrial contour is characteristic of a submucosal leiomyoma.
Fibroids in this location are a known structural cause of implantation failure and early pregnancy loss.
3
Analyze the uterine contour abnormality on MRI.
A deep external fundal cleft (>1 cm) signifies a fusion defect, diagnostic of a bicornuate uterus.
Differentiating between fusion anomalies (bicornuate) and resorption anomalies (septate) requires assessing the external fundal contour.
4
Interpret the direct visualization findings on hysteroscopy.
Avascular fibrous bands traversing the cavity confirm intrauterine synechiae, or Asherman syndrome.
Prior endometrial trauma leads to scarring, which mechanically obliterates the cavity and causes amenorrhea or infertility.

Anahtar Kavram

Structural etiologies of female infertility and their characteristic diagnostic imaging findings.
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Obstetrics and Gynecology Alıştırma Soruları — USMLE Step 2 CK — Sayfa 51 | Examkin