Keywords in Stem

• “Pudendal nerve block” – Directly points to the target nerve for anesthesia.
• “Landmark” – Indicates the question is asking for an anatomical point of needle insertion.

The pudendal nerve is consistently located near the ischial spine, making it the essential landmark for performing a pudendal nerve block during labor.

Explanation 

(Option B) Ischial spine:

• ✔ Correct landmark for pudendal nerve block.
• The pudendal nerve passes posterior to the ischial spine and medial to the sacrospinous ligament.
• During a transvaginal pudendal nerve block, the ischial spine is palpated through the vaginal wall as a bony prominence.
• A needle is inserted near the ischial spine to deliver local anesthetic around the pudendal nerve, providing pain relief in the perineum and lower vagina during late labor or episiotomy.

 (Option A) Pubic symphysis:

• Not related to pudendal nerve.
• This midline structure is an anterior bony landmark, associated more with bladder and pelvic bone anatomy.
• It is not close to the course of the pudendal nerve.

 (Option C) Sacral promontory:

• Too high and posterior.
• The sacral promontory marks the border between the lumbar spine and sacrum, and is part of the pelvic inlet.
• It is not near the ischial spine or pudendal nerve, and thus not used for a pudendal block.

 (Option D) Iliac crest:

• Lateral and superior landmark.
• The iliac crest is the uppermost edge of the ilium, used for lumbar puncture (L4 level) identification.
• It is not near the pelvic outlet or pudendal nerve.

 (Option E) Greater sciatic foramen:

• Incorrect approach site.
• While the pudendal nerve exits the pelvis through the greater sciatic foramen, the block is not performed here.
• It re-enters via the lesser sciatic foramen and becomes accessible near the ischial spine, which is the correct landmark.

Key Concept

Pudendal nerve block is performed transvaginally by palpating the ischial spine, where the pudendal nerve lies close to the sacrospinous ligament. This provides anesthesia to the perineum, vulva, and lower vagina — crucial for instrumental deliveries or episiotomy.

Subject: Obstetrics & Gynecology (Pelvic Anatomy)

System: Reproductive System – Nerve Supply 

Topic: Anatomy – Pelvic Nerve Landmarks and Nerve Blocks

Anatomy – Pelvic Nerve Landmarks and Nerve Blocks

Summary Point

Pudendal nerve block is the most important for obstetric perineal anesthesia, and the ischial spine is the consistent landmark for accurate nerve localization.

                                           Pudendal Nerve Block

Keywords in Stem 

• Prominent sacral promontory
• Narrow interspinous distance

Reason:

These features indicate midpelvic narrowing, a classic cause of cephalopelvic disproportion, leading to labor arrest/failure to progress.

Classic Triad:

Pelvic inlet contraction + midpelvis narrowing + labor arrest → strongly points to cephalopelvic disproportion (CPD).

Explanation

(Option C) Cephalopelvic disproportion:

• Cephalopelvic disproportion (CPD) refers to a mismatch between the size of the fetal head and the maternal pelvis, preventing the baby from descending through the birth canal.
• The prominent sacral promontory and narrow interspinous diameter are classic signs of an android or anthropoid pelvis, both of which are associated with narrow midpelvis, leading to mechanical obstruction.
• CPD commonly presents as failure to progress during labor, especially during the active phase of the first stage or during descent in the second stage.

(Option A) Shoulder dystocia:

• Occurs when the fetal anterior shoulder gets impacted behind the maternal pubic symphysis after the head is delivered.
• More commonly associated with macrosomia, diabetes, or post-term pregnancy.
• Not directly related to pelvic shape or narrow interspinous distance, but more to shoulder-to-head ratio.

(Option B) Prolonged latent phase:

• Refers to slow cervical dilation in the early phase of labor (latent phase).
• Usually related to ineffective uterine contractions or sedation, not pelvic anatomy.
• A narrow pelvis more commonly affects the active phase or descent, not the latent phase.

(Option D) Cord prolapse:

• Involves the umbilical cord slipping past the presenting part.
• More common in cases of malpresentation (breech, transverse lie) or with artificial rupture of membranes when the presenting part is not engaged.
• Not associated with pelvic architecture.

(Option E) Postpartum hemorrhage (PPH):

• Usually caused by uterine atony, retained placenta, trauma, or coagulopathy.
• Not linked with pelvic shape or interspinous diameter.
• May occur in prolonged labor but is not the most direct risk based on the pelvic exam findings described.

Key Concept

A narrow midpelvis — characterized by a prominent sacral promontory and reduced interspinous diameter — increases the risk of cephalopelvic disproportion (CPD), leading to failure to progress during labor.

This is a classic sign of mechanical obstruction in labor due to pelvic anatomy, most commonly seen in android pelvis.

Subject: Obstetrics & Gynecology (Obstetrical Anatomy)

System: Female Reproductive System – Obstetric Pelvimetry – ANATOMY OF REPRODUCTIVE AND GENITAL TRACT – Detailed anatomy of male and female Pelvis – Bones 

Topic: Obstetrics – Pelvic Types and Their Impact on Labor (Obstetric Pelvimetry)

Obstetrics – Pelvic Types and Their Impact on Labor (Obstetric Pelvimetry)

Keywords in the Stem to Identify the Correct Option (Müllerian agenesis – MRKH syndrome):

• Primary amenorrhea
  → Suggests an underlying congenital or hormonal abnormality in a pubertal-age girl.
• Normal breast and axillary hair development
  → Indicates normal estrogen production, ruling out hypogonadism or androgen insensitivity.
• Blind-ending vagina + absent uterus on ultrasound
  → Classic for Müllerian agenesis (MRKH) where upper vagina and uterus fail to develop.

Classic Triad of MRKH Syndrome in the Stem:

1. Primary amenorrhea
2. Normal secondary sexual characteristics (breasts, axillary hair)
3. Absent uterus and blind vagina

This triad strongly points toward MRKH syndrome (Müllerian agenesis).

Explanation 

(Option D) Müllerian agenesis (MRKH syndrome):

• Also known as Mayer-Rokitansky-Küster-Hauser syndrome, this is a congenital disorder characterized by the aplasia or hypoplasia of the Müllerian ducts, leading to the absence or underdevelopment of the uterus and upper two-thirds of the vagina.
• Patients are phenotypic females with normal secondary sexual characteristics (breasts, axillary/pubic hair), but absence of uterus and upper vagina due to Müllerian duct agenesis.
• Ovarian function is normal, so estrogen-dependent changes (breast development) occur normally.

(Option A) Androgen insensitivity syndrome (AIS):

• These individuals are genetically male (46,XY) but resistant to androgens.
• They present with female external genitalia and breast development, but absent pubic/axillary hair and no uterus or ovaries.
• Ovaries are absent, and testes are usually intra-abdominal or inguinal.

 (Option B) Turner syndrome:

• Characterized by 45,X karyotype with streak ovaries, leading to low estrogen, no breast development, and primary amenorrhea.
• Usually associated with short stature, webbed neck, and cardiac/renal anomalies.
• Uterus is present due to the female phenotype.

 (Option C) Transverse vaginal septum:

• This is a structural outflow tract abnormality, with normal uterus and ovaries.
• Presents with cyclic pelvic pain, hematocolpos, and primary amenorrhea.
• Vaginal canal may be short or obstructed, but uterus is present on imaging.

 (Option E) Kallmann syndrome:

• A GnRH deficiency disorder associated with anosmia, hypogonadism, and delayed or absent puberty.
• Presents with absent breast development, low FSH/LH, and normal uterus.
• Ovaries are present but under-stimulated.

Key Concepts 

• Müllerian agenesis (MRKH) = Normal female phenotype, breast and hair development, but absent uterus and upper vagina, normal ovaries.
• Differentiated from AIS by presence of pubic/axillary hair and 46,XX karyotype.

Subject: Obstetrics & Gynecology (Gynecological Anatomy)

• Closely related to Embryology (for developmental origin of Müllerian ducts)

System: Female Reproductive System – ANATOMY OF REPRODUCTIVE AND GENITAL TRACT – Developmental defects in the female genitourinary tract – Structural problems of pelvic organs 

Topic: Gynecology – Primary Amenorrhea Due to Congenital Anomalies of the Female Reproductive Tract

Alternative Topic: Gynecology – Disorders of Sexual Development (DSD)

Gynecology – Primary Amenorrhea Due to Congenital Anomalies of the Female Reproductive Tract

Gynecology – Disorders of Sexual Development (DSD)

Notes:

• DSD involves discordance between chromosomal, gonadal, or phenotypic sex.
• Important to differentiate based on karyotype, internal structures, secondary sexual characteristics, and hormonal profile.

Keywords in the Stem to identify correct option

• “24th week”
  ➤ Indicates mid-second trimester, when hPL levels peak and begin exerting metabolic effects.
• “Rising postprandial glucose levels”
  ➤ Suggests insulin resistance, a hallmark of hPL activity in pregnancy.

These keywords point to the metabolic role of hPL in increasing maternal insulin resistance to prioritize fetal glucose supply.

Explanation 

(Option C) Increases maternal insulin resistance to supply glucose to fetus:

• Human placental lactogen (hPL) is a hormone produced by the syncytiotrophoblast of the placenta. Its primary function is to alter maternal metabolism to ensure a continuous supply of glucose and amino acids to the developing fetus. It achieves this by acting as an antagonist to insulin. This causes the mother’s cells to become less sensitive to insulin, leading to maternal insulin resistance. As a result, glucose remains in the bloodstream longer after meals, making more available for placental transfer and fetal uptake. This physiological change, while beneficial for the fetus, can lead to elevated maternal blood glucose levels, particularly after eating, and is the underlying mechanism for gestational diabetes.
• Human placental lactogen (hPL) plays a crucial role in a pregnant woman’s metabolism, and its action explains the rising postprandial glucose levels.

(Option A) Enhances maternal thyroid activity:

• This is incorrect. While pregnancy does increase thyroid gland activity, this is primarily driven by human chorionic gonadotropin (hCG), which has a similar structure to thyroid-stimulating hormone (TSH) and can weakly stimulate the thyroid. hPL does not have a significant role in enhancing maternal thyroid activity.

(Option B) Promotes fetal surfactant production:

• This is incorrect. The production of fetal surfactant, which is crucial for lung maturation, is primarily stimulated by fetal cortisol. While hPL has some metabolic effects, it is not the main hormone responsible for the direct promotion of surfactant production.

(Option D) Inhibits uterine contractility in the third trimester:

• This is incorrect. Uterine contractility is primarily inhibited by progesterone, which maintains uterine quiescence throughout most of the pregnancy. hPL does not have a significant role in inhibiting uterine contractions.

(Option E) Suppresses fetal cortisol synthesis:

• This is incorrect. Fetal cortisol is essential for the maturation of many fetal organs, including the lungs, and its synthesis is regulated by the fetal hypothalamic-pituitary-adrenal axis. hPL does not suppress fetal cortisol synthesis; in fact, the two hormones have distinct and largely unrelated physiological roles.

Key Concepts

• Human Placental Lactogen (hPL): A hormone produced by the placenta that acts as an insulin antagonist, increasing maternal insulin resistance to ensure adequate glucose supply for the fetus.
• Gestational Diabetes: A condition of impaired glucose tolerance that develops during pregnancy, often due to the insulin-antagonistic effects of hPL and other placental hormones.
• Insulin Resistance: A state where the body’s cells don’t respond effectively to insulin, leading to higher blood glucose levels. This is a normal physiological adaptation in pregnancy, but can become pathological.

Subject: Obstetrics & Gynecology (Physiology)

System: Female Reproductive System – Endocrine System + Pregnancy-related Metabolic Physiology – ANATOMY OF REPRODUCTIVE AND GENITAL TRACT – Placenta – Function 

Topic: Physiology – Endocrine Adaptations in Pregnancy

Physiology – Endocrine Adaptations in Pregnancy

Summary Key Point

Pregnancy involves complex endocrine adaptations—especially from placenta-derived hormones—that prioritize fetal growth by altering maternal metabolism, particularly glucose and fat metabolism.

Human Placental Lactogen (hPL) in Pregnancy

This diagram illustrates a pregnant woman with a labeled placenta and fetus, highlighting the role of human placental lactogen (hPL) in pregnancy. It explains how hPL is produced by the placenta, increases maternal insulin resistance, and promotes lipolysis, ensuring adequate glucose supply to the fetus—a key adaptation of maternal endocrine physiology.

Keywords in the Stem to identify correct option

1. “Massive postpartum hemorrhage” – points toward ischemic pituitary injury.
2. “Failure of lactation” – indicates prolactin deficiency, classic post-partum pituitary problem.
3. “Amenorrhea” – shows gonadotropin deficiency (LH/FSH).

Classic Triad (for Sheehan syndrome):

• Postpartum hemorrhage + Failure of lactation + Amenorrhea

Explanation

(Option E) Sheehan syndrome:

• Also known as postpartum pituitary gland necrosis. It is caused by massive blood loss (postpartum hemorrhage) during or after childbirth, which leads to a reduction in blood flow to the pituitary gland. This can cause the pituitary gland tissue to die, resulting in a deficiency of various pituitary hormones, including those necessary for lactation (prolactin) and the menstrual cycle (gonadotropins)
• Leads to pan-hypopituitarism, commonly presenting as:
  • Failure of lactation (due to prolactin deficiency)
  • Amenorrhea (due to FSH/LH deficiency)
  • Fatigue, hypotension, hypothyroid or adrenal insufficiency signs (secondary)
• Onset is usually weeks to months after complicated delivery with hemorrhage.
• Early recognition is key because hormone replacement can prevent serious complications.

(Option A) Addison disease:

• Primary adrenal insufficiency due to autoimmune destruction of the adrenal cortex.
• Presents with fatigue, hypotension, hyperpigmentation, hyponatremia, and hyperkalemia.
• Does not typically cause postpartum lactation failure or amenorrhea.

(Option B) Graves disease:

• Autoimmune hyperthyroidism.
• Presents with weight loss, heat intolerance, palpitations, goiter, exophthalmos.
• Would not cause pituitary hormone deficiency or lactation failure.

(Option C) Hashimoto thyroiditis:

• Autoimmune hypothyroidism.
• Can cause fatigue, cold intolerance, weight gain, and sometimes menstrual irregularities.
• Usually not associated with massive postpartum hemorrhage or multiple pituitary hormone deficiencies.

(Option D) Kallmann syndrome:

• Congenital hypogonadotropic hypogonadism with anosmia.
• Causes delayed or absent puberty and infertility.
• Not acquired postpartum; patient had normal prior menstruation and pregnancy.

Key Concept
Sheehan syndrome is postpartum hypopituitarism caused by ischemic necrosis of the pituitary after severe hemorrhage. Key clinical features include lactation failure, amenorrhea, fatigue, and other hormone deficiencies. It is an acquired, obstetric-related pituitary disorder.

Subject: Obstetrics & Gynecology 

System: Female Reproductive System (Pituitary/Hypothalamic-Pituitary Axis) – REPRODUCTIVE PHYSIOLOGY – Endocrine – Pituitary Hormones

Topic: Obstetrics – Reproductive Endocrinology: Postpartum Hypopituitarism (Sheehan Syndrome)

Obstetrics – Reproductive Endocrinology: Postpartum Hypopituitarism (Sheehan Syndrome)

Key Concept

Postpartum pituitary necrosis → failure of prolactin, gonadotropins.

Differential Diagnosis

(For postpartum hypopituitarism / Sheehan Syndrome)

Key Point

• Sheehan syndrome is distinguished by history of massive postpartum hemorrhage + failure of lactation + amenorrhea—the classic triad.

Obstetrics – Reproductive Endocrinology: Postpartum Hypopituitarism (Sheehan Syndrome)

This diagram illustrates the pathophysiology and clinical features of Sheehan Syndrome, a condition of postpartum hypopituitarism caused by massive postpartum hemorrhage leading to pituitary gland ischemia. Key points highlighted include:

• Massive Postpartum Hemorrhage: Severe blood loss during or after delivery is the primary cause, leading to ischemic necrosis of the anterior pituitary.
• Pituitary Gland: The anterior pituitary is particularly susceptible to ischemic damage during hypovolemic shock.
• Clinical Features (Panhypopituitarism / Piceua Syndrome):
  • Failure of lactation: Due to prolactin deficiency.
  • Amenorrhea: Due to gonadotropin (LH, FSH) deficiency.
  • Fatigue and hypotension: Due to secondary adrenal and thyroid hormone deficiencies.

Keywords in the Stem to identify correct option

• “Early labour” – Indicates the patient is transitioning toward active labour, where contraction frequency increases.
• “Contractions every 5 minutes, lasting 45 seconds” – Describes current latent phase; the question asks what is expected in active labour.

Reason: These keywords help differentiate between latent phase (current status) and the expected contraction pattern in active labour, which is the focus of the question.

Explanation 

(Option D). 3–5 every 10 minutes

• This is the normal contraction pattern in the active phase of labour.
• During active labour, uterine contractions become more frequent, stronger, and regular, typically occurring every 2–3 minutes, or 3–5 times in 10 minutes, with each lasting 45–60 seconds.
• This pattern ensures effective cervical dilatation and fetal descent.
• CTG would show normal baseline with accelerations, no decelerations, and this frequency of uterine contractions.

(Option A) 1 every 30 minutes:

• Extremely infrequent; would suggest inefficient or latent labour, not active labour.
• May raise concerns about labour dystocia or a need for augmentation.

(Option B) 1 every 15 minutes:

• Still too infrequent for active labour.
• Seen more in very early latent phase or irregular contractions (Braxton Hicks).

(Option C) 1 every 10 minutes:

• Too infrequent for active phase.
• This may be acceptable in early latent labour, but not once cervix is dilated >4–6 cm.

(Option E) 8–10 every 10 minutes:

• Too frequent and may indicate uterine hyperstimulation (tachysystole).
• Can compromise fetal oxygenation and is potentially harmful.

Key Concept

In active labour, the uterus contracts 3–5 times every 10 minutes, each lasting around 45–60 seconds, ensuring progressive cervical dilation. More or less than this range indicates inefficient labour or hyperstimulation.

Subject: Obstetrics & Gynecology (Obs Physiology)

System: Female Reproductive System (Female – Uterus and Labour Physiology) – Antenatal and Natal Care – Labor and Puerperium – Physiology of Labor (1st, 2nd, 3rd Stage) – Physiology of Labor (1st Stage)

Topic: Obstetrics – Diagnosis and Clinical Assessment of Labour Progress (Active Phase)

Obstetrics – Diagnosis and Clinical Assessment of Labour Progress (Active Phase)

Differential Diagnosis – Irregular or Inadequate Uterine Contractions During Labour

When a woman in early or active labour shows abnormal contraction patterns (too few, too frequent, or ineffective), consider the following differentials:

Uterine Contractions at Various Stages of Labor

This diagram clearly shows:

• The frequency and duration of uterine contractions during the latent phase, active phase, and second stage of labour.
• It highlights the increase in contraction frequency from early labour to active labour, which directly addresses the MCQ’s focus on expected contraction frequency during active labour.
• The active phase is clearly marked with contractions occurring 3–5 times every 10 minutes, matching the correct answer.

This makes it the best visual aid for understanding the physiological changes in contraction patterns during labour progression relevant to the question.

Keywords in the Stem to identify correct option

• “extends into the parametrium bilaterally”
  Indicates tumor invasion beyond the cervix into parametrium, a hallmark of stage IIB.
• “does not reach the pelvic sidewalls”
  Excludes stage IIIB, which involves pelvic sidewall extension.

No classic triad is present in this stem; it’s primarily focused on local tumor extension landmarks.

Explanation 

(Option D) IIB:

• Tumor invades the parametrium but does not reach the pelvic sidewall.
• Can be unilateral or bilateral parametrial involvement.
• Correct answer as the tumor extends bilaterally into parametrium without reaching sidewalls.

More detailed explanation of the right option (D. IIB):

• Stage IIB is defined as cervical cancer where the tumor has extended beyond the cervix into the parametrium, but it has not yet reached the pelvic sidewalls. This indicates more local spread than stages IB or IIA, but less extensive than stage IIIB where sidewall involvement or hydronephrosis occurs. The parametrium is the fibrous tissue lateral to the cervix and uterus, so involvement here signals deeper local invasion, which often affects treatment choices such as combined chemoradiotherapy.

(Option A) IB:

• Tumor confined strictly to the cervix but clinically visible or larger than microscopic disease.
• No spread beyond the cervix or into surrounding tissues (parametrium or vagina).
• Not correct here since the tumor extends beyond the cervix into parametrium.

(Option B) IIA:

• Tumor invades beyond the uterus but not into the parametrium.
• Involvement includes upper two-thirds of the vagina without parametrial involvement.
• Not correct here because parametrium involvement is present.

(Option C) IIIA:

• Tumor extends to the lower third of the vagina but does not involve the pelvic sidewall.
• No parametrium involvement required for this stage.
• Not correct since the question states no vaginal involvement.

(Option E) IIIB:

• Tumor extends to the pelvic sidewall and/or causes hydronephrosis or non-functioning kidney.
• Represents more advanced local disease.
• Not correct here since pelvic sidewalls are not involved.

Key Concept

FIGO Stage IIB cervical cancer is characterized by tumor spread into the parametrium without reaching the pelvic sidewalls, indicating locally advanced but not yet extensively invasive disease beyond the parametrium.

Subject: Obstetrics & Gynecology (Pathology)

• Pathology (cervical cancer staging is a clinical-pathological correlation) and Clinical Oncology (cancer staging)

System: Female Reproductive System (specifically the cervix and adjacent pelvic structures) – PATHOLOGY IN RELATION TO OBSTETRICS AND GYNECOLOGY – Malignancies – Gynecological malignancies and staging – Cervical Cancer – Pathology and Staging

Topic: Cervical Cancer – FIGO Clinical Staging and Tumor Spread

Cervical Cancer – FIGO Clinical Staging and Tumor Spread

Differential Diagnoses

(Consider when a patient presents with a cervical mass or lesion suspicious for cervical cancer)

Note: 

Clinical examination combined with biopsy and imaging is key to differentiate cervical cancer from these conditions. The presence of parametrial invasion is highly suggestive of invasive cervical cancer rather than benign or inflammatory causes.

Cervical Cancer – FIGO Clinical Staging and Tumor Spread

The uploaded image provides a visual and textual overview of the FIGO (International Federation of Gynecology and Obstetrics) clinical staging system for cervical cancer. It illustrates the anatomical locations of the uterus, cervix, vagina, parametrium, and pelvic sidewalls.

The diagram specifically highlights key stages and their corresponding definitions:

• Stage I: Tumor is confined to the cervix.
• Stage IB: Clinically visible lesion confined to the cervix.
• Stage IIA: Tumor involves the upper two-thirds of the vagina, but there is no parametrial involvement.
• Stage IIB: The tumor extends into the parametrium but does not reach the pelvic sidewall.
• Stage III: Tumor extends to the pelvic sidewall and/or the lower third of the vagina.
• Stage IIIA: Involvement of the pelvic sidewall and/or… (The text is cut off, but this stage specifically involves the lower third of the vagina without extending to the pelvic sidewall).

Keywords in the Stem to identify correct option

1. “Cervical os is dilated” – Indicates miscarriage cannot be stopped; rules out threatened or missed miscarriage.
2. “Products of conception visible but not expelled” – Shows miscarriage is in progress but tissue not yet passed, differentiating it from incomplete miscarriage.
3. Classic triad: “Heavy vaginal bleeding + Crampy pain + Dilated cervical os” – Classic presentation of inevitable miscarriage.

Explanation

(Option C) Inevitable miscarriage:

• Definition: A miscarriage that cannot be stopped because the cervical os is dilated and the uterus is actively trying to expel the products of conception.
• Clinical features: Heavy bleeding, crampy pain, dilated cervix, products of conception may be visible at the cervical os but not yet expelled.
• Management: Often requires expectant, medical, or surgical management to ensure complete evacuation and prevent complications.

(Option A) Threatened miscarriage:

• Cervix remains closed, bleeding may be mild, pain minimal.
• Products of conception still in uterus.
• In this case, cervical os is dilated, so it is not threatened miscarriage.

(Option B) Incomplete miscarriage:

• Some products of conception have already been expelled, cervical os dilated, continued bleeding and cramping.
• Key difference: this patient has no tissue expelled yet, so it is not incomplete.

(Option D) Missed miscarriage:

• Fetus has died but remains in uterus, cervical os closed, minimal or no bleeding/pain.
• Not consistent with this clinical scenario.

(Option E) Septic miscarriage:

• Miscarriage complicated by infection: fever, foul-smelling discharge, uterine tenderness.
• No infection signs here.

Key Concept 

• Inevitable miscarriage occurs when cervix is dilated, bleeding and cramping are present, and products are still in the uterus.
• Differentiation from incomplete miscarriage: no tissue has been expelled yet, although it may be visible at the cervical os.

Subject: Obstetrics & Gynecology (specifically Obstetrics – Early Pregnancy Complications)

System: Female Reproductive System (Uterus, Cervix, Pregnancy-related structures) – PATHOLOGY IN RELATION TO OBSTETRICS AND GYNECOLOGY – Implantation and Early Pregnancy – Miscarriage  

Topic: Early Pregnancy Complications – Miscarriage (Inevitable, Threatened, Incomplete, Missed, Septic)

Early Pregnancy Complications – Miscarriage

Differential Diagnosis for Early Pregnancy Vaginal Bleeding (Miscarriage)

Note: 

In this MCQ scenario, the classic triad (heavy bleeding + crampy pain + dilated cervical os) with products visible but not expelled points strongly to inevitable miscarriage, making other differentials less likely but important to consider if diagnosis is unclear.

Early Pregnancy Complications – Miscarriage

This diagram visually compares the five main types of miscarriage—Threatened, Inevitable, Incomplete, Missed, and Septic—showing cervical os status, bleeding severity, pain, and the position of products of conception, along with brief management notes for each type. It highlights key clinical differences to aid in quick diagnosis and management decisions.

Keywords in the Stem to identify correct option

1. “6 weeks of amenorrhea” – Suggests early pregnancy where ultrasound may not yet detect intrauterine gestation, pointing toward need for serial β-hCG.
2. “No intrauterine gestational sac on transvaginal ultrasound” – Classic clue for ectopic pregnancy or very early pregnancy, making quantitative β-hCG rise the key diagnostic tool.
3. “Mild pelvic pain + positive pregnancy test” – Part of the classic ectopic pregnancy triad: amenorrhea, abdominal/pelvic pain, vaginal bleeding (here mild pain only); supports need for serial β-hCG.

Explanation 

(Option A) Quantitative serum β-hCG and repeat after 48 hours:

• Quantitative β-hCG is the most useful test in this scenario.
• In early pregnancy, β-hCG should approximately double every 48 hours.
• In ectopic pregnancy, β-hCG often rises more slowly or plateaus, suggesting abnormal implantation.
• Serial measurements help differentiate early intrauterine pregnancy vs ectopic pregnancy before ultrasound findings are conclusive.

(Option B) Serum progesterone level:

• Low progesterone (<5 ng/mL) may indicate nonviable pregnancy.
• However, it cannot reliably distinguish ectopic from failing intrauterine pregnancy, so it is less specific.

(Option C) Serum LH level:

• LH is used to predict ovulation and does not help diagnose pregnancy or ectopic pregnancy.
• Not relevant in this clinical scenario.

(Option D) MRI pelvis:

• MRI is rarely needed in early pregnancy evaluation.
• Ultrasound and β-hCG are usually sufficient; MRI is reserved for complicated or ambiguous cases.

(Option E) Urinary β-hCG:

• A urine pregnancy test confirms pregnancy but cannot quantify hCG or monitor its rise.
• Cannot reliably help differentiate ectopic from early intrauterine pregnancy.

Key Concept 

• Serial quantitative serum β-hCG is the most helpful investigation when transvaginal ultrasound does not show an intrauterine gestational sac.
• Abnormal rise or plateau of β-hCG suggests ectopic pregnancy or failing intrauterine pregnancy.

Subject: Obstetrics & Gynecology

System: Female Reproductive System (Early Pregnancy) – PATHOLOGY IN RELATION TO OBSTETRICS AND GYNECOLOGY – Implantation and Early Pregnancy – Ectopic Pregnancy  

Topic: Early Pregnancy Complications – Ectopic Pregnancy: Diagnosis

Early Pregnancy Complications –

Ectopic Pregnancy: Diagnosis

This table highlights the diagnostic approach, emphasizing that serial quantitative β-hCG is the key investigation when ultrasound is inconclusive.

Differential Diagnosis of

Suspected Ectopic Pregnancy

This table focuses on conditions that mimic ectopic pregnancy in early pregnancy.

Early Pregnancy Complications –

Ectopic Pregnancy: Diagnosis

The diagram illustrates the diagnostic pathway for suspected ectopic pregnancy. It shows absence of an intrauterine gestational sac on ultrasound, compares normal vs ectopic β-hCG rise patterns, and outlines the stepwise approach: positive pregnancy test → transvaginal ultrasound → serial quantitative serum β-hCG for confirmation when no intrauterine sac is seen.

Keywords in the Stem to identify correct option

1. Absent fetal movement for 5 days – suggests fetal demise.
2. Overlapping fetal skull bones – classic hallmark of IUFD, directly pointing to Spalding sign.

Classic triad (if present):

• Absent fetal cardiac activity + Absent fetal movement + Overlapping skull bones → Strongly indicates intrauterine fetal death (IUFD).

Explanation 

(Option E) Spalding sign:

• Classic sign of intrauterine fetal death (IUFD).
• On ultrasound or radiograph: overlapping of fetal skull bones due to softening and collapse of cranial bones after fetal demise.
• Usually appears 1–2 weeks after fetal death.
• More detailed: It indicates advanced fetal maceration, confirming the fetus has been dead in utero for some days.

(Option A) Snowstorm appearance:

• Seen in complete hydatidiform mole (CHM) on ultrasound.
• Characterized by heterogeneous echogenic mass with numerous cystic spaces in the uterus.
• Not related to fetal demise; more a trophoblastic disease finding.

(Option B) Double bubble sign:

• Seen in duodenal atresia on prenatal US or X-ray.
• Shows two adjacent fluid-filled structures (stomach and proximal duodenum).
• Not related to absent fetal movement or IUFD.

(Option C) Banana sign:

• Seen in Arnold-Chiari II malformation (spina bifida).
• Refers to banana-shaped cerebellum due to posterior fossa crowding.
• Not related to fetal death.

(Option D) Pseudogestational sac:

• Occurs in ectopic pregnancy, mimicking an intrauterine gestational sac.
• Usually small, centrally located, without yolk sac or fetal pole.
• Not applicable in a 26-week intrauterine pregnancy.

Key Concept
Spalding sign is a hallmark ultrasound/radiologic feature of intrauterine fetal death, seen as overlapping cranial bones. Recognizing this helps differentiate IUFD from other fetal anomalies or early pregnancy complications.

Subject: Obstetrics & Gynecology

System: Female Reproductive System (Feto-maternal) – PATHOLOGY IN RELATION TO OBSTETRICS AND GYNECOLOGY – Implantation and Early Pregnancy – Intrauterine Death  

Topic: Intrauterine Fetal Death (IUFD) – Ultrasound/Radiologic Signs

Intrauterine Fetal Death (IUFD) –

Ultrasound/Radiologic Signs

Differential Diagnoses for

(The ultrasound/radiologic finding of overlapping fetal skull bones (Spalding sign)

Key Point

• Spalding sign is pathognomonic for intrauterine fetal death; 
• Most differentials are distinguished by presence of fetal cardiac activity, timing, or associated anomalies.

Intrauterine Fetal Death (IUFD) – Ultrasound/Radiologic Signs

The diagram illustrates key diagnostic signs of IUFD, including Spalding sign (overlapping skull bones), absence of fetal cardiac activity, and exaggerated fetal head molding, helping in the radiologic/ultrasound confirmation of fetal demise.

Keywords in the Stem to identify correct option

1. “35-week abruption with fetal demise” – Classic trigger for DIC in obstetrics.
2. “Oozing from IV sites and postpartum bleeding disproportionate to loss” – Suggests consumptive coagulopathy rather than primary platelet or factor defect.
3. “Low fibrinogen, prolonged PT” – Hallmark lab pattern of DIC (consumption of clotting factors).

Classic triad in stem

Bleeding + Abnormal labs (low fibrinogen, prolonged PT) + Triggering obstetric event (placental abruption/fetal demise) → points to DIC.

Explanation 

(Option D) DIC (Disseminated Intravascular Coagulation):

• Triggered by placental abruption, especially with fetal demise.
• Pathophysiology: massive tissue factor release → widespread clotting → consumption of clotting factors and platelets → bleeding.
• Lab findings: low fibrinogen, prolonged PT/PTT, thrombocytopenia, elevated D-dimer.
• Clinical: oozing from IV sites, disproportionate postpartum bleeding, ecchymoses.

(Option A) HELLP syndrome:

• Hemolysis, Elevated Liver enzymes, Low Platelets.
• Usually presents with RUQ pain, nausea, hypertension, and thrombocytopenia.
• Does not typically cause prolonged PT or low fibrinogen as the primary issue.

(Option B) AFE (Amniotic Fluid Embolism):

• Rare, sudden onset cardiopulmonary collapse during labor or postpartum.
• May cause DIC, but classic presentation includes respiratory distress and hypotension first.

(Option C) Von Willebrand disease:

• Congenital bleeding disorder causing mucosal bleeding, easy bruising, prolonged bleeding.
• Lab pattern usually: prolonged bleeding time, may have low vWF, PT and fibrinogen often normal.

(Option E) Hemophilia carrier status:

• Usually asymptomatic unless extreme factor deficiency.
• Mainly affects males, females may have mild bleeding.
• Lab pattern: prolonged aPTT, normal PT, fibrinogen usually normal.

Key Concept 

Placental abruption, especially with fetal demise, can trigger DIC, which presents with widespread bleeding, low fibrinogen, prolonged PT, and oozing from IV sites. 

Early recognition is crucial for management.

Subject: Obstetrics & Gynecology

System: Female Reproductive System (Hematologic / Coagulation system – secondary to obstetric complication) – PATHOLOGY IN RELATION TO OBSTETRICS AND GYNECOLOGY – Obstetric Complications – Obstetric Hemorrhage – Antepartum Hemorrhage (APH)

Topic: Obstetrics – Intrapartum/Postpartum Hemorrhage: Disseminated Intravascular Coagulation (DIC) Secondary to Placental Abruption

DIC secondary to placental abruption in obstetrics

Differential Diagnosis for

Bleeding in late pregnancy / postpartum

This table highlights why DIC is the most likely diagnosis in the context of placental abruption with fetal demise and abnormal labs.

Disseminated Intravascular Coagulation (DIC)

Secondary to Placental Abruption

The diagram illustrates how placental abruption leads to massive tissue factor release, triggering DIC through widespread consumption of clotting factors and platelets. This results in low fibrinogen, prolonged PT/PTT, thrombocytopenia, and excessive bleeding manifesting as postpartum hemorrhage and oozing from IV sites.

Keywords in the Stem to identify correct option

• Monochorionic diamniotic twins → shared placenta → risk of vascular anastomoses.
• Polyhydramnios in one sac + oligohydramnios in the other → classic for Twin-to-Twin Transfusion Syndrome (TTTS).

Classic “Poly-Oligo Sequence” = diagnostic clue for TTTS.

Explanation 

(Option B) Arteriovenous placental anastomoses:

• The condition described, with one twin’s sac having an excess of amniotic fluid (polyhydramnios) and the other having a lack of fluid (oligohydramnios), is characteristic of twin-to-twin transfusion syndrome (TTTS). This syndrome occurs in monochorionic pregnancies, which share a single placenta.
• In TTTS, unequal blood flow through vascular anastomoses (connections) on the placenta leads to one twin (the donor) pumping blood to the other (the recipient). The donor twin becomes anemic and has oligohydramnios due to reduced blood volume and urine output. Conversely, the recipient twin becomes polycythemic and develops polyhydramnios due to increased blood volume and subsequent increased urine production.
  • Donor twin → oligohydramnios, growth restriction, anemia.
  • Recipient twin → polyhydramnios, hypervolemia, cardiac strain.
• This is the classic cause of poly/oligo sequence in monochorionic twins.

(Option A) Unequal fertilization of ova:

• Fertilization always involves a single sperm–egg fusion per ovum; twins arise from either two ova (dizygotic) or one ovum splitting (monozygotic).
• Does not explain twin-to-twin fluid imbalance.

(Option C) Rh isoimmunization:

• Maternal antibodies attack fetal RBCs → hemolysis, anemia, hydrops.
• Affects both twins equally (not one sac polyhydramnios and other oligohydramnios).

(Option D) Cord entanglement:

• Occurs in monoamniotic twins, not in diamniotic twins.
• Leads to cord accidents, acute hypoxia, or demise, not chronic poly/oligo fluid imbalance.

(Option E) Fetal infection:

• Causes growth restriction, hydrops, or miscarriage.
• Does not cause the discordant amniotic fluid (poly/oligo) picture.

Key Concept 

In monochorionic twin pregnancies, poly/oligohydramnios sequence is diagnostic of Twin-to-Twin Transfusion Syndrome (TTTS), caused by arteriovenous placental anastomoses between the twins’ circulations.

Subject: Obstetrics & Gynecology (Obs)

System: Female Reproductive System (Placental/Fetoplacental circulation) + Secondary involvement: Fetoplacental circulation (placental vascular system)- PATHOLOGY IN RELATION TO OBSTETRICS AND GYNECOLOGY – Obstetric Complications – Multiple Pregnancy – Fetal Complications

Topic: Obstetrics – Multiple Pregnancy (Complications: Twin-to-Twin Transfusion Syndrome – TTTS)

Obstetrics – Multiple Pregnancy

(Complications: Twin-to-Twin Transfusion Syndrome – TTTS)

Differential Diagnosis – Poly-Oligo Sequence in Twins

Key Point

Among these, TTTS is the classic cause of polyhydramnios in one sac + oligohydramnios in the other in monochorionic twins.

Twin-to-Twin Transfusion Syndrome (TTTS) 

in Monochorionic Diamniotic Twins

The diagram illustrates monochorionic diamniotic twins with Twin-to-Twin Transfusion Syndrome (TTTS). It shows the shared placenta with abnormal arteriovenous anastomoses, leading to a donor twin with oligohydramnios and a recipient twin with polyhydramnios — the classic poly-oligo sequence seen on ultrasound.

Keywords in the Stem to identify correct option 

• Thalassemia major → implies chronic anemia & hypoxia, even with transfusions.
• Fetal growth restriction (FGR) → classical complication of maternal chronic anemia.

Explanation 

(Option D) Chronic maternal anemia:

• In thalassemia major, even with transfusions, chronic maternal anemia and hypoxia persist due to ineffective erythropoiesis and iron overload.
• While transfusions help, they often do not fully correct the underlying chronic anemia and its effects on the mother’s cardiovascular system and oxygen-carrying capacity.
• The body’s long-term adaptation to chronic anemia can lead to a state of compromised oxygen delivery to the placenta, resulting in placental insufficiency. This insufficiency impairs the transfer of nutrients and oxygen to the fetus, leading to FGR.
• This chronic maternal anemia is the most important risk factor for FGR in thalassemic pregnancies.

(Option A) Maternal hypertension:

• Hypertension in pregnancy (chronic or preeclampsia) is a well-known cause of uteroplacental insufficiency and FGR.
• But in this case, no mention of hypertension is given, so this is unlikely.

(Option B) Placenta previa:

• Placenta previa usually causes antepartum hemorrhage (APH) and is not a classic cause of FGR.
• Placental implantation issues may rarely contribute to growth problems, but FGR is not a typical finding in previa.

(Option C) Infection:

• Congenital infections (TORCH, syphilis, malaria, etc.) can cause symmetric IUGR.
• However, the stem does not mention maternal fever, infection risk factors, or ultrasound findings suggestive of infection (e.g., microcephaly, calcifications, hydrops).

(Option E) Congenital malformations:

• Some anomalies do cause FGR (especially chromosomal), but the stem does not mention any ultrasound structural abnormalities.
• Less likely compared to maternal anemia in this scenario.

Key Concept 

In thalassemia major pregnancies, chronic maternal anemia remains a major contributor to fetal growth restriction, even with transfusion support. Other causes like hypertension, previa, infection, or anomalies are possible but less likely in this specific clinical context.

Subject: Obstetrics & Gynecology (Obs)

System: Female Reproductive System (Hematology/Placental–Fetal Growth Restriction) – COMMON CONGENITAL ANOMALIES – Blood disorders – Thalassemia

Topic: Obstetrics – Pregnancy Complications due to Maternal Hematological Disorders (Thalassemia Major and Fetal Growth Restriction)

Obstetrics – Pregnancy Complications due to Maternal Hematological Disorders (Thalassemia Major and Fetal Growth Restriction)

Key Point

 In thalassemia major, even with transfusions, chronic maternal anemia and hypoxia remain the main drivers of FGR in pregnancy.

Maternal Anemia in Pregnancy → Effect on Fetus (IUGR/FGR)

Key Point
Chronic maternal anemia → reduced oxygen and nutrient supply to placenta → chronic hypoxia → FGR/IUGR, low birth weight, stillbirth risk.

Differential Diagnosis

for Fetal Growth Restriction (FGR/IUGR) in Pregnancy with Maternal Anemia

(Thalassemia Major context)

Key Point
While chronic maternal anemia (like thalassemia) is a direct cause of FGR, other causes such as hypertension, placental insufficiency, infections, and congenital anomalies should be considered in differential diagnosis when evaluating a growth-restricted fetus.

Maternal Anemia in Pregnancy → Effect on Fetus (FGR/IUGR)

The diagram illustrates how maternal anemia leads to placental hypoxia, which in turn causes fetal growth restriction (FGR/IUGR). It shows the stepwise impact: maternal anemia → reduced oxygen delivery → impaired placental function → restricted fetal growth.

Keywords in the Stem to identify correct option

• HBsAg and HBeAg positive → means mother is highly infectious (very high risk of vertical transmission).
• Immediate postnatal prophylaxis → tells you timing is crucial (within 12 hours).

These keywords together indicate the need for the most effective and immediate prevention → HBIG + Hepatitis B vaccine within 12 hours.

Explanation 

(Option C) HBIG + Hepatitis B vaccine within 12 hours:

• Combination of active + passive immunity.
• HBIG provides immediate protection, while vaccine induces long-term immune response.
• When given within 12 hours, efficacy is >90–95% in preventing vertical transmission.
• This is the Gold standard recommended by WHO and CDC for infants of HBsAg-positive mothers, especially if also HBeAg positive.

More Explanation 

• This combination works by immediate neutralization of circulating virus (HBIG) and induction of long-term immunity (vaccine).
• Timing is critical: must be given within 12 hours of birth for maximum efficacy.
• Subsequent doses of vaccine at 1 and 6 months complete the active immunization series.

(Option A) Hepatitis B vaccine only:

• Provides active immunity by stimulating the baby’s immune system.
• Alone, it reduces infection risk but is not sufficient in infants of highly infectious mothers (HBeAg+).
• Efficacy ~70–80% alone, lower than combination.

(Option B) HBIG only:

• Provides passive immunity with immediate antibodies against HBV.
• Protects for a few months but does not induce long-term immunity.
• Alone, efficacy ~70–75%, not enough for high-risk neonates.

(Option D) HBIG after 1 week + vaccine at 6 weeks:

• Delayed prophylaxis is ineffective.
• HBV can infect newborn hepatocytes very early (during birth).
• By 1 week or 6 weeks, the virus may already have established infection → protection is useless.

(Option E) No intervention needed:

• Transmission risk from HBsAg + HBeAg + mother is up to 90% if untreated.
• Doing nothing leads to very high rates of chronic infection in infants.

Key Concept 

The most effective strategy to prevent neonatal HBV infection from HBsAg and HBeAg positive mothers is combined HBIG + vaccine within 12 hours of birth, providing >95% protection through both passive and active immunity.

Subject: Obstetrics & Gynecology (Obs)

• Obstetrics (Obs) – because it deals with maternal HBsAg/HBeAg status and perinatal vertical transmission.
• Pediatrics – because the focus is on newborn prophylaxis (neonatal HBV prevention).
• Microbiology (Virology) – since Hepatitis B virus transmission and immunity are the core concepts.

System: Female Reproductive System (Hepatobiliary System (Liver + Viral Hepatitis)) – INFECTIONS – Modes of Transmission

Topic: Obstetrics – Maternal Infections (Hepatitis B in Pregnancy: Prevention of Mother-to-Child Transmission)

Obstetrics – Maternal Infections (high-yield, exam-style)

This captures the major maternal infections in pregnancy with their fetal impact + management/prevention in one glance.

Obstetrics – Maternal Infections

(Hepatitis B in Pregnancy: Prevention of Mother-to-Child Transmission)

Key Exam Point
HBIG + Hepatitis B vaccine within 12 hrs of birth is the most effective way (>95% efficacy) to prevent mother-to-child transmission of HBV.

Differential Diagnosis

(Relevant to Obstetrics – Maternal Infections (Hepatitis B in Pregnancy: Prevention of Mother-to-Child Transmission))

These are other maternal infections that can also be vertically transmitted and mimic the “vertical transmission” concern of HBV in pregnancy:

Why this table matters for your MCQ:

• The main differential diagnosis is with other vertically transmitted infections (TORCH + HBV/HCV/HIV).
• HBV is unique because effective prophylaxis exists (HBIG + vaccine within 12 hrs).

Obstetrics – Maternal Infections (Hepatitis B in Pregnancy: 

Prevention of Mother-to-Child Transmission)

The diagram illustrates the pathway of Hepatitis B transmission risk in pregnancy and highlights the critical neonatal prophylaxis steps. It shows that mothers who are HBsAg and HBeAg positive have a high vertical transmission risk, but this can be reduced to <5% if the newborn receives HBIG + Hepatitis B vaccine within 12 hours, followed by the complete vaccination series.

Keywords in the Stem to identify correct option

• Chorioretinitis → strongly points toward congenital toxoplasmosis (ocular involvement is classic).
• Hydrocephalus + Intracranial calcifications → together with chorioretinitis form the classic triad of congenital toxoplasmosis.
• Exposure to cats → risk factor for Toxoplasma gondii infection.

Classic triad 

(chorioretinitis, hydrocephalus, intracranial calcifications) makes Toxoplasmosis the only correct answer.

Explanation 

(Option D) Toxoplasmosis:

• Caused by Toxoplasma gondii, a protozoan parasite.
• Acquired through ingestion of oocysts from cat feces, undercooked meat, or transplacental transmission during maternal infection.
• Classic triad in congenital toxoplasmosis:

1. Chorioretinitis (eye inflammation leading to blindness)
2. Hydrocephalus (due to obstruction from CNS inflammation)
3. Intracranial calcifications (diffuse, typically in basal ganglia)

• Early infection may cause miscarriage; later infection causes neurologic and ocular disease.

(Option A) Cytomegalovirus (CMV):

• Congenital CMV is the most common congenital infection.
• Classic features: periventricular calcifications, microcephaly, hearing loss, seizures, blueberry muffin rash.
• Unlike toxoplasmosis, calcifications are periventricular rather than diffuse.

(Option B) Rubella:

• Congenital rubella syndrome (CRS) triad:
  1. Sensorineural deafness
  2. Cataracts
  3. Cardiac defects (e.g., PDA, pulmonary artery stenosis)
• May also cause blueberry muffin rash and microcephaly.
• Ocular chorioretinitis and hydrocephalus are not typical.

(Option C) Herpes Simplex Virus (HSV):

• Congenital/neonatal HSV usually presents with:
  • Vesicular skin lesions
  • Sepsis-like illness with hepatitis and DIC
  • CNS disease (encephalitis, seizures)
• Not associated with calcifications + triad described in the stem.

(Option E) Syphilis:

• Congenital syphilis features:
  • Snuffles (profuse nasal discharge), Hutchinson teeth, saddle nose deformity, saber shins
  • Skin rashes, hepatosplenomegaly
  • Later findings: deafness, keratitis
• No hydrocephalus or calcification triad.

Key Concept 

The classic triad of chorioretinitis, hydrocephalus, and intracranial calcifications with history of cat exposure in pregnancy is diagnostic of congenital toxoplasmosis. Differentiation from CMV is based on site of calcifications (diffuse vs. periventricular).

Subject: Obstetrics & Gynecology & Pediatrics

• Obstetrics (maternal exposure → fetal infection), Microbiology (parasite: Toxoplasma gondii).
• Pediatrics → Neonatal Infections (Congenital TORCH infections)

System: Female Reproductive System – INFECTIONS – Complications – Perinatal

Topic: Obstetrics – Maternal Infections in Pregnancy – TORCH Infections – Toxoplasmosis in Pregnancy and Fetal Complications

Obstetrics – Maternal Infections in Pregnancy – TORCH Infections – Toxoplasmosis in Pregnancy and Fetal Complications

Exam Key Point
In Obstetrics, this falls under Maternal Infections – TORCH group. Toxoplasmosis in pregnancy is characterized by asymptomatic maternal disease but serious fetal complications, most classically the triad of chorioretinitis, hydrocephalus, and intracranial calcifications.

Differential Diagnosis

(for your MCQ, focusing on other TORCH infections that can mimic congenital toxoplasmosis)

Key Exam Differentiator

• Toxoplasmosis → Diffuse intracranial calcifications + chorioretinitis + hydrocephalus (Classic Triad)
• CMV → Periventricular calcifications + microcephaly + sensorineural hearing loss

Obstetrics – Maternal Infections in Pregnancy – TORCH Infections: Toxoplasmosis and Fetal Complications

The diagram illustrates the TORCH infections, highlighting toxoplasmosis in pregnancy as a maternal risk due to cat exposure, and demonstrates its fetal complications, including the classic triad of chorioretinitis, hydrocephalus, and intracranial calcifications. It links maternal infection with vertical transmission and resulting neonatal outcomes.