Adolescent pregnancy is associated with unique risks due to incomplete pelvic growth, hormonal changes, and limited nutritional reserves. Girls <18 years often have smaller pelvic diameters, predisposing them to cephalopelvic disproportion. Hemoglobin should normally be 12–16 g/dL in females, but iron deficiency anemia is common in adolescents. Normal maternal blood pressure is <120/80 mmHg; adolescents are less likely to have chronic hypertension compared to older women. Chromosomal abnormalities risk is strongly linked to advanced maternal age >35 years, not adolescence.

Rationale for correct answer

3. Cephalopelvic disproportion is more likely in adolescents due to incomplete pelvic maturation. A smaller bony pelvis increases the chance of obstructed labor. The question stem highlights her young age (16 years), which is the main factor raising the risk for CPD.

Rationale for incorrect answers

1. Gestational diabetes mellitus occurs more frequently in women >25 years, especially with obesity or family history. Adolescents generally have higher insulin sensitivity, and the pathophysiology does not favor increased risk in this group.

2. Chromosomal abnormalities, such as trisomy 21, are linked to advanced maternal age because of meiotic nondisjunction. The risk at age 16 is extremely low compared to women >35 years.

4. Placenta previa incidence increases with maternal age, multiparity, and uterine scarring from surgeries. A primigravida adolescent without prior uterine surgery has no significant predisposition to placenta previa.

Take home points

• Adolescent pregnancy increases risk of cephalopelvic disproportion due to incomplete pelvic growth.
• Gestational diabetes mellitus is more common in older pregnant women.
• Chromosomal abnormalities are strongly associated with advanced maternal age.
• Placenta previa risk rises with prior uterine surgery, advanced maternal age, and multiparity, not adolescence.

Chromosomal abnormalities result from errors in meiotic division, particularly nondisjunction, leading to conditions such as trisomy 21 (Down syndrome). The risk of nondisjunction increases with advancing maternal age, especially ≥35 years. Normal karyotype is 46 chromosomes. The baseline risk for trisomy 21 at age 25 is approximately 1 in 1,250, while at age 35 it rises to about 1 in 350.

Rationale for correct answer

4. Maternal age ≥35 years is strongly associated with chromosomal nondisjunction events during oogenesis. This significantly increases the risk of Down syndrome and other trisomies. The question directly asks for the age group linked to increased chromosomal abnormality risk, making this option correct.

Rationale for incorrect answers

1. The age group 18–24 years carries a very low risk for chromosomal abnormalities, with Down syndrome occurring in about 1 in 1,400 live births at age 20. Nondisjunction errors are uncommon in this group.

2. Women aged 25–30 years have only a slightly increased risk compared to teenagers, with trisomy 21 risk around 1 in 1,000. This is not considered a high-risk age group.

3. Ages 31–34 years show a gradual increase in risk, with trisomy 21 risk at age 32 being about 1 in 900. However, this group is not defined as high risk until ≥35 years.

Take home points

• Risk of chromosomal abnormalities increases significantly after maternal age 35.
• Nondisjunction is the primary mechanism leading to trisomies such as Down syndrome.
• Younger maternal age groups have a very low baseline risk.
• Counseling and screening are emphasized for women ≥35 years.

Adolescent pregnancy carries medical and psychosocial risks due to biologic immaturity, inadequate prenatal care, and poor nutritional status. Young mothers <18 years are more likely to experience preterm birth (<37 weeks) and deliver infants with low birth weight (<2,500 g). Hemoglobin is often <12 g/dL, reflecting iron deficiency anemia. Adolescent mothers are also more vulnerable to intimate partner violence, with reported prevalence rates up to 20–30%. Normal pregnancy blood pressure is <120/80 mmHg, and risk of preeclampsia is not decreased in adolescence. Cesarean delivery may be required due to cephalopelvic disproportion.

Rationale for correct answer

1. Preterm birth is more common in adolescents because of biologic immaturity and inadequate cervical competence, as well as poor access to prenatal care. This raises risk for neonatal morbidity and mortality.

3. Low birth weight is frequent due to maternal malnutrition, iron deficiency, and increased risk of intrauterine growth restriction. Infants <2,500 g are more likely in adolescent pregnancies.

5. Intimate partner violence risk is elevated in adolescents, related to power imbalances, dependency, and limited social support. This contributes to adverse maternal and fetal outcomes.

Rationale for incorrect answers

2. The risk of preeclampsia is not decreased in adolescents; in fact, it may be increased, especially in first pregnancies due to immunologic factors. A blood pressure ≥140/90 mmHg is diagnostic for hypertensive disorders in pregnancy.

4. Adolescents do not have reduced likelihood of cesarean delivery. In fact, rates may be higher due to cephalopelvic disproportion from incomplete pelvic growth, leading to obstructed labor.

Take home points

• Adolescent pregnancy increases risk of preterm birth and low birth weight.
• Hypertensive disorders of pregnancy are not less common in adolescents.
• Cesarean delivery may be more frequent due to cephalopelvic disproportion.
• Psychosocial risks such as intimate partner violence are more prevalent in adolescents.

Advanced maternal age (≥35 years) is linked to obstetric and fetal risks due to oocyte aging, impaired glucose tolerance, and increased placental dysfunction. Risk of trisomy 21 rises from 1 in 350 at age 35 to 1 in 100 at age 40. Normal fasting plasma glucose is <100 mg/dL, but gestational diabetes mellitus is more common with maternal age >35 due to reduced insulin sensitivity. Placenta previa incidence is higher because of age-related endometrial changes. Stillbirth and preterm birth risks increase, not decrease, in advanced maternal age pregnancies.

Rationale for correct answers

1. Gestational diabetes mellitus risk increases with maternal age due to reduced insulin sensitivity and higher rates of obesity. This is strongly associated with advanced maternal age.

2. Down syndrome risk increases sharply after 35 years because of meiotic nondisjunction. Oocyte aging leads to chromosomal errors.

4. Placenta previa is more frequent in women ≥35 years due to endometrial scarring and impaired placental implantation. Advanced maternal age is a recognized risk factor.

Rationale for incorrect answers

3. Stillbirth risk is not reduced with age. In fact, women ≥35 years have higher rates of stillbirth, likely related to placental insufficiency and medical comorbidities.

5. Preterm birth is not lower in advanced maternal age. The risk is increased, partly due to obstetric complications such as hypertension, diabetes, and placenta previa.

Take home points

• Advanced maternal age ≥35 years increases risk of gestational diabetes.
• Chromosomal abnormalities, especially trisomy 21, are strongly age-related.
• Placenta previa incidence rises with older maternal age.
• Both stillbirth and preterm birth risks increase with advanced maternal age.

Maternal diabetes mellitus affects pregnancy due to maternal hyperglycemia, altered insulin metabolism, and abnormal placental function. Poor glycemic control leads to excess glucose crossing the placenta, causing fetal hyperinsulinemia and accelerated growth. Normal fasting plasma glucose is <100 mg/dL, and hemoglobin A1C should remain <6.5% during pregnancy. Complications include macrosomia, congenital malformations, neonatal hypoglycemia, and stillbirth.

Rationale for correct answer

2. Macrosomia occurs when maternal hyperglycemia causes excess transplacental glucose transfer. The fetus responds with hyperinsulinemia, which acts as a growth hormone, leading to birth weight >4,000 g. Poorly controlled diabetes is the direct cause in this scenario.

Rationale for incorrect answers

1. Microcephaly is not a classic complication of maternal diabetes. It is more commonly linked to congenital infections such as Zika virus, rubella, or cytomegalovirus, rather than hyperglycemia.

3. Spina bifida results from neural tube defects associated with folate deficiency, not from maternal diabetes. Normal maternal folate level should be >4 ng/mL to prevent such defects.

4. Low birth weight (<2,500 g) is usually associated with maternal hypertension, intrauterine growth restriction, or placental insufficiency. In diabetes, the opposite effect (excess growth) is more common due to increased nutrient availability.

Take home points

• Poorly controlled maternal diabetes leads to fetal macrosomia.
• Macrosomia is caused by fetal hyperinsulinemia from maternal hyperglycemia.
• Neural tube defects and microcephaly are not direct outcomes of diabetes.
• Low birth weight is linked to placental insufficiency, not poorly controlled diabetes.

Chronic hypertension in pregnancy is defined as blood pressure ≥140/90 mmHg present before conception or before 20 weeks of gestation. It leads to impaired uteroplacental perfusion, abnormal vascular remodeling, and increased placental ischemia. Normal blood pressure is <120/80 mmHg, and mean arterial pressure should be 70–105 mmHg. This condition predisposes to placental abruption, intrauterine growth restriction, preeclampsia, and stillbirth.

Rationale for correct answer

3. Placental abruption is strongly linked to chronic hypertension because long-standing elevated pressure damages spiral arteries, reducing placental attachment stability. Ischemic injury and vascular rupture increase risk of premature placental separation, leading to bleeding and fetal compromise.

Rationale for incorrect answers

1. Neonatal hypoglycemia is more commonly associated with infants of diabetic mothers due to fetal hyperinsulinemia in response to maternal hyperglycemia. It is not a direct complication of chronic hypertension.

2. Macrosomia, defined as fetal weight >4,000 g, is linked to maternal diabetes mellitus due to excess transplacental glucose. In chronic hypertension, placental insufficiency more often causes restricted growth rather than overgrowth.

4. Congenital anomalies are not specifically associated with maternal chronic hypertension. They are more related to teratogenic exposures, poorly controlled diabetes, and genetic causes. Hypertension mainly causes placental complications rather than structural defects.

Take home points

• Chronic hypertension in pregnancy increases risk of placental abruption.
• Placental abruption results from ischemic vascular damage and poor placental attachment.
• Macrosomia and neonatal hypoglycemia are associated with maternal diabetes, not hypertension.
• Congenital anomalies are not a direct consequence of chronic hypertension.

Maternal thyroid disorders in pregnancy alter metabolism, impair neurodevelopment, and disturb placental function. Thyroid hormones regulate fetal brain growth, myelination, and neuronal differentiation. Normal thyroid-stimulating hormone (TSH) in the 1st trimester is 0.1–2.5 mIU/L, free thyroxine (T4) is 0.8–1.7 ng/dL, and triiodothyronine (T3) is 80–200 ng/dL. Untreated hypothyroidism leads to impaired cognitive function, growth restriction, and miscarriage, while uncontrolled hyperthyroidism increases risk of preeclampsia, preterm birth, and fetal thyrotoxicosis.

Rationale for correct answer

3. Neurodevelopmental issues occur when maternal hypothyroidism causes inadequate transfer of thyroid hormones essential for fetal brain development. Deficiency during early gestation leads to intellectual impairment, reduced IQ, and motor delays. The lack of maternal thyroid hormone supply directly explains the fetal complications.

Rationale for incorrect answers

1. Placental abruption is mainly associated with chronic hypertension, preeclampsia, trauma, smoking, and cocaine use. Thyroid disorders do not directly damage placental attachment or cause premature separation.

2. Fetal alcohol spectrum disorder results from maternal alcohol consumption during pregnancy. It is characterized by growth restriction, facial anomalies, and neurobehavioral impairment, unrelated to thyroid hormone imbalance.

4. Gestational hypertension is defined as blood pressure ≥140/90 mmHg after 20 weeks without proteinuria. Thyroid dysfunction is not a primary cause. Hypertension is more linked to vascular or placental pathology, not thyroid hormone imbalance.

Take home points

• Maternal thyroid hormones are critical for fetal brain development, especially in early gestation.
• Untreated hypothyroidism increases risk of neurodevelopmental delay and reduced IQ in offspring.
• Hyperthyroidism in pregnancy causes maternal and fetal complications but not direct alcohol-like syndromes.
• Placental abruption and gestational hypertension are vascular disorders, not endocrine-driven thyroid effects.

Gestational diabetes mellitus results from impaired glucose tolerance, maternal hyperglycemia, and excess fetal insulin production. Normal fasting plasma glucose is <100 mg/dL, 1-hour postprandial glucose should be <140 mg/dL, and 2-hour postprandial glucose should be <120 mg/dL in pregnancy. Poor control leads to fetal hyperinsulinemia, which acts as a growth-promoting hormone. This causes macrosomia, neonatal hypoglycemia, and obstetric complications such as shoulder dystocia. Intrauterine growth restriction is more associated with placental insufficiency from maternal hypertension. Congenital rubella syndrome results from viral infection, not hyperglycemia.

Rationale for correct answer

1. Macrosomia develops because maternal hyperglycemia increases glucose transfer to the fetus. Fetal pancreatic hyperinsulinemia stimulates fat deposition, leading to birth weight >4,000 g.

2. Neonatal hypoglycemia occurs after birth because the infant’s pancreas continues producing high insulin levels while maternal glucose supply is cut off. Normal neonatal glucose should be >45 mg/dL; values below this indicate hypoglycemia.

4. Shoulder dystocia is a direct consequence of macrosomia, where the fetal shoulder becomes impacted behind the maternal pubic symphysis during delivery. It is a recognized obstetric emergency in diabetic pregnancies.

Rationale for incorrect answers

3. Intrauterine growth restriction is not typical of gestational diabetes. It is more commonly linked to maternal hypertension, preeclampsia, or uteroplacental insufficiency, where fetal nutrient supply is limited.

5. Congenital rubella syndrome results from maternal rubella infection in the first trimester, leading to cataracts, deafness, and cardiac defects. It is unrelated to glucose metabolism or gestational diabetes.

Take home points

• Poorly controlled gestational diabetes causes macrosomia and related birth trauma.
• Neonatal hypoglycemia results from persistent fetal hyperinsulinemia after birth.
• Intrauterine growth restriction is linked to hypertension, not diabetes.
• Congenital rubella syndrome is viral, not metabolic in origin.

Preeclampsia is a hypertensive disorder of pregnancy characterized by elevated blood pressure, proteinuria, and end-organ dysfunction after 20 weeks gestation. Normal blood pressure is <120/80 mmHg, while preeclampsia is diagnosed at ≥140/90 mmHg with proteinuria ≥300 mg/24 h or protein/creatinine ratio ≥0.3. Severe cases may show thrombocytopenia (<100,000/µL), elevated liver enzymes (AST/ALT >40 U/L), or serum creatinine >1.1 mg/dL. Nursing care focuses on monitoring, seizure prevention, and maternal-fetal stabilization.

Rationale for correct answers

1. Monitoring blood pressure is essential because preeclampsia is defined by hypertension and progression to severe ranges (≥160/110 mmHg) increases maternal and fetal risk.

2. Administering magnesium sulfate is indicated to prevent seizures (eclampsia). Normal serum magnesium is 1.7–2.4 mg/dL, and therapeutic levels for seizure prophylaxis are 4–7 mEq/L.

4. Assessing for proteinuria is critical because preeclampsia involves abnormal renal glomerular permeability. Dipstick testing or 24-hour urine collection confirms diagnosis and severity.

5. Providing dietary counseling is important to maintain adequate protein and balanced nutrition. Sodium restriction is not generally recommended, but patients should avoid excessive processed foods and maintain hydration.

Rationale for incorrect answers

3. Encouraging ambulation is unsafe in preeclampsia. Patients are at risk of seizures, hypertension crises, and placental abruption. Bed rest or activity restriction is often recommended in severe cases to reduce maternal-fetal stress.

Take home points

• Preeclampsia is diagnosed after 20 weeks with hypertension and proteinuria or end-organ signs.
• Magnesium sulfate is the drug of choice for seizure prophylaxis.
• Proteinuria assessment is central to diagnosis and monitoring.
• Ambulation may increase risks; close monitoring and rest are safer strategies.

Rubella infection in pregnancy is a viral illness that can severely impair fetal development, cause teratogenic effects, and damage multiple organ systems. The rubella virus crosses the placenta, especially in the first trimester when fetal organs are forming. Normal maternal rubella IgG titer >10 IU/mL indicates immunity, while non-immune mothers are at high risk. Congenital rubella syndrome leads to sensorineural deafness, cataracts, congenital heart disease, microcephaly, and growth restriction.

Rationale for correct answer

3. Rubella infection in the first trimester directly causes congenital rubella syndrome. Viral replication in fetal tissues disrupts organogenesis, leading to the classic triad of deafness, cataracts, and cardiac anomalies. The risk of fetal malformation is highest when infection occurs before 12 weeks.

Rationale for incorrect answers

1. Cytomegalovirus is the most common congenital viral infection and may cause microcephaly, periventricular calcifications, and sensorineural hearing loss, but it does not cause congenital rubella syndrome.

2. Toxoplasmosis, caused by Toxoplasma gondii, can result in chorioretinitis, hydrocephalus, and intracranial calcifications. It is transmitted through undercooked meat or cat feces exposure, not associated with congenital rubella syndrome.

4. Group B Streptococcus is a bacterial infection causing neonatal sepsis, pneumonia, and meningitis if transmitted during delivery. It does not produce teratogenic effects in utero and is unrelated to rubella.

Take home points

• Rubella infection in the first trimester causes congenital rubella syndrome.
• Classic triad: sensorineural deafness, cataracts, and congenital heart disease.
• Cytomegalovirus and toxoplasmosis cause congenital infections but not rubella syndrome.
• Group B Streptococcus leads to neonatal sepsis, not congenital malformations.

Syphilis is a sexually transmitted infection caused by Treponema pallidum that can cross the placenta and cause severe congenital anomalies, fetal death, and systemic disease. Normal maternal screening involves nontreponemal tests (VDRL, RPR) and treponemal-specific tests (FTA-ABS, TP-PA). Congenital syphilis may present with hepatosplenomegaly, anemia (hemoglobin <13 g/dL in neonates), rash, Hutchinson teeth, saddle nose, and sensorineural deafness. It is included in the TORCH infections (Toxoplasmosis, Other [syphilis], Rubella, Cytomegalovirus, Herpes simplex virus).

Rationale for correct answer

3. Syphilis is part of the “O” in TORCH and can cross the placenta at any stage of pregnancy. It causes congenital syphilis with manifestations such as hydrops fetalis, hepatomegaly, skin lesions, and later findings including Hutchinson teeth and saddle nose deformity.

Rationale for incorrect answers

1. Chlamydia is associated with neonatal conjunctivitis and pneumonia but is not classified under TORCH infections. It does not typically cause congenital structural anomalies.

2. Gonorrhea can cause ophthalmia neonatorum and neonatal sepsis but is not part of TORCH and does not produce congenital anomalies in utero.

4. Trichomoniasis causes preterm rupture of membranes, preterm birth, and low birth weight but does not cause congenital anomalies and is not part of TORCH.

Take home points

• TORCH infections include toxoplasmosis, syphilis, rubella, cytomegalovirus, and herpes simplex.
• Syphilis is the “O” in TORCH and causes congenital anomalies and stillbirth.
• Chlamydia, gonorrhea, and trichomoniasis cause neonatal infections but not TORCH anomalies.
• Screening and treatment of syphilis in pregnancy prevent congenital transmission.

Group B Streptococcus (GBS) is a gram-positive bacterium that colonizes the genitourinary tract and can be transmitted during vaginal delivery. Neonates exposed to GBS are at high risk of early-onset sepsis, pneumonia, and meningitis. Normal maternal screening is performed at 35–37 weeks of gestation using vaginal and rectal swabs. Prophylactic intravenous penicillin G or ampicillin during labor reduces neonatal infection risk without affecting uterine contractions, hemorrhage, or maternal long-term colonization.

Rationale for correct answer

2. The primary reason for giving intrapartum antibiotics in GBS-positive mothers is to prevent neonatal GBS sepsis, which can occur within the first 7 days of life and has a high mortality rate.

Rationale for incorrect answers

1. Prophylactic antibiotics are not given to prevent maternal postpartum infection. GBS rarely causes maternal endometritis or wound infection; the intervention specifically targets neonatal transmission.

3. Antibiotics do not influence coagulation pathways and therefore have no effect on maternal hemorrhage risk. Hemorrhage prevention relies on uterotonics and active management of the third stage of labor.

4. Antibiotics do not stimulate uterine contractions. Uterine contractility is managed with oxytocin, prostaglandins, or other uterotonics, not antimicrobial therapy.

Take home points

• GBS is screened for at 35–37 weeks of gestation.
• Main neonatal risks: sepsis, pneumonia, and meningitis.
• Intrapartum IV penicillin or ampicillin prevents early-onset neonatal disease.
• Maternal infection prevention is not the primary goal of prophylaxis.

TORCH infections are a group of congenital infections including toxoplasmosis, other (syphilis, varicella-zoster, parvovirus B19), rubella, cytomegalovirus, and herpes simplex virus. They cross the placenta and cause teratogenic effects. Manifestations include microcephaly, hepatosplenomegaly, growth restriction, rash, and ocular abnormalities. Normal newborn head circumference is 32–36 cm. Normal glucose levels in neonates are 40–60 mg/dL within the first 24 hours.

Rationale for correct answer

1. Microcephaly occurs due to impaired brain development from intrauterine infection. Viral invasion such as cytomegalovirus and rubella directly damages neural progenitor cells, resulting in reduced cranial growth.

3. Sensorineural hearing loss is linked to cytomegalovirus and rubella infections. Viral damage to the inner ear structures and auditory nerve occurs in utero, leading to irreversible deficits after birth.

4. Congenital cataracts develop primarily from rubella infection. Viral replication in the developing lens leads to opacity formation and impaired visual development that can cause lifelong blindness if untreated.

Rationale for incorrect answers

2. Neonatal hypoglycemia is not a direct complication of TORCH infections. It is typically associated with maternal diabetes, intrauterine growth restriction, or perinatal stress. TORCH pathogens primarily cause structural anomalies and neurologic deficits rather than acute metabolic derangements.

5. Shoulder dystocia is a mechanical complication of labor, not an outcome of TORCH infections. It is caused by fetal macrosomia, maternal diabetes, or abnormal pelvic anatomy, not intrauterine infection. TORCH-related complications are congenital abnormalities, not intrapartum mechanical problems.

Take home points

• TORCH infections cross the placenta and damage fetal organs.
• Microcephaly, hearing loss, and cataracts are common complications.
• Hypoglycemia is metabolic, not infectious in origin.
• Shoulder dystocia is mechanical, not congenital.

Vertical transmission refers to the passage of infection from mother to fetus during pregnancy, labor, or delivery. Major pathogens include HIV, GBS, HSV, and TORCH organisms. Prevention strategies involve screening, prophylactic treatment, and safe delivery methods. Normal maternal blood glucose is 70–99 mg/dL fasting and 70–140 mg/dL postprandial, but glucose control does not directly prevent infection spread.

Rationale for correct answers

1. Administering penicillin for GBS-positive mothers during labor prevents neonatal sepsis, pneumonia, and meningitis by reducing bacterial colonization in the birth canal.

2. Educating patients on avoiding undercooked meat reduces toxoplasmosis risk, since Toxoplasma gondii cysts survive in raw or poorly cooked animal tissue and can cross the placenta.

3. Screening for HIV at the initial prenatal visit ensures early detection and initiation of antiretroviral therapy, which reduces mother-to-child transmission rates from about 25% to less than 2%.

5. Recommending cesarean delivery for active HSV lesions prevents neonatal exposure to herpes simplex virus during passage through the birth canal, thereby reducing risk of neonatal herpes infection.

Rationale for incorrect answers

4. Monitoring blood glucose levels is important for detecting gestational diabetes, but it does not prevent vertical transmission of infections. Hyperglycemia increases risk of macrosomia and neonatal hypoglycemia, but it is unrelated to infectious disease transmission from mother to fetus.

Take home points

• Vertical transmission occurs during pregnancy, labor, or delivery.
• Key prevention: maternal screening, prophylaxis, safe food handling, and delivery planning.
• HIV, HSV, GBS, and toxoplasmosis are major targets for prevention.
• Blood glucose monitoring prevents metabolic complications, not infection spread.

Maternal opioid use causes neonatal abstinence syndrome due to chronic in-utero exposure to opioids such as heroin, methadone, or oxycodone. These drugs cross the placenta and stimulate fetal opioid receptors. After birth, the abrupt drug withdrawal leads to neurologic and autonomic symptoms including irritability, tremors, diarrhea, and seizures. Normal neonatal respiratory rate is 30–60 breaths/min, heart rate 120–160 beats/min, and glucose 40–60 mg/dL in the first 24 hours.

Rationale for correct answer

2. Neonatal abstinence syndrome develops because opioids readily cross the placenta and accumulate in the fetal system. Following delivery, drug supply is interrupted, causing withdrawal marked by hypertonia, high-pitched cry, and poor feeding. These symptoms are well recognized consequences of chronic maternal opioid use.

Rationale for incorrect answers

1. Fetal alcohol spectrum disorder results from maternal alcohol consumption, not opioid use. Alcohol causes microcephaly, smooth philtrum, thin upper lip, and growth retardation, whereas opioids cause withdrawal, not teratogenic facial abnormalities.

3. Congenital heart defects are most often associated with chromosomal abnormalities (e.g., trisomy 21) or maternal rubella infection. Opioid exposure does not directly interfere with cardiac septation or outflow tract formation, making this an incorrect consequence.

4. Placenta previa is linked to uterine scarring, multiparity, and advanced maternal age. It occurs when the placenta implants over the cervical os, unrelated to opioid exposure. Opioids act pharmacologically, not structurally, and do not determine placental implantation sites.

Take home points

• Maternal opioid use leads to neonatal abstinence syndrome after delivery.
• Symptoms include tremors, irritability, diarrhea, seizures, and feeding difficulty.
• Alcohol, not opioids, causes fetal alcohol spectrum disorder.
• Placenta previa and congenital heart defects are unrelated to opioid use.

Lead exposure in pregnancy causes miscarriage and neurodevelopmental delays due to its ability to cross the placenta and accumulate in fetal tissues. Lead interferes with neurologic development by disrupting synapse formation and neurotransmitter release. Blood lead levels should be <5 µg/dL in children and <10 µg/dL in adults to be considered safe. Elevated levels increase risks of low birth weight, preterm delivery, and impaired cognition.

Rationale for correct answer

2. Lead exposure is strongly linked to miscarriage and developmental delays. Lead crosses the placenta and accumulates in fetal bone and brain tissue. This results in impaired synaptogenesis, neuronal death, and long-term cognitive deficits. Miscarriage is associated with maternal blood lead levels >10 µg/dL.

Rationale for incorrect answers

1. Mercury exposure, particularly methylmercury from contaminated fish, primarily causes neurotoxicity manifesting as impaired motor skills, cerebral palsy-like features, and sensory deficits. While harmful, it is less directly associated with miscarriage compared to lead.

3. Air pollution increases risks of low birth weight, intrauterine growth restriction, and preterm birth, but evidence for miscarriage and direct neurodevelopmental delay is weaker compared to lead exposure. The impact is more related to hypoxia and placental inflammation.

4. Radiation, especially doses >100 mGy, is associated with growth restriction, microcephaly, and increased childhood cancer risk. However, miscarriage and developmental delay are more consistently documented with lead exposure at much lower levels, making radiation less likely in this context.

Take home points

• Lead exposure in pregnancy is a major cause of miscarriage and developmental delay.
• Mercury mainly causes neurotoxicity and motor deficits, not miscarriage.
• Air pollution contributes to low birth weight and preterm birth.
• Radiation at high doses causes growth restriction and microcephaly, but not primarily miscarriage.

Sudden infant death syndrome (SIDS) is the unexplained death of an infant under 1 year, usually during sleep. Maternal smoking is the strongest modifiable risk factor, as nicotine causes impaired autonomic regulation, reduced arousal, and hypoxemia in the fetus. Normal infant respiratory rate is 30–60 breaths/min and heart rate is 120–160 beats/min; disruption of autonomic control increases risk of apnea and death during sleep.

Rationale for correct answer

2. Smoking during pregnancy and after delivery exposes the fetus and infant to nicotine and carbon monoxide. This reduces oxygen delivery, impairs brainstem respiratory control, and increases SIDS risk by 2–4 times compared to nonsmoking mothers.

Rationale for incorrect answers

1. Caffeine consumption during pregnancy is linked to low birth weight and miscarriage at high intake (>200–300 mg/day), but it is not a major contributor to SIDS. It does not significantly impair neonatal respiratory regulation.

3. High sugar intake predisposes to gestational diabetes and macrosomia but has no established link to sudden infant death. It affects metabolic health, not respiratory arousal mechanisms.

4. Sedentary lifestyle increases maternal obesity risk and complications such as preeclampsia and gestational diabetes, but it does not directly cause SIDS. Infant mortality in this case is more related to perinatal complications than unexplained sudden death.

Take home points

• SIDS is unexplained infant death under 1 year, often during sleep.
• Maternal smoking is the strongest modifiable risk factor.
• Caffeine and high sugar intake affect pregnancy outcomes but not SIDS.
• Sedentary lifestyle increases maternal risk, not infant sudden death.

Fetal alcohol spectrum disorder (FASD) results from maternal alcohol consumption during pregnancy. Ethanol freely crosses the placenta and interferes with neurodevelopment, cellular differentiation, and organogenesis. Manifestations include facial dysmorphia, intrauterine growth restriction, and lifelong cognitive impairment. Normal birth weight is 2.5–4.0 kg, and growth below the 10th percentile indicates restriction. There is no safe threshold of alcohol during pregnancy.

Rationale for correct answer

1. Facial dysmorphia occurs due to alcohol-induced disruption of neural crest cell migration. Classic features include smooth philtrum, thin upper lip, and short palpebral fissures.

3. Growth restriction results from impaired placental blood flow and direct fetal toxicity of ethanol, leading to birth weights <2.5 kg or below the 10th percentile.

4. Neurodevelopmental deficits are long-term consequences of prenatal alcohol exposure, presenting as poor memory, attention deficits, and reduced IQ, caused by neuronal apoptosis and abnormal brain development.

Rationale for incorrect answers

2. Neonatal abstinence syndrome is due to maternal opioid use, not alcohol exposure. It results from withdrawal after delivery and manifests with tremors, irritability, and seizures, unlike structural teratogenic effects of alcohol.

5. Congenital rubella syndrome is caused by maternal rubella infection, not alcohol. It is characterized by cataracts, sensorineural hearing loss, and congenital heart defects, which are unrelated to ethanol teratogenicity.

Take home points

• Alcohol in pregnancy causes fetal alcohol spectrum disorder.
• Classic features: facial dysmorphia, growth restriction, and lifelong neurodevelopmental impairment.
• Opioids, not alcohol, cause neonatal abstinence syndrome.
• Rubella infection, not alcohol, causes congenital rubella syndrome.

Environmental toxin exposure in pregnancy poses risks of miscarriage, growth restriction, and neurodevelopmental deficits. Substances such as mercury, lead, air pollutants, and radiation cross the placenta and disrupt fetal organogenesis. Safe maternal blood lead level is <10 µg/dL, while methylmercury intake should be <0.1 µg/kg/day. Radiation exposure >100 mGy increases fetal malformation risk.

Rationale for correct answer

1. Educating patients to avoid high-mercury fish such as shark, swordfish, and king mackerel prevents methylmercury accumulation, which causes fetal neurotoxicity and cerebral palsy-like features.

3. Screening for lead exposure is critical in high-risk groups (old housing, contaminated water, occupational exposure). Lead crosses the placenta, and maternal levels >10 µg/dL are associated with miscarriage and cognitive impairment.

5. Advising limited radiographic imaging minimizes unnecessary fetal radiation exposure. Doses above 100 mGy increase risk of microcephaly, growth restriction, and childhood cancer, making judicious imaging essential.

Rationale for incorrect answers

2. Encouraging outdoor activities in high-pollution areas increases maternal exposure to particulate matter and carbon monoxide. These impair placental oxygen delivery and raise risks of preterm birth and low birth weight, making this harmful rather than protective.

4. Administering folic acid prevents neural tube defects but does not counteract mercury, lead, or radiation toxicity. Its mechanism is through DNA synthesis and repair, not detoxification, so it is not an intervention against environmental toxins.

Take home points

• Mercury, lead, and radiation are major teratogens during pregnancy.
• Avoiding high-mercury fish prevents fetal neurotoxicity.
• Screening for lead exposure reduces miscarriage and neurodevelopmental risk.
• Limiting radiation exposure is essential to prevent fetal malformations.

Intimate partner violence is a major psychosocial risk factor during pregnancy. It is linked to increased maternal morbidity, poor fetal outcomes, and heightened risk of depression. Pregnant women experiencing violence often present with low birth weight infants (<2500 g), preterm birth (<37 weeks), and maternal complications such as anemia (Hb <12 g/dL) and hypertension (normal <120/80 mmHg). Chronic stress from abuse increases cortisol, leading to placental dysfunction and impaired fetal growth.

Rationale for correct answer

2. Intimate partner violence is a psychosocial condition that significantly increases the risk of poor pregnancy outcomes. It causes maternal stress, depression, inadequate prenatal care, and substance use, all of which increase fetal morbidity and mortality. The question specifically asks for a psychosocial factor, making this the correct choice.

Rationale for incorrect answers

1. Gestational diabetes is a medical, not psychosocial, condition. It is associated with fetal macrosomia (>4000 g), neonatal hypoglycemia (normal 40–60 mg/dL), and polyhydramnios. However, it does not represent a psychosocial factor, and thus it is not the correct answer to this question.

3. Placental abruption is a direct obstetric complication caused by premature separation of the placenta, leading to hemorrhage and fetal distress. It presents with abdominal pain, vaginal bleeding, and non-reassuring fetal heart tones (normal baseline 110–160 bpm). It is a physical complication, not a psychosocial risk factor.

4. Multiple gestation is a biological condition that increases obstetric risk such as preterm birth, preeclampsia, and intrauterine growth restriction. It does not fall under psychosocial factors, which relate to social, emotional, or behavioral conditions affecting pregnancy outcomes.

Take home points

• Intimate partner violence is a psychosocial risk factor that worsens pregnancy outcomes.
• Gestational diabetes and multiple gestation are biological risk factors, not psychosocial.
• Placental abruption is an obstetric complication, not psychosocial in nature.
• Psychosocial risk factors influence maternal mental health and indirectly impact fetal well-being.

Intimate partner violence during pregnancy requires screening, privacy, and appropriate referral for safety. Violence leads to maternal stress, trauma, poor prenatal care, and adverse fetal outcomes like preterm birth (<37 weeks) and low birth weight (<2500 g). Nurses must conduct private, sensitive questioning because disclosure is unlikely in the presence of the abuser. Universal screening is recommended during prenatal visits to ensure early detection and intervention.

Rationale for correct answer

2. Conducting private, sensitive screening is the essential nursing intervention for suspected intimate partner violence. Asking nonjudgmental questions in a safe, confidential environment allows accurate identification of abuse and timely referral to resources, thereby reducing maternal and fetal morbidity.

Rationale for incorrect answers

1. Administering magnesium sulfate is indicated for preeclampsia or eclampsia to prevent seizures. It has no role in identifying or addressing intimate partner violence, which requires psychosocial screening and intervention.

3. Ordering a non-stress test evaluates fetal well-being by monitoring fetal heart rate (normal baseline 110–160 bpm). While useful in obstetric complications, it does not address the underlying psychosocial risk factor of intimate partner violence.

4. Monitoring blood glucose levels is appropriate for gestational diabetes management. Normal fasting glucose in pregnancy is <95 mg/dL, but this is unrelated to psychosocial risk factors such as intimate partner violence.

Take home points

• Intimate partner violence requires private, sensitive screening during prenatal visits.
• Magnesium sulfate is used for eclampsia, not psychosocial risks.
• Non-stress tests assess fetal well-being but do not screen for abuse.
• Glucose monitoring is specific to gestational diabetes, not intimate partner violence.

Multiple gestation increases uterine distension, raising the risk of preterm birth, preeclampsia, and intrauterine growth restriction. In twin pregnancies, preterm birth is the most frequent complication, with over 50% delivering before 37 weeks (normal term = 37–42 weeks). Neonates born preterm face risks including respiratory distress syndrome due to surfactant deficiency (normal surfactant adequate after 34–36 weeks) and feeding difficulties. Increased placental demands also predispose to anemia (Hb <12 g/dL) and gestational hypertension (normal BP <120/80 mmHg).

Rationale for correct answer

2. Preterm birth is the most common complication of multiple gestation. Uterine overdistension, hormonal changes, and increased uteroplacental insufficiency lead to early labor, often before 37 weeks, making this the correct answer.

Rationale for incorrect answers

1. Postpartum depression is a psychosocial condition associated with hormonal shifts, lack of support, and stress. While it may occur after any pregnancy, it is not a direct obstetric complication unique to multiple gestation.

3. Neural tube defects such as spina bifida occur due to folate deficiency and genetic predisposition. They are not more common specifically because of multiple gestation, though nutritional demands are higher in twin pregnancies.

4. Congenital rubella syndrome results from maternal rubella infection during pregnancy. It is unrelated to multiple gestation and presents with deafness, cataracts, and congenital heart disease, not a complication caused by twin pregnancy.

Take home points

• Multiple gestation most commonly leads to preterm birth due to uterine overdistension.
• Neural tube defects are linked to folate deficiency, not multiple gestation itself.
• Congenital rubella syndrome results from maternal infection, not twin pregnancy.
• Postpartum depression is psychosocial, not a direct complication of multiple gestation.

Intimate partner violence during pregnancy causes physical trauma, chronic stress, and inadequate prenatal care, leading to serious maternal and fetal complications. Trauma increases catecholamines and cortisol, impairing uteroplacental perfusion and raising the risk of miscarriage (loss before 20 weeks), preterm labor (<37 weeks), and placental abruption (premature placental separation). These complications stem from both direct physical injury and indirect physiologic stress. Normal pregnancy carries miscarriage risk of 10–15%, but this risk rises with violence. Placental abruption can cause hypovolemia and fetal distress (normal FHR baseline 110–160 bpm).

Rationale for correct answer

1. Miscarriage can occur from direct abdominal trauma or severe maternal stress. Disruption of placental attachment and uterine perfusion contributes to early pregnancy loss.

2. Preterm labor is strongly associated with intimate partner violence. Stress hormones and trauma can trigger uterine contractions, leading to delivery before 37 weeks gestation.

3. Placental abruption results from trauma to the abdomen or chronic vascular stress, leading to premature placental separation. This causes vaginal bleeding, abdominal pain, and compromised fetal oxygenation.

Rationale for incorrect answers

4. Fetal macrosomia (>4000 g) is usually associated with gestational diabetes due to maternal hyperglycemia and increased fetal insulin production. It is not a complication of intimate partner violence.

5. Neonatal hypoglycemia (plasma glucose <40 mg/dL in the first 24 hours) is also linked to infants of diabetic mothers due to excess insulin production in utero. It does not result from intimate partner violence.

Take home points

• Intimate partner violence can cause miscarriage, preterm labor, and placental abruption.
• Fetal macrosomia is associated with gestational diabetes, not abuse.
• Neonatal hypoglycemia is linked to maternal diabetes, not trauma.
• Trauma and stress responses are key mechanisms of violence-related pregnancy complications.

Placental abnormalities such as placenta previa and placental abruption compromise maternal perfusion, cause hemorrhage, and impair oxygen and nutrient transfer to the fetus. These conditions lead to maternal hemorrhage (normal pregnancy blood loss at delivery <500 mL vaginal, <1000 mL cesarean), fetal hypoxia due to disrupted placental oxygen exchange (normal umbilical venous PO₂ ≈ 30 mmHg), and preterm birth (<37 weeks) due to uteroplacental instability. Placental pathology does not directly cause metabolic conditions like neonatal hypoglycemia or congenital structural anomalies like heart defects.

Rationale for correct answers

1. Maternal hemorrhage occurs with placental abruption and placenta previa, where separation or abnormal implantation of the placenta leads to severe bleeding.

2. Fetal hypoxia results from impaired maternal-fetal oxygen transfer when the placenta detaches or is compromised, leading to abnormal fetal heart rate patterns.

4. Preterm birth is common with placental abnormalities, often due to bleeding, uteroplacental insufficiency, or iatrogenic delivery to save maternal or fetal life.

Rationale for incorrect answers

3. Neonatal hypoglycemia (plasma glucose <40 mg/dL in first 24 hours) is most commonly seen in infants of diabetic mothers or those with intrauterine growth restriction. It is not directly caused by placental abnormalities.

5. Congenital heart defects are structural anomalies from abnormal embryonic development, often linked to genetic syndromes or teratogens like rubella. They are not a complication of placental pathology.

Take home points

• Placental abnormalities cause maternal hemorrhage, fetal hypoxia, and preterm birth.
• Neonatal hypoglycemia is metabolic, often due to maternal diabetes.
• Congenital heart defects result from embryonic malformations, not placental disorders.
• Placenta previa and abruption threaten both maternal and fetal survival.

Folic acid deficiency is the primary cause of neural tube defects such as spina bifida and anencephaly. Neural tube closure normally occurs by day 28 of embryonic development, often before pregnancy is recognized. Adequate folate levels (normal serum folate >4 ng/mL) are essential for DNA synthesis, cell division, and neural tissue development. Women of childbearing age are advised to take 400–800 µg daily to prevent defects, with higher doses (up to 4 mg/day) recommended for those with prior affected pregnancies.

Rationale for correct answer

3. Folic acid deficiency impairs neural tube closure due to defective DNA synthesis and cell division. This leads to structural anomalies like spina bifida, making it the most associated nutrient deficiency.

Rationale for incorrect answers

1. Iron deficiency causes maternal anemia (Hb <12 g/dL in pregnancy) leading to fatigue, pallor, and low birth weight infants, but it is not linked to neural tube defects.

2. Calcium deficiency increases maternal risk of osteopenia and may contribute to hypertensive disorders of pregnancy. It does not affect neural tube development.

4. Vitamin D deficiency leads to maternal bone demineralization and neonatal rickets. It is not associated with neural tube closure failure.

Take home points

• Folic acid deficiency is the key cause of neural tube defects.
• Iron deficiency causes maternal anemia but not neural tube defects.
• Calcium deficiency contributes to bone and blood pressure complications, not neural tube defects.
• Vitamin D deficiency affects bone health but not neural tube closure.

Food insecurity during pregnancy leads to poor fetal growth due to inadequate caloric intake, micronutrient deficiencies, and chronic maternal stress. Restricted maternal nutrition reduces uteroplacental blood flow and nutrient transfer, resulting in intrauterine growth restriction (IUGR). IUGR is defined as estimated fetal weight below the 10th percentile for gestational age, with normal birth weight expected between 2500–4000 g at term. Infants affected are at risk of hypothermia, hypoglycemia (<40 mg/dL in first 24 hours), and long-term developmental delays.

Rationale for correct answer

2. Poor fetal growth occurs when maternal malnutrition and food insecurity limit nutrient supply. This results in IUGR and low birth weight, which are common outcomes of inadequate prenatal nutrition.

Rationale for incorrect answers

1. Macrosomia (>4000 g) is typically linked to gestational diabetes mellitus, not food insecurity, as it results from maternal hyperglycemia and excess fetal insulin.

3. Placenta previa, characterized by implantation of the placenta over the cervical os, is an anatomical abnormality unrelated to maternal nutrition or food insecurity.

4. Congenital heart defects arise from abnormal embryonic development influenced by genetic or teratogenic factors. They are not directly caused by food insecurity.

Take home points

• Food insecurity in pregnancy most often leads to poor fetal growth and low birth weight.
• Macrosomia results from maternal diabetes, not malnutrition.
• Placenta previa is a placental implantation disorder, not nutrition-related.
• Congenital heart defects are embryonic malformations, not outcomes of food insecurity.

Maternal obesity in pregnancy is linked to insulin resistance, altered placental function, and systemic inflammation, which increase risks of multiple complications. Obesity raises the likelihood of gestational diabetes mellitus, preeclampsia, cesarean birth, and macrosomia (>4000 g). Neonates face higher risks of shoulder dystocia during delivery, hypoglycemia (<40 mg/dL in first 24 hours), and later-life metabolic disease. Stillbirth risk is elevated in obese pregnancies due to impaired uteroplacental perfusion, with obesity classified as a significant modifiable maternal risk factor.

Rationale for correct answers

1. Increased risk of gestational diabetes mellitus occurs because maternal obesity causes insulin resistance and hyperglycemia, leading to abnormal glucose tolerance.

3. Higher incidence of shoulder dystocia occurs due to fetal macrosomia, common in pregnancies complicated by maternal obesity and diabetes.

5. Increased risk of preeclampsia is linked to obesity through vascular dysfunction, endothelial injury, and chronic inflammation, which raise maternal blood pressure above normal levels (<120/80 mmHg).

Rationale for incorrect answers

2. Decreased risk of macrosomia is incorrect because obesity increases, not decreases, the likelihood of fetal overgrowth due to excess maternal glucose and fat transfer.

4. Reduced likelihood of stillbirth is incorrect because obesity increases stillbirth risk. Mechanisms include impaired placental function, chronic hypoxia, and metabolic abnormalities.

Take home points

• Maternal obesity raises risk for gestational diabetes, preeclampsia, macrosomia, and shoulder dystocia.
• Obesity is linked to increased stillbirth risk, not reduced.
• Macrosomia (>4000 g) is a hallmark complication, not less common in obesity.
• Insulin resistance and inflammation are central mechanisms of obesity-related pregnancy risks.

Nutritional deficiencies in pregnancy increase risks of anemia, neural tube defects, poor fetal growth, and maternal complications. Iron deficiency anemia is the most common, defined as hemoglobin <11 g/dL in the 1st and 3rd trimesters, <10.5 g/dL in the 2nd trimester. Folate deficiency raises neural tube defect risk, prevented by 400–800 µg daily folic acid supplementation. Adequate dietary counseling on iron-rich foods (meat, legumes, leafy greens) improves hemoglobin and hematocrit (normal Hct in pregnancy: 33–44%). Food insecurity is a major barrier to adequate nutrition, requiring referrals to programs like WIC.

Rationale for correct answer

1. Educating on daily folic acid supplementation prevents neural tube defects by supporting DNA synthesis and neural tissue development.

2. Monitoring hemoglobin levels detects iron deficiency anemia early, allowing timely intervention to prevent maternal fatigue and fetal growth restriction.

4. Providing dietary counseling for iron-rich foods ensures adequate iron intake, enhancing hemoglobin production and preventing anemia-related complications.

5. Referring to WIC supports food-insecure patients by providing access to nutrient-rich foods, reducing risks of growth restriction and preterm birth.

Rationale for incorrect answers

3. Encouraging high-sugar diets is inappropriate. Excess sugar intake increases risk of gestational diabetes, macrosomia (>4000 g), and neonatal hypoglycemia (<40 mg/dL). It does not correct nutritional deficiencies.

Take home points

• Folic acid supplementation prevents neural tube defects.
• Iron deficiency anemia is common; monitor hemoglobin and diet.
• Food insecurity requires nursing referrals to support programs like WIC.
• High-sugar diets increase risks of gestational diabetes, not correct deficiencies.

Rh incompatibility occurs when an Rh-negative mother carries an Rh-positive fetus. Hemolysis results from maternal IgG antibodies crossing the placenta and destroying fetal red blood cells. Anemia and hydrops fetalis may occur in severe cases. Normal maternal hemoglobin is 12–16 g/dL and hematocrit is 36–46%. Antibody screening is performed at the first prenatal visit and repeated at 28 weeks if the mother is Rh-negative. Prophylaxis with anti-D immunoglobulin prevents maternal sensitization and protects future pregnancies.

Rationale for correct answer

2. Administration of RhoGAM at 28 weeks is standard to prevent maternal alloimmunization. The drug binds fetal Rh-positive cells that may enter maternal circulation before antibodies form. This prophylaxis decreases risk of hemolytic disease of the newborn in subsequent pregnancies.

Rationale for incorrect answers

1. Hepatitis B vaccine is not indicated in this situation unless the mother is unvaccinated or high risk. It does not prevent alloimmunization and is unrelated to Rh factor status. The timing of hepatitis B vaccination is independent of maternal Rh typing.

3. Screening for Group B Streptococcus is done between 35–37 weeks, not at 28 weeks. The rationale is that colonization status can change during pregnancy, so screening earlier may not provide accurate guidance for intrapartum prophylaxis.

4. Pap smears are not indicated routinely during pregnancy unless cervical screening is due. Performing a Pap smear at 28 weeks offers no benefit in preventing Rh incompatibility and is not part of standard prenatal care at this gestational age.

Take home points

• RhoGAM is given at 28 weeks and within 72 hours postpartum if the baby is Rh-positive.
• Hemolytic disease of the newborn results from maternal IgG antibodies destroying fetal red blood cells.
• GBS screening is done at 35–37 weeks, not 28 weeks.
• Hepatitis B vaccination is unrelated to Rh alloimmunization prevention.

Fundal height measurement is a simple clinical tool used in pregnancy to monitor fetal growth and estimate gestational age after 20 weeks. From 20–36 weeks, the fundal height in centimeters usually corresponds to gestational age in weeks ±2 cm. Normal amniotic fluid index is 8–24 cm. Deviations may suggest intrauterine growth restriction (IUGR) or macrosomia. Measurement reliability decreases after 36 weeks due to fetal descent.

Rationale for correct answer

3. After 20 weeks, fundal height in centimeters approximates gestational age in weeks, allowing assessment of fetal growth and amniotic fluid volume. This provides a non-invasive method for monitoring intrauterine development.

Rationale for incorrect answers

1. Fundal height does not directly assess maternal weight gain. Maternal weight gain is measured using a scale, and normal recommended gain for a woman with normal BMI is 11.5–16 kg.

2. Determination of fetal lie and presentation is done using Leopold’s maneuvers and ultrasound, not fundal height measurement. Fundal height does not indicate fetal orientation.

4. Fetal heart rate variability is monitored using electronic fetal monitoring or Doppler auscultation, not fundal height. Variability is assessed in beats per minute and reflects fetal well-being.

Take home points

• Fundal height correlates with gestational age between 20–36 weeks within ±2 cm.
• Deviations may indicate IUGR, macrosomia, or abnormal amniotic fluid volume.
• Leopold’s maneuvers, not fundal height, assess fetal lie and presentation.
• Fetal heart rate variability requires electronic monitoring, not abdominal measurement.

Preeclampsia is a hypertensive disorder of pregnancy characterized by hypertension, proteinuria, and potential end-organ dysfunction after 20 weeks gestation. Normal blood pressure in pregnancy is <140/90 mmHg. Proteinuria is significant if ≥300 mg/24 h. Severe features include systolic ≥160 mmHg or diastolic ≥110 mmHg, thrombocytopenia <100,000/µL, creatinine >1.1 mg/dL, and symptoms such as headache or visual disturbances. Complications include eclampsia, HELLP syndrome, and fetal growth restriction.

Rationale for correct answer

3. Severe, persistent headaches and blurred vision at 34 weeks are classic signs of preeclampsia with severe features. These result from cerebral vasospasm and edema due to endothelial dysfunction, requiring urgent evaluation and management to prevent seizures.

Rationale for incorrect answers

1. Gestational diabetes mellitus usually presents with polyuria, polydipsia, and polyphagia due to glucose intolerance. It is diagnosed with an oral glucose tolerance test. It does not cause neurologic symptoms such as headaches and blurred vision.

2. Iron deficiency anemia presents with fatigue, pallor, tachycardia, and low hemoglobin (<11 g/dL in pregnancy). It does not cause hypertension, headache, or visual disturbances.

4. Urinary tract infection in pregnancy typically causes dysuria, frequency, urgency, and suprapubic discomfort. Severe cases may cause flank pain or fever but not hypertension with neurologic symptoms.

Take home points

• Preeclampsia is defined as hypertension after 20 weeks with proteinuria or end-organ dysfunction.
• Severe features include headache, visual changes, thrombocytopenia, renal impairment, and liver dysfunction.
• Complications include eclampsia, HELLP syndrome, and intrauterine growth restriction.
• Differentiation from gestational diabetes, anemia, and UTI relies on symptom-specific clinical findings.

First trimester screening is used to assess the risk of aneuploidy such as trisomy 21 and trisomy 18 between 11–14 weeks gestation. It combines nuchal translucency ultrasound measurement with maternal serum levels of free β-hCG and PAPP-A. Increased nuchal translucency (>3.0 mm) is associated with chromosomal abnormalities and congenital heart disease. Normal crown-rump length is used to standardize NT measurements. This screening provides early risk stratification before diagnostic testing.

Rationale for correct answer

3. Nuchal translucency ultrasound is a standard component of first trimester aneuploidy screening. Increased NT thickness indicates abnormal lymphatic fluid accumulation in the fetal neck, often associated with trisomy 21, trisomy 18, and congenital heart defects.

Rationale for incorrect answers

1. Maternal serum alpha-fetoprotein is part of the second trimester quadruple screen, not the first trimester screen. Elevated levels are linked to neural tube defects, while low levels may indicate trisomy 21.

2. The one-hour glucose tolerance test is performed between 24–28 weeks gestation to screen for gestational diabetes mellitus. It is not used for aneuploidy risk assessment.

4. Group B Streptococcus culture is performed at 35–37 weeks to identify carriers who require intrapartum antibiotic prophylaxis. It has no role in first trimester aneuploidy screening.

Take home points

• First trimester screening combines NT ultrasound, free β-hCG, and PAPP-A.
• Increased NT thickness (>3.0 mm) suggests aneuploidy and congenital heart disease.
• Second trimester screening uses MSAFP, hCG, estriol, and inhibin A.
• GTT and GBS culture are performed later in pregnancy for different purposes.

Foodborne infections in pregnancy increase risk of maternal illness and fetal complications due to immunologic changes. Pregnant women are more susceptible to pathogens such as Listeria monocytogenes, Toxoplasma gondii, and Salmonella. Raw seafood may harbor parasites, viruses, and bacteria, posing risks of miscarriage, stillbirth, or neonatal sepsis. Normal maternal white blood cell count in pregnancy is 6,000–16,000/µL due to physiologic leukocytosis. Safe food handling, cooking meat to ≥74°C, and avoiding unpasteurized products are essential preventive measures.

Rationale for correct answer

3. Raw sushi should be avoided because it may contain Listeria and other pathogens. Infection during pregnancy can cross the placenta and cause miscarriage, stillbirth, or neonatal sepsis. Cooking eliminates these risks, making raw seafood unsafe.

Rationale for incorrect answers

1. Cooked chicken breast is safe in pregnancy if thoroughly cooked to an internal temperature of ≥74°C. Proper cooking destroys harmful pathogens such as Salmonella and Campylobacter.

2. Pasteurized milk is safe because pasteurization kills Listeria and other harmful bacteria. Unpasteurized milk, not pasteurized, poses infection risks in pregnancy.

4. Fully cooked vegetables are safe and provide essential vitamins, minerals, and fiber. Risk occurs only with raw or improperly washed vegetables that may harbor Toxoplasma gondii oocysts.

Take home points

• Raw sushi and undercooked seafood should be avoided in pregnancy due to infection risks.
• Pasteurized dairy products are safe; unpasteurized products should be avoided.
• Thorough cooking of meat to ≥74°C prevents bacterial foodborne illness.
• Raw unwashed vegetables may carry Toxoplasma; cooking ensures safety.

Preterm premature rupture of membranes (PPROM) involves fluid leakage from the vagina due to rupture of the amniotic sac before labor. Amniotic fluid normally ranges from 500–1,000 mL at term, with an amniotic fluid index (AFI) of 8–24 cm. Leakage increases risk of infection, preterm birth, and umbilical cord prolapse. Differentiating true amniotic fluid leakage from urinary incontinence can be confirmed with tests such as nitrazine (alkaline pH) and ferning. Prompt medical evaluation is critical for maternal-fetal safety.

Rationale for correct answer

3. Fluid leakage from the vagina is a danger sign because it suggests rupture of membranes, which places the fetus at risk for infection and cord prolapse. Immediate medical evaluation is necessary to prevent complications.

Rationale for incorrect answers

1. Mild ankle swelling is common in late pregnancy due to increased venous pressure and fluid retention. It is generally benign unless associated with hypertension or proteinuria, which would suggest preeclampsia.

2. Occasional heartburn results from progesterone-induced relaxation of the lower esophageal sphincter and uterine pressure on the stomach. While uncomfortable, it is not a warning sign.

4. Fatigue is a common symptom throughout pregnancy due to hormonal changes, increased metabolic demands, and anemia risk. It does not require urgent evaluation unless severe or associated with other symptoms.

Take home points

• Vaginal fluid leakage is an urgent warning sign requiring immediate evaluation.
• Mild ankle swelling and heartburn are common discomforts, not emergencies.
• Fatigue is expected in pregnancy but should be monitored if severe or persistent.
• Ruptured membranes increase risk of infection, preterm labor, and cord prolapse.

Alcohol consumption in pregnancy poses significant risks because ethanol freely crosses the placenta, and the fetal liver cannot metabolize it effectively. This leads to fetal alcohol spectrum disorders (FASD), characterized by growth restriction, neurodevelopmental delay, and craniofacial abnormalities. There is no safe threshold; even small amounts can disrupt organogenesis. Normal newborn head circumference is 32–36 cm, but alcohol exposure may cause microcephaly. Abstinence from alcohol is the only proven preventive measure.

Rationale for correct answer

3. There is no known safe amount of alcohol consumption in pregnancy. Any exposure increases risk of teratogenic effects, especially during the first trimester when organogenesis occurs, but risks persist throughout gestation.

Rationale for incorrect answers

1. Moderate alcohol consumption after the first trimester is not safe. The fetal brain continues developing throughout pregnancy, and alcohol can still cause growth and neurodevelopmental impairment.

2. It is not only heavy drinking that causes harm; even light or occasional drinking has been linked to subtle cognitive and behavioral issues. No level is safe.

4. Red wine is not permissible in pregnancy, regardless of its antioxidant content. The ethanol in wine carries the same teratogenic risks as other alcoholic beverages.

Take home points

• No amount of alcohol is safe at any point in pregnancy.
• Alcohol causes fetal alcohol spectrum disorders with lifelong effects.
• Both heavy and light alcohol use can impair fetal growth and brain development.
• Prevention requires total abstinence during pregnancy.

Pre-gestational diabetes mellitus in pregnancy increases risk of congenital anomalies due to hyperglycemia during organogenesis (first 8 weeks). Poor control causes oxidative stress, disrupting cardiac, neural tube, and skeletal development. Normal fasting glucose is 70–99 mg/dL, and HbA1c target in pregnancy is <6–6.5%. Poorly controlled diabetes also increases risks of macrosomia, spontaneous abortion, polyhydramnios, and neonatal hypoglycemia.

Rationale for correct answer

3. Congenital anomalies are strongly associated with pre-gestational diabetes and poor glycemic control, particularly affecting the heart, neural tube, and musculoskeletal system. This risk is highest during early embryogenesis.

Rationale for incorrect answers

1. Fetal alcohol syndrome results from maternal alcohol use, not diabetes. It causes microcephaly, growth restriction, and facial dysmorphisms, unrelated to hyperglycemia.

2. Neonatal abstinence syndrome is caused by maternal opioid use, leading to withdrawal symptoms after birth. It is not linked to maternal diabetes.

4. Poor maternal glycemic control increases risk of respiratory distress syndrome due to delayed—not premature—lung maturation. High maternal glucose and insulin levels suppress fetal surfactant production, delaying pulmonary maturity.

Take home points

• Poor glycemic control in pre-gestational diabetes increases congenital anomaly risk.
• Common malformations involve the cardiac, neural tube, and skeletal systems.
• Alcohol and opioid use cause separate fetal syndromes, not related to diabetes.
• Hyperglycemia delays fetal lung maturation, raising risk of RDS.

Hepatitis B virus (HBV) infection in pregnancy is a major cause of vertical transmission to the newborn, particularly during delivery. Screening for hepatitis B surface antigen (HBsAg) at the first prenatal visit identifies women with active infection. Normal liver enzymes (ALT 7–56 U/L, AST 10–40 U/L) may be elevated in infection but screening focuses on transmission risk. Newborns of HBsAg-positive mothers must receive hepatitis B vaccine and hepatitis B immune globulin (HBIG) within 12 hours of birth to prevent chronic infection.

Rationale for correct answer

3. Screening for HBsAg in pregnancy is done to prevent vertical transmission. Early identification ensures immediate neonatal prophylaxis with HBV vaccine and HBIG, which reduces transmission risk from 90% to <5%.

Rationale for incorrect answers

1. Immunity to hepatitis B is determined by hepatitis B surface antibody (anti-HBs), not HBsAg. Presence of anti-HBs indicates vaccination or recovery from past infection.

2. HBsAg screening does not assess liver function. Liver function is measured with ALT, AST, bilirubin, and albumin, not HBsAg.

4. Maternal vaccination decisions are based on serology for anti-HBs and HBc antibodies, not HBsAg alone. HBsAg screening specifically targets prevention of neonatal transmission.

Take home points

• HBsAg screening at the first prenatal visit detects maternal infection.
• Vertical transmission risk is highest at delivery without prophylaxis.
• Newborns of HBsAg-positive mothers need HBV vaccine + HBIG within 12 hours.
• Anti-HBs, not HBsAg, indicates maternal immunity to hepatitis B.

Anatomy scan (Level II ultrasound) performed at 18–22 weeks gestation evaluates fetal structural development. It provides detailed assessment of organs, skeletal structures, placental location, and amniotic fluid volume (normal AFI 8–24 cm). This scan identifies congenital anomalies such as cardiac defects, neural tube defects, and abdominal wall defects. It also confirms fetal number, gender if desired, and growth parameters. Early detection allows for counseling, prenatal interventions, or delivery planning for affected fetuses.

Rationale for correct answer

3. The primary benefit of the anatomy scan is detection of structural anomalies. Detailed imaging identifies congenital defects in the heart, brain, spine, kidneys, and limbs, allowing timely management and family counseling.

Rationale for incorrect answers

1. Fetal heart tones are typically assessed via Doppler starting at 10–12 weeks. Anatomy scan is not intended primarily for confirming heart activity.

2. Gestational diabetes screening is performed at 24–28 weeks using glucose tolerance testing. Anatomy scan does not assess maternal glucose metabolism.

4. Maternal risk for preeclampsia is assessed through blood pressure monitoring, urine protein evaluation, and maternal history. Ultrasound does not predict preeclampsia risk.

Take home points

• Anatomy scan at 18–22 weeks evaluates fetal structural development and detects congenital anomalies.
• Placental location and amniotic fluid volume are also assessed.
• Fetal heart tones and maternal conditions are evaluated through other methods.
• Early detection allows for prenatal counseling and delivery planning.

Comprehensive prenatal history is critical for identifying risk factors that may affect maternal or fetal health. It includes family history, past medical and surgical history, obstetric history, and social history, including substance use. Normal maternal hemoglobin is 12–16 g/dL, and hematocrit 36–46%; abnormalities in history may indicate increased risk for anemia or other complications. Dietary habits are assessed if they impact health or pregnancy outcomes, but personal preferences unrelated to medical conditions are not essential.

Rationale for correct answers

1. A detailed family history identifies genetic disorders that may affect the fetus, such as cystic fibrosis, sickle cell disease, or trisomies. This informs risk assessment and potential genetic counseling.

2. Past surgical history is important because previous abdominal or pelvic surgeries may affect pregnancy management, labor, or delivery options. Knowledge of prior procedures aids in planning safe maternal care.

4. Social history, including substance use (tobacco, alcohol, illicit drugs), is crucial to assess risks for fetal growth restriction, preterm birth, or congenital anomalies. It guides counseling and intervention.

Rationale for incorrect answers

3. Current preferences for newborn clothing are not medically relevant to prenatal risk assessment and do not impact pregnancy management.

5. Dietary restrictions unrelated to medical conditions are not essential in the initial prenatal history unless they affect nutritional adequacy or pregnancy outcomes. Focus is on medically significant nutrition needs.

Take home points

• Comprehensive prenatal history identifies maternal, fetal, and genetic risk factors.
• Family history and past surgical history guide risk assessment and delivery planning.
• Social history, including substance use, directly impacts fetal outcomes.
• Non-medically relevant preferences or dietary habits are not critical components.

Routine prenatal physical assessment focuses on monitoring maternal and fetal well-being throughout pregnancy. Key components include maternal vital signs, fetal heart tones, and fundal height. Normal blood pressure is <140/90 mmHg, heart rate 60–100 bpm, respiratory rate 12–20/min, and temperature 36.5–37.5°C. Fundal height in centimeters approximates gestational age between 20–36 weeks ±2 cm. These assessments help identify complications such as preeclampsia, fetal growth restriction, or multiple gestation.

Rationale for correct answer

1. Maternal vital signs are monitored at every prenatal visit to detect hypertension, tachycardia, or fever. Abnormal readings may indicate preeclampsia, infection, or other maternal complications.

2. Fetal heart tones are assessed to ensure fetal well-being. Normal fetal heart rate ranges from 110–160 bpm, and deviations may signal fetal distress requiring further evaluation.

3. Fundal height is measured to monitor fetal growth and amniotic fluid volume. Deviations >2 cm from gestational age may indicate intrauterine growth restriction, macrosomia, or oligohydramnios/polyhydramnios.

Rationale for incorrect answers

4. A detailed neurological examination of the mother is not routinely performed unless there are specific symptoms such as headaches, vision changes, or neurological deficits. It is not part of standard prenatal visits.

5. Extensive gynecological examination is not required at every visit. Pelvic exams are typically done at the initial visit and selectively based on risk factors or complications. Routine subsequent visits focus on maternal and fetal assessments.

Take home points

• Maternal vital signs monitor for hypertension, infection, and maternal complications.
• Fetal heart tones ensure fetal well-being and detect distress early.
• Fundal height tracks fetal growth and amniotic fluid status.
• Neurological and extensive gynecological exams are done only when indicated.

Initial prenatal laboratory testing is essential to assess maternal hematologic, immunologic, and infectious status to optimize maternal and fetal outcomes. Common tests include CBC to detect anemia (normal hemoglobin 12–16 g/dL, hematocrit 36–46%), blood type and Rh factor to identify alloimmunization risk, and rubella titer to determine immunity (positive ≥1:10). These tests help guide prophylaxis, vaccination, and management decisions early in pregnancy. Other tests may include syphilis, HIV, hepatitis B, and urine studies depending on epidemiology and risk factors.

Rationale for correct answer

1. CBC is routinely performed at the initial prenatal visit to detect anemia, leukopenia, or thrombocytopenia. Maternal hemoglobin below 11 g/dL in the first trimester indicates iron-deficiency anemia, guiding supplementation.

2. Blood type and Rh factor identify potential Rh incompatibility. Rh-negative mothers require RhoGAM prophylaxis to prevent hemolytic disease of the newborn in future pregnancies.

4. Rubella titer determines immunity. Nonimmune women (titer <1:10) are counseled to avoid pregnancy until vaccination, as rubella infection can cause congenital rubella syndrome.

Rationale for incorrect answers

3. Hepatitis C antibody screening is not routinely performed at the initial prenatal visit unless the patient has specific risk factors such as intravenous drug use, history of blood transfusions before 1992, or known HCV exposure. Universal screening is not standard practice.

5. Thyroid function tests are not routinely done in all pregnant women. Screening is indicated only for those with a history of thyroid disease, symptoms suggestive of hypo- or hyperthyroidism, or high-risk factors such as autoimmune disease or previous pregnancy complications.

Take home points

• CBC, blood type/Rh, and rubella titer are standard first-trimester labs.
• Anemia is defined as hemoglobin <11 g/dL in the first trimester.
• Rh-negative mothers require prophylaxis to prevent hemolytic disease of the newborn.
• Hepatitis C and thyroid function tests are performed selectively based on risk or history.