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By week 26, the fetus exceeds 400 grams. A weight of 300–400 grams corresponds more closely to fetal parameters seen around week 20–22, not week 26.

A weight of 1–1.2 kg is typical around week 28–30, during early third trimester. At week 26, the fetus has not yet accumulated enough fat and muscle to reach this mass.

Weights of 1.5–2 kg occur in the late third trimester, generally around weeks 32–34. This is beyond the expected weight for a fetus at 26 weeks.

Magnesium sulfate is used for neuroprotection in preterm infants <32 weeks and for seizure prophylaxis in preeclampsia, not lung maturation. It does not stimulate surfactant production.

Oxytocin is a uterotonic agent used to induce or augment labor, not to promote fetal lung maturity. Its administration would worsen preterm labor outcomes by promoting contractions.

Nifedipine is a calcium channel blocker used as a tocolytic to delay preterm labor. While it can prolong pregnancy, it does not directly influence surfactant production or lung development.

Testing at 24–26 weeks is too early to accurately predict colonization status at term, since GBS colonization can change. Early testing may miss new colonization or clear existing transient colonization.

At 28–30 weeks, GBS screening is still premature. Colonization detected at this point does not reliably indicate presence at delivery, potentially leading to unnecessary or missed prophylaxis.

While 32–34 weeks is closer to delivery, it is still earlier than recommended. Testing at this stage may not reflect GBS status at term, reducing accuracy and predictive value.

The fetal liver produces immunoglobulins like IgM but cannot produce IgG in significant quantities. IgM is the first antibody synthesized by the fetus but does not confer maternal-derived passive immunity.

Amniotic fluid contains nutrients, hormones, and fetal waste products but does not deliver immunoglobulins systemically. While some immune cells may be present, it does not function in providing passive immunity.

Placental hormones (e.g., hCG, progesterone, estrogens) support pregnancy maintenance and fetal development but do not play a role in immune protection. They do not transfer antibodies or confer immune function.

Oxygen transport to the fetus occurs via placental gas exchange, not surfactant. Oxygenated maternal blood diffuses through the placenta to the fetal circulation, independent of pulmonary function before birth.

While surfactant has minor immune-modulatory functions, its primary role is not infection prevention. Other components like alveolar macrophages and immunoglobulins play a more significant role in pulmonary immune defense.

Fetal breathing movements are controlled by the central nervous system and are not driven by surfactant. These movements begin around week 20 and help condition respiratory muscles, but surfactant is not their initiator.