Which of the following are the primary functions of the placenta? Select all that apply
Transfer of oxygen from maternal blood to fetal blood.
Excretion of fetal waste products into the maternal circulation.
Transfer of immunoglobulins (antibodies) from the mother to the fetus.
Production of fetal hemoglobin.
Regulation of fetal blood pressure.
Correct Answer : A,B,C
The placenta is a vital organ for fetal development, facilitating maternal-fetal exchange. It performs gas exchange, nutrient delivery, and waste removal between maternal and fetal blood without direct blood mixing. The placenta also transfers immunoglobulins, mainly immunoglobulin G (IgG), providing passive immunity to the fetus. It produces hormones essential for pregnancy maintenance but does not produce fetal hemoglobin or regulate fetal blood pressure directly. Normal placental weight ranges from 400 to 600 grams at term.
Rationale for correct answers
A. The placenta facilitates the transfer of oxygen from maternal blood to fetal blood via diffusion through the placental membrane, critical for fetal oxygenation.
B. It acts as an interface for the excretion of fetal waste products such as carbon dioxide and urea into maternal circulation for elimination.
C. The placenta transfers maternal immunoglobulins, especially IgG, across the syncytiotrophoblast to the fetal circulation, providing passive immunity.
Rationale for incorrect answers
D. Fetal hemoglobin (HbF) is synthesized by the fetal liver and bone marrow, not by the placenta.
E. Regulation of fetal blood pressure is controlled by fetal cardiovascular and renal systems, not directly by the placenta.
Take home points
- The placenta transfers oxygen and nutrients and removes fetal wastes.
- It mediates passive immunity by transferring maternal antibodies to the fetus.
- Placenta does not synthesize fetal hemoglobin or regulate fetal blood pressure.
- Placental function is essential for fetal survival and growth.
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Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is C
Explanation
Blastocyst adhesion is a critical step in implantation where the blastocyst attaches to the endometrial lining. This process is mediated by cell adhesion molecules such as integrins and cadherins, which facilitate specific binding between trophoblast cells and the extracellular matrix of the uterine epithelium. Integrins are transmembrane receptors that recognize extracellular matrix proteins like fibronectin, while cadherins mediate calcium-dependent cell-cell adhesion. This interaction occurs around day 6-7 post-fertilization and is essential for successful implantation and establishment of pregnancy.
Rationale for correct answers
C. Integrins and cadherins mediate blastocyst adhesion by promoting specific binding between the trophoblast and uterine epithelium. These molecules regulate the attachment and communication necessary for the blastocyst to invade and implant properly.
Rationale for incorrect answers
A. Estrogen and luteinizing hormone are endocrine hormones involved in ovulation and endometrial preparation but do not directly mediate cellular adhesion during blastocyst attachment.
B. Fibrin and collagen are extracellular matrix components but are not the primary molecules facilitating blastocyst adhesion; rather, they form structural scaffolds.
D. Histamine and prostaglandins are involved in inflammatory responses and uterine contractions but do not mediate the adhesive interactions of the blastocyst.
Take home points
- Integrins and cadherins are the key adhesion molecules enabling blastocyst attachment to the endometrium.
- Hormones like estrogen prepare the endometrium but do not directly mediate adhesion.
- Extracellular matrix proteins support tissue structure but are not primary adhesion mediators.
- Implantation requires coordinated molecular and cellular interactions for successful pregnancy.
Correct Answer is ["A","C","E"]
Explanation
Fetal growth restriction (FGR) is a condition where the fetus fails to achieve its genetically predetermined growth potential, often due to placental insufficiency, leading to chronic hypoxia and nutrient deprivation. Oligohydramnios, defined as an amniotic fluid index less than 5 cm or a single deepest pocket less than 2 cm, frequently accompanies FGR. Amniotic fluid volume depends primarily on fetal urine production, lung fluid secretion, and swallowing. Placental dysfunction, fetal renal anomalies, and altered fetal circulation can decrease urine output, reducing amniotic fluid and causing oligohydramnios.
Rationale for correct answers
A. Reduced fetal urine output occurs secondary to placental insufficiency, which causes hypoxia and redistribution of blood flow, limiting kidney perfusion and thus decreasing urine production—the major source of amniotic fluid in the third trimester.
C. Congenital anomalies of the fetal renal system impair urine formation or excretion, directly reducing amniotic fluid volume, as fetal urine constitutes up to 90% of amniotic fluid after 16 weeks gestation.
E. A shift in fetal blood flow away from the kidneys (known as blood flow redistribution or “brain-sparing”) prioritizes vital organs during hypoxia, reducing renal perfusion and urine output, thus contributing to oligohydramnios.
Rationale for incorrect answers
B. Increased fetal swallowing of amniotic fluid is not a typical compensatory mechanism in FGR; rather, swallowing usually maintains normal fluid balance and is not significantly increased in FGR or oligohydramnios.
D. Absence of functional kidneys (e.g., bilateral renal agenesis) leads to anuria and severe oligohydramnios, but this is a specific congenital anomaly rather than a common cause of FGR-related oligohydramnios.
Take home points
- Placental insufficiency decreases fetal renal perfusion, reducing urine output and amniotic fluid.
- Fetal renal congenital anomalies can impair urine production, leading to oligohydramnios.
- Fetal blood flow redistribution prioritizes brain over kidneys, reducing renal function.
- Oligohydramnios is a frequent finding in FGR and indicates compromised fetal well-being.
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