PLACENTAL TRANSPORT AND FETAL NUTRITION
• The intervillous space is the compartment where maternal-fetal transfer takes place. Placental villi form a large (approximately 10 m2) exchange surface at term and placental transfer is of great importance in the nutrition of the fetus.
Passive Diffusion
• Most of the molecules with a molecular weight below 500 daltons pass in this way. Insulin, steroid hormones and thyroid hormones pass through, albeit at a very slow rate.
• Oxygen, carbon dioxide, water, most electrolytes and anesthetic gases pass through the placenta by passive diffusion.
Facilitated Diffusion
• Glucose (GLUT-1 and GLUT-3), lactate (as lactic acid) cross the placenta by facilitated diffusion.
Active Transport
• Essential amino acids, iodine, calcium, phosphorus, ascorbic acid (Vit C), iron and folic acid pass through the placenta by active transport.
Specific Receptor Mediated Endocytosis
• LDL (250,000 DA) and IgG (160,000 DA) cross the placenta by endocytosis.
IgA, IgM, heparin, erythropoietin, TSH, ACTH, triacylglycerol and coagulation factors do not cross the placenta.
FETAL CIRCULATION SYSTEM
• Fetal circulatory system shows some differences from adults. Chief among these is that fetal blood does not need the pulmonary artery system to be oxygenated, and therefore blood from the right ventricle bypasses the lungs. Again, fetal heart chambers work in parallel, not in series, and myocardium and brain receive the most oxygen-rich blood.
• In the 3rd week of pregnancy, blood vessels begin to appear in the chorionic villi. In the 4th week, the cardiovascular system is formed and the real circulation begins.
• Nutrients and oxygen from the placenta are transported to the fetus through a single umbilical vein. The most oxygen-rich blood is located in the ductus venosus, with an oxygen saturation of approximately 85% . The umbilical vein divides into two in the liver: the ductus venosus and the portal sinus. The ductus venosus bypasses the liver and pours directly into the inferior vena cava . Since it does not give blood to other organs, this blood with high oxygen content goes directly to the heart . On the other hand, as the portal sinus gives blood to the liver via hepatic veins, the amount of oxygen in its content decreases. This blood, which is deoxygenated in the liver, is then poured into the inferior vena cava.
Thus, the blood coming to the heart via the inferior vena cava becomes a mixture of well-oxygenated blood carried by the ductus venosus and deoxygenated blood coming from below the level of the liver and diaphragm (oxygen saturation about 70%).
• The well-oxygenated part of the blood in the inferior vena cava pouring into the right atrium goes to the left atrium (oxygen saturation approximately 70%), left ventricle (oxygen saturation approximately 65%) and from there to the brain via the foramen ovale; The deoxygenated part of the blood is poured into the right ventricle and goes to other parts of the body. This different distribution of blood according to oxygen content is provided by the flow of the blood in the inferior vena cava and the structure of the right atrium. Well-oxygenated blood flows in the middle part of the inferior vena cava, while deoxygenated blood flows in the outer part near the vessel wall. Thus, when it is poured into the right atrium, the chambers called crista dividens in the atrium direct the oxygenated blood flowing faster and in the middle part to the foramen ovale; It directs the deoxygenated blood flowing in the outer part close to the vessel wall to the tricuspid valve.
• Less oxygenated blood from the brain, which is poured into the right atrium via the vena cava superior (oxygen saturation about 29%), is also poured into the right ventricle (approximately 55% saturation).
Because of all these flow systems, the oxygen content of the blood in the right ventricle is 15-20% less than in the left ventricle.. 90% of the blood exiting the right ventricle is poured directly into the abdominal aorta (about 60% oxygen saturation) by bypassing the lungs via the ductus arteriosus (oxygen saturation approximately 52%). 10% of the blood goes to the lungs. This deoxygenated blood carried by the abdominal aorta is transported to the placenta via the a.iliaca interna (hypogastric arteries) that separates from the common iliac arteries and the umbilical arteries (oxygen saturation approximately 58-60%).
Some fetal structures and their adult counterparts
• Umbilical artery - Medial umbilical folds
· Umbilical vein - Lig. teres hepatis
· Ductus arteriosus - Lig. arteriosus
• Ductus venosus - Lig. venosum
• Urachus (Allantois) - Median umbilical ligament
FETAL HEMOPOETIC SYSTEM
• Hemopoiesis begins in the embryo at the earliest and first in the yolk sac . Gower 1, Gower 2 and Portland hemoglobins are made here until the gestational week 8-10 . From the 8-10 week onwards, the hematopoiesis passes to the liver. Hemoglobin F (Hbf) is produced in the liver during this period. After the 16th week of pregnancy, the main site of hematopoiesis becomes the bone marrow, and hemoglobin A (HbA) begins to be made from there.
• Since fetal HbF has a high affinity for oxygen, it 'binds more oxygen under the same conditions' than adult HbA. As pregnancy progresses, HbF begins to decrease in the fetus, and at term, 75% of the fetal blood is HbF. After birth, HbF gradually decreases and is replaced by HbA.
• Fetus starts to make procoagulant, fibrinolytic and anticoagulant proteins at the 12th week of intrauterine. These proteins, which are found in high amounts in the mother, cannot cross the placenta.
• While the level of prealbumin, one of the plasma proteins, decreases as pregnancy progresses, other proteins increase.
FETAL IMMUNE SYSTEM
• The transmission of IgG from mother to fetus begins approximately at the 16th week of pregnancy, and the highest transmission occurs in the last 4 weeks of pregnancy. Therefore, IgG levels are even lower in preterm infants. In a normal fetus, very small amounts of IgM are made and IgM cannot cross the placenta. Therefore, high amounts of IgM in the fetus reflect the fetus's own immune response and mostly due to intrauterine fetal infections due to rubella, CMV or toxoplasma.
While IgG production in the fetus starts after the 20th gestational week; IgA, D and E cannot be made in the fetus.
• B lymphocytes are seen in the liver at the 9th week, and in the blood and spleen at the 12th week. T lymphocytes are released from the thymus at 14 weeks.
FETAL NERVOUS SYSTEM
• While the brain and spinal cord are formed from the wall of the neural tube, the ventricular system is developing from its lumen. At the end of the 6th week, the neural tube is closed (cranial end closes on 38th day, caudal end on 40th day according to SAT). By week 6, three primary vesicles (prosencephalon, mesencephalon, and rhombencephalon) appear at the cranial end of the neural tube. In the 7th week, five secondary vesicles develop. The structures that will develop from these vesicles in the future are as follows;
► Telencephalon; cerebral hemisphere
► Diencephalon; Thalamus
► Mesencephalon; midbrain
► Metencephalon; Pons and cerebellum
► Myelencephalon; Medulla oblongata
• Neuronal proliferation peaks at 3-4 months. Neuronal migration also occurs simultaneously and makes picks in the month 3-5.
• The development of the CNS continues throughout pregnancy and until the second postpartum year. The spinal cord reaches S1 level at 24 weeks intrauterine, L3 level at birth and L1 level in adult. Myelination of the spinal cord begins in the 6th month of pregnancy and continues until the end of the 1st year.
FETAL GASTROINTESTINAL SYSTEM
• After the embryological formation of the yolk sac, various extensions (foregut, midgut and hindgut) emerge to form the digestive system.
► Builds evolving from Foregut; Pharynx, lower respiratory tract, esophagus, stomach, proximal duodenum, liver, pancreas and biliary tract
► Structures evolving from Midgut; Distal duodenum, jejunum, ileum, cecum, appendix and right colon
► Structures evolving from Hindgut; Superior part of left colon, rectum and anal canal
• Fetal swallowing starts in the week 10-12 . In the same period, peristalsis appears in the small intestines and glucose absorption can be done. There is no ability to suck before 24 weeks. Meconium passage may occur in the mature fetus with normal intestinal peristalsis or with vagal stimulation due to cord compression. In addition, meconium passage occurs with the stimulation of arginine vasopressin (AVP) release from the pituitary gland of the fetus remaining in the hypoxic environment.
• Fetal liver enzymes are at a very low level compared to adults. For this reason, fetal liver cannot conjugate the already increased bilirubin load due to short-lived erythrocytes, and from the 12th week, unconjugated bilirubin is released into the amnion, from which it passes to the mother via the placenta.
FETAL URINARY SYSTEM
• In the embryo, pronephros is at 2 weeks, mesonephros is at 5 weeks, and metanephros is at 9-12 weeks. starts a week. While the kidneys and ureters develop from the intermediate mesoderm; The bladder and urethra also develop from the urogenital sinus.
• At the 14th week of pregnancy, loops of Henle form and reabsorption begins. Fetal kidneys begin to produce urine at 12 weeks. Fetal urine is hypotonic. Renal functions increase as pregnancy progresses.
FETAL RESPIRATORY SYSTEM
• Fetal respiratory movements can be detected in the 11th week.
• The anatomical development of the lungs occurs in 4 stages.
► Pseudoglandular stage (between 5-17 weeks); An intrasegmental bronchiole tree develops.
► Canalicular stage (between 16-25 weeks); Each terminal bronchiole divides into several respiratory bronchioles, and respiratory bronchioles into numerous saccular ducts.
► Terminal sac period (starts after 25 weeks); Respiratory bronchioles transform into primitive pulmonary alveoli (terminal sac).
► Alveolar stage; Although the complete transition is not certain, it usually starts at 32 weeks.
• Surfactant prevents the collapse of alveoli after birth and type II pneumocytes begin to synthesize surfactant at 24 weeks. 90% of the surfactant is composed of lipids and the remaining 10% is composed of proteins. The major apoprotein in the structure of surfactant is Surfactant Protein A (SP-A).
• Phospholipids provide the basis for the surface tension reducing effect of the surfactant. 80% of glycerophospholipids are phosphatidylcholine (lecithins). The main component responsible for the functionality of the surfactant is a specific lecithin called dipalmitolphosphatidylcholine (DPPC) and it constitutes 50% of all lecithins. Phosphatidylglycerol (PG), the second important component, is present at a rate of 8-15%. Another component is phosphatidylinositol (PI).
FETAL ENDOCRINE SYSTEM
• While the adenohypophysis develops from the oral ectoderm (Rathke's sac) in the embryo, the neurohypophysis develops from the neuroectoderm. The middle pituitary begins to disappear before term (a MSH, beta-endorphin).
• At the 7th week of pregnancy, the fetal pituitary gland begins to make ACTH, at the 13th week, growth hormone and LH begin to be made, and at the end of the 17th week, the production of all pituitary hormones begins. Fetal neurohypophysis 10-12. It begins to secrete oxytocin and arginine vasopressin (AVP).
• Thyroid gland begins to secrete within a week 10-12. TSH, thyroxine and TBG can be detected in fetal serum at 11 weeks. Free T4, free T3 and TBG increase continuously throughout fetal life, and at 36 weeks, when compared to adults, serum TSH concentrations are high, whereas total and free T3 levels are low and T4 levels are normal. This shows that the fetal thyroid gland is not sensitive to feedback mechanisms until term. The fetus retains more iodine than the mother.
• The placenta deiodinates maternal thyroid hormones, preventing their effective transmission to the fetus (converts T4 and T3 to reverse T3, which is ineffective); however, since this is within a limited capacity, the placenta cannot deiodinate all thyroid hormones in the overproduction of maternal thyroid hormones. Thyroid-stimulating immunoglobulins and long-acting thyroid stimulator (LATS) pass directly to the fetus.
• Fetal adrenals are hypertrophic. The reason for this is that the fetal zone, which disappears after birth, is overactive in intrauterine life. This zone secretes large amounts of adrenal steroids and synthesizes aldosterone.
• In the fetal pancreas, glucagon can be detected at week 8 and insulin at week 12. However, the fetus is unresponsive to hypoglycemia. By week 16, most of the pancreatic enzymes are present. Insulin is a growth hormone in all tissues of the fetus.