Flashcards in Lecture 12: Placental Physiology & Developmental Disorders Deck (19)
This is not at a function of the placenta:
A. Diffusion of oxygen and carbon dioxide
B. Attaches fetus to mother’s uterine wall
C. Diffusion of foodstuffs
D. Excretion of waste products
Ans: B. Placenta is attached to the uterus but the it is more of a trading surface than an adhesion membrane to the developing embryo
Functions of Placenta
• Diffusion of oxygen and carbon dioxide
• Diffusion of foodstuffs
• Excretion of waste products
Which is a characteristic of the early placenta?
A. It is thin
B. It has high permeability
C. It has large surface area
D. Total diffusion conductance is miniscule
Early placenta: • Thick • Permeability low • Small surface area • Total diffusion conductance is miniscule
Late placenta: • Thin • Permeability high • Large surface area • Large increase in placental diffusion
Reasons why adequate oxygenation of the fetus can occur with low pressure gradient is:
A. Maternal hemoglobin has a higher affinity for oxygen
B. Fetal hemoglobin has a higher affinity for oxygen.
C. Maternal hemoglobin has 50% more concentration than fetal
D. Fetus is nourished with less amount of oxygen as compared to the mother
Diffusion of Oxygen and Carbon Dioxide
Oxygen pressure gradient (near end of pregnancy): • PO2 of mother: 50 mm Hg • PO2 of fetus: 30 mm Hg
Reasons why adequate oxygenation can occur with such a low pressure gradient (mean diffusion gradient pressure = 20 mm Hg)
• Fetal hemoglobin has a higher affinity for oxygen.
• Fetal blood hemoglobin concentration is about 50% greater than maternal.
• Bohr effect
How does the Bohr Effect contribute to the distribution of O2 from the mother?
A. Increase capacity of fetal blood to combine with O2
B. Decrease capacity of fetal blood to combine with O2
C. Increase capacity of maternal blood to combine with O2
D. Fetal blood becomes more acidic
Bohr effect: • Hemoglobin can carry more oxygen at a low PCO2• Fetal blood coming into placenta carries more CO2.
• Excess CO2 diffuses into maternal blood.
• Fetal blood becomes more alkaline
• Maternal blood becomes more acidic.
• Changes cause: • Increase in capacity of fetal blood to combine with oxygen • Decrease in capacity of maternal blood to combine with oxygen
Double Bohr effect: • Refers to the double shift in the maternal blood and in the fetal blood.
Bohr effect: shift of oxygen-hemoglobin dissociation curve to right and downward forces oxygen away from the hemoglobin and delivers increased amounts of oxygen to the tissues.
How is glucose transported to fetal blood?
A. Directly via placenta
B. Due to higher affinity of fetal blood
C. Via trophoblast cells
D. Slow diffusion
Carbon dioxide diffusion: • PCO2 of fetal blood = 2-3X higher than maternal blood.
Diffusion of foodstuffs: • Facilitated diffusion of glucose via trophoblast cells
• Slower diffusion of fatty acids into fetal blood
Excretion of waste products: • Urea, uric acid, and creatinine diffuse from fetus to maternal blood.
Human chorionic gonadotropin functions include:
A. Exerts interstitial cell-stimulating effect on testes of male fetus, resulting in the production of testosterone until birth
B. Causes the involuted not of corpus luteum
C. Causes Corpus Luteum to decrease secretion of progesterone and estrogens
D. It allows the shrinkage of corpus luteum
Secreted by the syncytial trophoblast cells into maternal fluids
• Measurable secretion 8-9 days after ovulation.
• Maximal secretion during 10th – 12th week of pregnancy.
• Lower levels secreted 16th through 20th weeks
• Functions: • Prevents involution of corpus luteum
• Causes CL to increase secretion of progesterone and estrogens
• Causes increased growth in CL
• Exerts interstitial cell-stimulating effect on testes of male fetus:
• Results in production of testosterone until birth
What is not a function of estrogen secreted by syncytiotrophoblast:
A. Uterine and breast enlargement
B. Relaxation of pelvic ligaments
C. Increase secretion of progesterone
D. Enlargement of maternal external genitalia
Secreted by syncytiotrophoblast cells of placenta
• Toward end of pregnancy, secretion level is 30X mother’s normal level
• Placental estrogens are formed almost entirely from androgenic
Formed in mother’s and fetal’s adrenal glands, Converted by trophoblast cells into estradiol, estrone, and estriol
Uterine enlargement, Breast enlargement, Growth of breast ductal structure, Enlargement of maternal external genitalia, Relaxation of pelvic ligaments, May also affect aspects of fetal
Which is the function of progesterone?
A. Prevents involution of corpus luteum
B. Causes corpus luteum to increase secretion of progesterone and estrogens
C. Causes increased growth in corpus luteum
D. Causes decidual cells to develop in the endometrium
• Secreted in small quantities early by corpus luteum
• Secreted in large quantities by placenta
Causes decidual cells to develop in the endometrium
Decreases contractility of pregnant uterus
Increases secretions of fallopian tubes and uterus
May work with estrogen to prepare breasts for lactation
Human chorionic somatomammotropin functions to:
A. Causes decidual cells to develop in the endometrium
B. Decreases contractility of pregnant uterus
C. Causes decreased insulin sensitivity and decreased utilization of glucose by mother
D. Increases secretions of fallopian tubes and uterus
Human Chorionic Somatomammotropin
• Secreted by placenta beginning in 5th week of pregnancy
• Functions: • Causes decreased insulin sensitivity and decreased utilization of glucose by mother
• General metabolic hormone
Placental immunology deals with:
A. expression of major histocompatibility antigens by
syncytiotrophoblast and cytotrophoblast (placental components)
B. Enhance mother’s immunity during pregnancy
C. Decidual immune barrier
D. Activation of mother’s immune system components (i.e., T cells) by molecules formed on fetal placental surface.
Theories Regarding Placental Immunology
• Lack of expression of major histocompatibility antigens by syncytiotrophoblast and cytotrophoblast (placental components)
• Paralysis of mother’s immune system during pregnancy.
• Decidual immune barrier.
• Inactivation of mother’s immune system components (i.e., T cells) by molecules formed on fetal placental surface.
Primary errors of morphogenesis. They are usually
multifactorial, involving a number of etiological agents including genetic and environmental factors.
Malformations: Malformations are primary errors of morphogenesis. They are usually multifactorial, involving a number of etiological agents including genetic and environmental factors.
Disruptions:Disruptions are disturbances in otherwise normal morphogenetic processes. Examples include amniotic bands.
Deformations: Deformations are also disturbances in otherwise normal morphogenetic processes. These are typically caused by abnormal biomechanical forces such as uterine constraints. Clubfoot is an example.
Sequences: A sequence is a series (cascade) of events triggered by one initiating factor (sort of like the complement cascade or the hemostatic cascade discussed previously). An example used earlier in your text is oligohydramnios (decreased amniotic fluid) which leads to a variety of events, including fetal compression and other problems stemming from the fetal compression.
Syndromes: Syndromes are constellations of congenital anomalies that are thought to be pathologically related but cannot be explained on the basis of a single local initial event. They are often caused by a single event such as a viral infection.
When is the critical period?
A. Before 8th week
B. 4th week
C. After 8th week
D. 6th week
developmental insults during the first three weeks of development are unlikely to result in defective development.
Explain why major structural anomalies are unlikely to occur
after the eighth week of pregnancy.
Causes of Congenital Anomalies
There are three groups of causes of congenital anomalies:
Congenital deficiency of galactosyl-1-phosphate uridyltransferase. Results in tissue accumulation of
B. Cystic fibrosis
C. Trisomy 13
Gene mutations: (refer to Table 8.5)
• These include inborn errors of metabolism, which are rare.
• They are inherited most commonly as autosomal recessive or X-linked diseases. A
few are inherited as dominant traits.
• Often affect enzymes and biochemical pathways
• Phenylketonuria: Congenital deficiency of phenylalanine
4-monooxygenase. Causes inadequate formation of L-tyrosine, elevation of serum L-phenylalanine, excretion of phenylpyruvic acid, and accumulation of phenylalanine.
• Galactosemia: Congenital deficiency of galactosyl-1-phosphate uridyltransferase. Results in tissue accumulation of galactose 1-phosphate.
• Cystic fibrosis: Inherited disorder that affects mostly the lungs but also the pancreas, liver, kidneys, and intestine. CF is inherited in an autosomal recessive manner with mutations in both copies of the cystic fibrosis transmembrane conductance regulator (CFTR) protein gene. The CFTR protein is a membrane protein chloride channel/transporter.
Female patient presenting with underdeveloped sex
characteristics, low hairline, broad chest, folds on her neck. Patient is also sterile with normal intelligence. Upon genetic testing the genotype of the patient is likely to reveal that the patient has:
A. Trisomy 21
B. Trisomy 13
C. Turner syndrome
D. Poly X syndrome
Genotype: • X0 (i.e., a total of 45 chromosomes and only one X chromosome)
Incidence: • 1 in 3000
Characteristics: • Female with underdeveloped sex characteristics
• Low hairline • Broad chest • Folds on neck • Usually sterile • Usually of normal intelligence
Genotype: • XXX
Incidence: • 1 in 1000
Characteristics: • Usually tall and thin • Often fertile • Most have normal intelligence
What is a hazards of prematurity in fetal growth:
A. Preterm premature rupture of placental membranes
B. Intrauterine infections
C. Necrotizing enterocolitis
D. Uterine, cervical, and placental structural abnormalities
Prematurity and Growth Restrictions
• Prematurity and fetal growth restrictions are the second most common cause of neonatal mortality.
• Major risk factors of prematurity: • Preterm premature rupture of placental membranes
• Intrauterine infections:
• Uterine, cervical, and placental structural abnormalities
• Multiple gestation
• Hazards of prematurity: • Hyaline membrane disease
• Necrotizing enterocolitis
• Interventricular hemorrhage
• Long-term complications incl. developmental delay
Fetal factors resulting in fetal growth restriction:
A. Congenital infections
B. Umbilical-placental vascular anomalies
C. Placenta previa
D. Placental thrombosis and infarction
• Fetal factors resulting in fetal growth restriction:
• Placental factors resulting in fetal growth restriction
Umbilical-placental vascular anomalies
Placental thrombosis and infarction
Placental genetic mosaicism
Maternal factors resulting in fetal growth restriction
A. Placental thrombosis and infarction
C. Multiple gestations
D. Placental genetic mosaicism
• Maternal factors resulting in fetal growth restriction
• Chronic hypertension
• Maternal use of drugs, narcotics, alcohol, nicotine
• Maternal malnutrition
There is an accumulation of edema fluid in the fetus during intrauterine growth. Doctors suspect cardiovascular defects such as congenital cardiac defects and arrhythmias. These factors lead to suspect this condition:
A. Neonatal Respiratory Distress Syndrome
B. Immune Hydrops
D. Nonimmune hydrops
Neonatal Respiratory Distress Syndrome: This condition is related to immaturity of the lungs &, is related to premature birth. Fundamental deficiency is in the lack of pulmonary surfactant
• Hydrops refers to the accumulation of edema fluid in the fetus during intrauterine growth.
• Until recently, the most common cause was hemolytic anemia caused by blood group incompatibility between mother and fetus.
• Causes: Immune hydrops, Nonimmune hydrops
• Caused by blood group incompatibility between mother and fetus. Fetal red cells reach the maternal blood stream during last trimester or during childbirth itself. Major factor is the D antigen of the Rh group. ABO incompatibility is generally not a problem, because maternal antibodies remove any incompatible fetal RBCs that cross the placentaRh disease is not a problem with the first pregnancy. *
Major causes: • Cardiovascular defects such as congenital cardiac defects and arrhythmias, Chromosomal anomalies: Turner syndrome and trisomies 21 and 18
• Generally due to the cardiac structural aberrations that accompany these anomalies