Books: 'Placenta; Pregnancy'

1

P, Bischof, and Klopper Arnold, eds. Proteins of the placenta: Biochemistry, biology, and clinical application. Basel ; New York: Karger, 1985.

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2

International Conference on Placenta (1990 Tokyo, Japan). Placenta: Basic research for clinical application. Edited by Soma H. Basel: Karger, 1991.

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3

Lantbruksuniversitet, Sveriges, ed. Studies of the endometrium and placenta during early pregnancy in the pig: Morphology, growth factors and steroid receptors. Uppsala: Sveriges Lantbruksuniversitet, 1996.

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4

Pulkkinen, Pekka. Smoking and pregnancy: With a special reference to fetal growth and certain trace element distribution between mother, placenta, and fetus. Tampere: University of Tampere, 1989.

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5

Color atlas of obstetric and gynecologic pathology. St. Louis: Mosby, 1997.

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6

Matsuto, Mochizuki, and Hussa Robert O, eds. Placental protein hormones: Proceedings of the Satellite Symposium on Placental Protein Hormones, Kobe, Japan, 14-15 July 1988. Amsterdam: Excerpta Medica, 1988.

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7

N, Fitch, and Paradice B. A, eds. Pathology of the human embryo and previable fetus: An atlas. New York: Springer-Verlag, 1990.

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8

International Congress on Placental and Endometrial Proteins (6th 1987 Nagoya-shi, Japan). Placental and endometrial proteins: Basic and clinical aspects : proceedings of the 6th International Congress on Placental and Endometrial Proteins, Nagoya, Japan, 13 December 1987. Utrecht, the Netherlands: VSP, 1988.

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9

Immunology of pregnancy and cancer. Commack, N.Y: Nova Science Publishers, 1993.

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10

Mothers, babies, and health in later life. 2nd ed. Edinburgh: Churchill Livingstone, 1998.

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11

Doppler blood flow measurement in uteroplacental and fetal vessels: Pathophysiological and clinical significance. Berlin: Springer-Verlag, 1990.

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12

(Editor), A. Klopper, and P. Bischof (Editor), eds. Proteins of the Placenta. S. Karger AG (Switzerland), 1985.

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13

Life's Vital Link: The Astonishing Role of the Placenta. Oxford University Press, 2018.

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14

Life's vital link: The astonishing role of the placenta. Oxford University Press, 2013.

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15

Redline, Raymond W., Theonia K. Boyd, and Drucilla J. Roberts. Placental and Gestational Pathology. University of Cambridge ESOL Examinations, 2018.

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16

Bonnet, Marie-Pierre, and Anne Alice Chantry. Placenta and uteroplacental perfusion. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198713333.003.0003.

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The placenta is a complex and changing organ necessary for normal fetal growth and development and for maintenance of a healthy pregnancy. It has three major functions: a protective function of the fetus, an endocrine function, and a metabolic function. The main functional unit of the placenta is the chorionic villous, responsible for the majority of the fetal–maternal exchanges. Migration of trophoblastic cells induces a remodelling of the uterine arteries, with vasodilatated and compliant vessels, unresponsive to maternal vasomotor control. Therefore, any significant change in maternal blood pressure, in particular in the context of general or regional anaesthesia, can directly impact on uteroplacental perfusion. Most anaesthetic drugs cross the placental barrier, but without significant consequences on the fetal well-being.

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17

Gluckman, Sir Peter, Mark Hanson, Chong Yap Seng, and Anne Bardsley. Maternal stress in pregnancy and breastfeeding. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198722700.003.0033.

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Acute and/or chronic stress in pregnancy is potentially detrimental to the health of both the mother and the developing fetus. The stress response triggers the release of glucocorticoids, mainly cortisol, into the maternal bloodstream, with subsequent effects on energy metabolism, growth processes, and in the functioning of the immune system and brain. The placenta provides a barrier to natural glucocorticoids, buffering the fetus from minor changes in maternal cortisol levels but can be saturated by high maternal levels of cortisol and under conditions of maternal under-nutrition or compromised placental function. Various outcomes can be affected, including birthweight and infant behaviour. Severe stress is not always easily avoided, but daily stress, and specifically that associated with pregnancy itself, should be minimized as much as possible.

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18

MD, Rebecca Baergen. Placental Pathology, An Issue of Surgical Pathology Clinics. Elsevier, 2013.

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19

Say No to Placenta Pics: And Other Uproarious Unsolicited Advice for Pregnant Women. Skyhorse Publishing Company, Incorporated, 2018.

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20

Parsons, Jillian M., and Allison Baerken. Say No to Placenta Pics: And Other Hilarious, Unsolicited Advice for Pregnant Women. Skyhorse Publishing Company, Incorporated, 2018.

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21

Eldridge, James, and Maq Jaffer. Obstetric anaesthesia and analgesia. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198719410.003.0033.

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This chapter discusses the anaesthetic management of the pregnant patient, for labour analgesia as well as surgical intervention. It begins with a description of the physiological and pharmacological changes of pregnancy. It describes methods of labour analgesia, including remifentanil, and epidural analgesia and its complications such as post-dural puncture headache. It describes anaesthesia for Caesarean section (both regional and general), failed intubation, antacid prophylaxis, post-operative analgesia, retained placenta, in utero fetal death, hypertensive disease of pregnancy (pre-eclampsia, eclampsia, and the hypertension, elevated liver enzymes, and low platelets (HELLP) syndrome), massive obstetric haemorrhage, placenta praevia and morbidly adherent placenta (placenta accreta, increta, and percreta), amniotic fluid embolism, maternal sepsis, and maternal resuscitation. It discusses co-morbidity in pregnancy, such as obesity and cardiac disease, and the patient who requires non-obstetric surgery while pregnant. It provides information on safe prescribing in pregnancy and breastfeeding.

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22

Lise, Cédard, and Firth Anthony, eds. Placental signals: Autocrine and paracine control of pregnancy. Rochester, N.Y: University of Rochester Press, 1992.

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23

1946-, Miller Richard K., Thiede Henry A, and Rochester Trophoblast Conference (12th : 1992 : Rochester, N.Y.), eds. HIV, perinatal infections, and therapy: The role of the placenta. Rochester, N.Y: University of Rochester Press, 1994.

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24

Placental Signals Autocrine and Paracine Control of Pregnancy (Trophoblast Research). University of Rochester Press, 1993.

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25

1962-, Baker Philip, and Sibley Colin, eds. The placenta and neurodisability. London: Mac Keith Press, 2006.

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26

Medforth, Janet, Linda Ball, Angela Walker, Sue Battersby, and Sarah Stables. Fetal emergencies during pregnancy, labour, and postnatally. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198754787.003.0023.

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Neonatal emergencies during pregnancy, labour, birth, and the postnatal period are covered. Blood tests during pregnancy and detecting deviations from the norm are included. Fetal emergencies and their management include: in utero transfer, hypoxia, asphyxia, cord presentation, cord prolapse, vasa/placenta praevia, shoulder dystocia, undiagnosed breech, and neonatal resuscitation. Guidelines for admission to a neonatal intensive care unit (NICU) and current neonatal morbidity and mortality data are included. The management of an intrauterine death or stillbirth is included.

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27

Thiede, Henry A. HIV, Perinatal Infections and Therapy: The Role of the Placenta (Trophoblast Research). University of Rochester Press, 1995.

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28

Gluckman, Sir Peter, Mark Hanson, Chong Yap Seng, and Anne Bardsley. Iodine in pregnancy and breastfeeding. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198722700.003.0019.

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Iodine is a key component of thyroid hormones. Development of the fetal brain and nervous system are dependent on thyroid hormones supplied by the mother via the placenta, increasing the maternal demand for iodine throughout pregnancy. Women with adequate iodine intake before conception (~150 #amp;#x03BC;g/day) can adapt to the increased demand for thyroid hormones during pregnancy, because the thyroid gland adjusts its hormonal output; but this depends on sufficient availability of dietary iodine and the integrity of the thyroid gland. Iodine deficiency causes congenital hypothyroidism, and in severe form, the irreversible brain damage associated with cretinism. Moderate iodine deficiency in pregnancy is associated with lower learning capacity, reduced IQ, hearing impairment, and increased risk of attention deficit disorder. Pregnant women should take a daily multivitamin that contains 150 #amp;#x00B5;g of iodine, unless they regularly consume concentrated food sources of iodine.

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29

Gluckman, Sir Peter, Mark Hanson, Chong Yap Seng, and Anne Bardsley. Vitamin B1 (thiamine) in pregnancy and breastfeeding. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198722700.003.0007.

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Vitamin B1 (thiamine) is involved in nervous system and muscle function and is essential for carbohydrate metabolism. Deficiency is common in Asia, where diets are often high in thiamine-depleted polished rice and can be low in other food sources. Pregnancy imposes an increasing requirement for thiamine over the course of gestation, and deficiency can lead to widespread metabolic disturbances affecting the placenta and fetus. Nutritional deficiency for thiamine is rare in people who consume a moderately varied diet that contains whole grains. However, excessive vomiting in pregnancy can cause thiamine depletion, in which case antenatal vitamins containing thiamine and other B vitamins may be beneficial.

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30

Gluckman, Sir Peter, Mark Hanson, Chong Yap Seng, and Anne Bardsley. Vitamin K in pregnancy and breastfeeding. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198722700.003.0016.

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Vitamin K is involved in blood clotting, and lack of this nutrient results in a hypocoagulable state, associated with a high risk of bleeding events. Deficiency is rare among adults, because vitamin K is widely available in foods. However, the placenta transmits vitamin K relatively poorly, leading to a general deficiency in full-term neonates, who are also particularly vulnerable to the effects of low vitamin K levels because of their immature clotting systems. Deficiency can lead to intracranial haemorrhage following birth trauma, or classic vitamin K deficiency bleeding. It is important to maintain adequate vitamin K status throughout pregnancy in order to avoid added risk to the neonate at birth and in the first few weeks of life. Supplementation of newborns by intramuscular injection should be universal.

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31

Gluckman, Sir Peter, Mark Hanson, Chong Yap Seng, and Anne Bardsley. Vitamin B12 (cobalamin) in pregnancy and breastfeeding. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198722700.003.0013.

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Vitamin B12 is required for the synthesis of fatty acids and myelin and so is crucial for normal neurological function and maintenance of the CNS. In conjunction with folate, it is involved in red blood cell formation and DNA synthesis, and in embryogenesis, it is important for proper neural tube formation and brain development. Maternal intake during pregnancy is important, as only newly absorbed vitamin B12, and not that stored in the maternal liver, is concentrated in the placenta. Despite the active transfer during pregnancy, the vitamin B12 content in the newborn is low, and the infant is dependent on breast milk for ongoing needs. Pregnant and lactating women should ensure that their diet contains sufficient (animal) sources of vitamin B12; those consuming vegan or strict vegetarian diets should either take vitamin B12 supplements or seek foods that have been fortified with vitamin B12.

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32

1940-, Hata Toshio, Takayama Masaomi 1938-, Taki Ichiro 1919-, Foidart Jean-Michel 1949-, Japanese Placenta Group Meeting, and European Placenta Group Meeting, eds. Placental molecules in hemodynamics, transport, and cellular regulation. Rochester, NY: University of Rochester Press, 1997.

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33

(Editor), Masaomi Takayama, Toshio Hata (Editor), Ichiro Taki (Editor), Jean-Michel Foidart (Editor), John Aplin (Editor), Peter Kaufmann (Editor), and Jean-Pierre Schaaps (Editor), eds. Placental Molecules in Hemodynamics, Transport and Cellular Regulation, Volume 9; and Early Pregnancy, Volume 10 (Trophoblast Research). University of Rochester Press, 1997.

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34

Glover, Vivette. Maternal Stress During Pregnancy and Infant and Child Outcome. Edited by Amy Wenzel. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199778072.013.006.

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Many independent prospective studies show maternal stress, anxiety, or depression during pregnancy poses an increased risk for her child to have a wide range of adverse outcomes including emotional problems, ADHD or conduct disorder, or impaired cognitive development. Several studies have shown that these adverse outcomes are independent of possible confounding factors, such as postpartum anxiety and depression. Most children are not affected, and those who are can be affected in different ways, probably due to different genetic vulnerabilities and the quality of postpartum care. An evolutionary explanation for the observed changes is proposed. Underlying mechanisms are just starting to be understood: altered function of the placenta, allowing more of the stress hormone cortisol to pass through to the fetus, may well be important, as may epigenetic changes. The implications are that improved emotional care of pregnant women should improve outcomes for their children to a clinically significant degree.

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35

Vasquez, Vanessa. Infection in the Pregnant Patient. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199976805.003.0059.

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Infections in pregnancy can result in significant complications for both the mother and fetus and can increase the risk of preterm labor. Fever in a pregnant woman also raises concern for its associated risk of preterm birth due to the release of prostaglandins and cytokines that stimulate uterine contractility. Infection can be passed to the neonate hematogenously or ascend from the genital tract. Treatment during pregnancy creates problems, as many antimicrobials cross the placenta and may have a teratogenic risk. Prophylaxis, vaccination, a high degree of suspicion, and early intervention can help improve morbidity and mortality. The pregnant patient should be asked important questions that include history of uterine tenderness and leakage of vaginal fluid, exposure to or symptoms of sexually transmitted infection, previous preterm labor, history of pregnancy complications, and a thorough social history.

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36

1932-, Battaglia Frederick C., Nestlé Nutrition Services, and Nestlé Nutrition Workshop (39th : 1996 : East Sussex, England), eds. Placental function & fetal nutrition. [Vevey, Switzerland]: Nestlé Nutrition Services, 1997.

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37

Rizzuto, Gabrielle A., and Anna I. Bakardjiev. Listeria monocytogenes. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190604813.003.0020.

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Listeria monocytogenes is a intracellular bacterial pathogen that causes serious foodborne illness in humans. Among all infectious diseases caused by gastrointestinal pathogens, listeriosis has the highest mortality rate, likely because of its ability to cross the gastrointestinal barrier and cause sepsis and infection of other organs such as the brain and placenta. Infection of the placenta leads to fetal infection, and otherwise healthy pregnant women have a significantly increased incidence of listeriosis than the general population, likely due to changes in the maternal cell-mediated immune response during pregnancy. Clinical manifestations include miscarriage, stillbirth, preterm labor, and neonatal infection and death. Neonates develop early-onset sepsis or late-onset meningitis. Physicians must evaluate pregnant women and neonates with febrile illnesses for listeriosis, since prompt treatment with antibiotics can cure it. It is important to note that L. monocytogenes is resistant to cephalosporins. Ampicillin is the treatment of choice in patients without penicillin allergy.

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38

R, Rosenfeld Charles, ed. The Uterine circulation. Ithaca, N.Y: Perinatology Press, 1989.

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39

Pastrakuljic, Aleksandra. The role of the placenta in adverse fetal outcomes associated with maternal cocaine use and cigarette smoking in pregnancy. 2000.

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40

Nora, Chiang C., Lee Charles C, and National Institute on Drug Abuse., eds. Prenatal drug exposure. Rockville, Md: U.S. Dept. of Health and Human Services, Public Health Service, Alcohol, Drug Abuse, and Mental Health Administration, National Institute on Drug Abuse, 1985.

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41

Waldmann, Carl, Neil Soni, and Andrew Rhodes. Obstetric emergencies. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199229581.003.0031.

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Pre-eclampsia 518Eclampsia 520HELLP syndrome 522Postpartum haemorrhage 524Amniotic fluid embolism 526Pre-eclampsia is a common complication of pregnancy, UK incidence is 3–5%, with a complex hereditary, immunological and environmental aetiology.Abnormal placentation is characterized by impaired myometrial spiral artery relaxation, failure of trophoblastic invasion of these arterial walls and blockage of some vessels with fibrin, platelets and lipid-laden macrophages. There is a 30–40%, reduction in placental perfusion by the uterine arcuate arteries as seen by Doppler studies at 18–24 weeks gestation. Ultimately the shrunken, calcified, and microembolized placenta typical of the disease is seen. The placental lesion is responsible for fetal growth retardation and increased risks of premature labour, abruption and fetal demise. Maternal systemic features of this condition are characterized by widespread endothelial damage, affecting the peripheral, renal, hepatic, cerebral, and pulmonary vasculatures. These manifest clinically as hypertension, proteinuria and peripheral oedema, and in severe cases as eclamptic convulsions, cerebral haemorrhage (the most common cause of death due to pre-eclampsia in the UK), pulmonary oedema, hepatic infarcts and haemorrhage, coagulopathy and renal dysfunction....

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42

Bhattacharya, Niranjan, and Phillip Stubblefield. Regenerative Medicine Using Pregnancy-Specific Biological Substances. Springer, 2011.

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43

Sibley, Colin, and Phillip Baker. The Placenta and Neurodisability (Clinics in Developmental Medicine (Mac Keith Press)). MacKeith Press, 2006.

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44

1948-, Morrish Donald, Miller Richard K. 1946-, Rochester Trophoblast Conference (13th : 1996 : Banff, Alta.), and Thomas G. Wegmann Memorial Symposium on Reproductive Immunology (1996 : Banff, Alta.), eds. Genetic regulation of placental development, and immunology. Rochester, N.Y: University of Rochester Press, 1998.

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45

Susan C. Modesitt M.D. (Foreword), ed. Gestational Trophoblastic Neoplasia: A Guide for Women Dealing with Tumors of the Placenta, such as Choriocarcinoma, Molar Pregnancy and Other Forms of GTN. Your Health Press, 2007.

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46

Johnson, Tara, and Meredith Schwartz Ph D. Gestational Trophoblastic Neoplasia: A Guide for Women Dealing with Tumors of the Placenta, such as Choriocarcinoma, Molar Pregnancy and Other Forms of GTN. Your Health Press, 2012.

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47

Frazier, Linda M., and Deborah Barkin Fromer. Reproductive and Developmental Disorders. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190662677.003.0027.

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This chapter describes reproductive disorders and developmental disorders, with a focus on their recognition and prevention. Certain hazardous exposures at sufficient doses during preconception among men and women have been shown to increase the risk for infertility, miscarriage (spontaneous abortion) and birth defects. Women’s exposures during pregnancy can cause fetal death, congenital anomalies, and neurodevelopmental disorders. Fathers’ occupational exposures can secondarily expose pregnant women through contamination of the home environment. Numerous chemical pollutants readily cross the placenta and are transmitted into breast milk. Prenatal and perinatal exposures have been linked to abnormal development of the immune system, childhood cancer, and learning disabilities. Specific examples, such as lead and dibromochloropropane, are provided in the chapter to illustrate general concepts. A final section addresses evaluation and control of risk.

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48

Gluckman, Sir Peter, Mark Hanson, Chong Yap Seng, and Anne Bardsley. The importance of nutrition and lifestyle to healthy development. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198722700.003.0001.

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Good fetal and infant nutrition, whether derived from the mother via the placenta during gestation or via breast milk after birth, consists of the macronutrients protein, carbohydrates, and fats, all of which are needed for building the fundamental components of the body, and micronutrients such as vitamins and trace elements, which are essential structural components and cofactors in metabolic processes. Understanding the concept of a ‘balanced diet’ and the implications of maternal body composition is critical for pregnant and breastfeeding women to ensure that their metabolic adaptation to pregnancy and lactation is appropriate and that their offspring gets the required nutrients in the appropriate amount and proportion to ensure optimal development. An unbalanced diet, or over- or under-nutrition, can increase the risks of low birthweight and gestational diabetes and result in unfavourable metabolic adjustments by the fetus.

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49

L, Power Michael, and Schulkin Jay, eds. Birth, distress, and disease: Placental-brain interactions. Cambridge: Cambridge University Press, 2005.

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50

Marrie, Thomas J. Q fever. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0018.

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Q fever is a wide spread illness affecting wild and domestic animals and man. The etiological agent Coxiella burnetii, has both a wild life and domestic animal cycle. In mammals, infection localizes to the endometrium and the mammary glands. The organism is reactivated during pregnancy reaching high concentrations in the placenta. At the time of parturition the organism is aerosolized. Inhalation of Coxiella burnetii by a susceptible animal results in Q fever. In man, Q fever may be acute (self limited febrile illness, pneumonia, hepatitis) or chronic (mostly endocarditis, but also osteomyelitis, endovascular infection, hepatitis [can be both acute and chronic] and Q fever in pregnancy). Abortion and stillbirth are manifestations of Q fever in domestic animals and in animal models of disease (such as a mouse model of Q fever in pregnancy ). A vaccine is available for abattoir workers, veterinarians and others at high risk for acquiring Q fever.

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Books on the topic 'Placenta; Pregnancy'

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