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Books on the topic 'Fetal size'

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Author: Grafiati

Published: 4 June 2021

Last updated: 21 February 2023

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1

Kautz, J. Edward. Effects of harvest on feral rock dove survival, nest success and population size. Washington, D.C: U.S. Dept. of the Interior, Fish and Wildlife Service, 1990.

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2

Briggs, Gerald G. Drugs in pregnancy and lactation: A reference guide to fetal and neonatal risk. 3rd ed. Baltimore: Williams & Wilkins, 1990.

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3

1935-, Freeman Roger K., and Yaffe Sumner J. 1923-, eds. Drugs in pregnancy and lactation: A reference guide to fetal and neonatal risk. 6th ed. Philadelphia, Pa: Lippincott Williams & Wilkins, 2002.

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4

Briggs, Gerald G. Drugs in pregnancy and lactation: A reference guide to fetal and neonatal risk on CD-ROM. [Philadelphia, Pa.]: Lippincott, Williams & Wilkins, 1999.

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5

Ried, Sibylle. Epilepsy, pregnancy, and the child. Oxford: Blackwell Science, 1996.

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6

1939-, Scanlon John W., ed. Perinatal anesthesia. Boston: Blackwell Scientific Publications, 1985.

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7

1935-, Freeman Roger K., and Yaffe Sumner J. 1923-, eds. Drugs in Pregnancy and Lactation. 7th ed. Baltimore: Lippincott Williams & Wilkins, 2005.

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8

P, Barker D. J., ed. Fetal and placental size and risk of hypertension in adult life. 1990.

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9

Anne, Dorita. The effect of colony size on fetal resorption and secondary sex ratio in domestic Chinchilla laniger. 1985.

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10

Archer, Nick, and Nicky Manning. Nuchal translucency and the heart. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199230709.003.0019.

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Introduction 264The nuchal scan 266Management 268Nuchal translucency describes sonolucent tissue in the posterior aspect of the fetal neck; the size can be measured with accuracy during the 1st trimester of pregnancy and an increase in the measurement is associated with an increased risk of chromosomal abnormality. If fetal karyotype is normal: ...

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11

Schreuder, Michiel F. Renal tubular dysgenesis. Edited by Adrian Woolf. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0350.

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Renal tubular dysgenesis involves the absence or incomplete differentiation of proximal tubular nephron segments. Due to the lack of a patent nephron, it is characterized by (fetal) anuria and subsequent oligohydramnios, pulmonary hypoplasia, premature birth with severe and refractory arterial hypotension, and fetal or neonatal death. The main cause for renal tubular dysgenesis is a genetic mutation in the renin–angiotensin system, which has shown an autosomal recessive trait. Maternal use of angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers during pregnancy can have similar blocking effects on the fetal renin–angiotensin system, which may lead to renal tubular dysgenesis. Even though there is no actual renal function, ultrasound usually shows kidneys of normal size and architecture with an intact corticomedullary differentiation. Most patients with renal tubular dysgenesis do not survive beyond the neonatal period. A few patients have been described to survive with respiratory support, vasopressor treatment, and dialysis.

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12

Wilton, Niall, Brian J. Anderson, and Bruno Marciniak. Anatomy, physiology, and pharmacology in paediatric anaesthesia. Edited by Jonathan G. Hardman and Neil S. Morton. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0069.

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Anaesthesia for children is tempered by changes that occur during both growth and development. Drug dose is affected by size and clearance maturation processes as well as the changing body composition that occurs with age. All organ systems undergo these maturation changes and most are complete within the first few years of life. Normal physiological variables in infancy and childhood are quite different from adults. The central nervous, cardiovascular, and respiratory systems are particularly important. Cerebral immaturity and plasticity impacts sensitivity to drugs, pain responses, and behaviour and increases potential harm from apoptosis with anaesthesia. The heart undergoes a transition from fetal to adult circulation during the first few weeks of life. Undiagnosed congenital defects are not uncommon. The neonate is very susceptible to conditions that trigger an increase in pulmonary vascular resistance, with reversion to fetal circulatory patterns. Respiratory anatomy and mechanics affect the propensity to apnoea, airway maintenance, artificial ventilation modalities, uptake of inhalational agents, and tracheal tube sizes. Metabolic rate and oxygen requirements increase with decreasing age. This physiology influences diverse aspects that include the rate of desaturation during apnoea, hypoglycaemia during starvation, cardiac output, drug metabolism, fluid requirements, and heat production or loss.

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13

Davidson, Andrew, Adrian Bosenberg, and Stephen Stayer. Neonatal anaesthesia. Edited by Jonathan G. Hardman and Neil S. Morton. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0070.

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Neonatal anaesthesia requires an understanding of how neonates differ from adults and older children in anatomy, physiology, and pharmacology. There are also pathological and surgical conditions in neonates that are associated with unique anaesthesia challenges. Organ systems are generally immature, reducing the clearance of many drugs, while different water and fat content results in altered volumes of distribution. Pharmacological management is further complicated by a lack of basic pharmacokinetic data for the use of most anaesthetic drugs in neonates. At birth, there is a transition from a fetal circulation. Some aspects of fetal physiology can persist and have an impact on anaesthesia care, for example, exaggerated hypoxic pulmonary vasoconstriction. Small size, organ immaturity, and reduced physiological reserve can also result in rapid changes to cardiovascular or respiratory status during surgery. Neonates are also very vulnerable to injury, particularly pulmonary or neurological damage. Even brief episodes of over-inflation or hyperoxia may have long-lasting effects on the lung. Safe neonatal anaesthesia thus requires appropriate equipment and ventilators, careful monitoring, and the rapid management of changes in circulatory or respiratory status. Neonates that need surgery often have other significant co-morbidities; for example, prematurity, sepsis, congenital cardiac disease, or a wide variety of syndromes. Safe anaesthesia requires a careful preoperative assessment looking for such co-morbidities and a good understanding of how these may have an impact on anaesthesia.

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14

A, Malecki Richard, and U.S. Fish and Wildlife Service., eds. Effects of harvest on feral rock dove survival, nest success and population size. Washington, D.C: U.S. Dept. of the Interior, Fish and Wildlife Service, 1991.

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15

Drugs in Pregnancy and Lactation: A Reference Guide to Fetal and Neonatal Risk. Williams & Wilkins, 1994.

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16

Alchi, Bassam, and David Jayne. The patient with antiphospholipid syndrome with or without lupus. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0164.

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Antiphospholipid syndrome (APS) is an autoimmune disorder characterized by recurrent arterial or venous thrombosis and/or pregnancy loss, accompanied by laboratory evidence of antiphospholipid antibodies (aPL), namely anticardiolipin antibodies (aCL), lupus anticoagulant (LA), and antibodies directed against beta-2 glycoprotein 1 (β‎‎‎2GP1). APS may occur as a ‘primary’ form, ‘antiphospholipid syndrome,’ without any known systemic disease or may occur in the context of systemic lupus erythematosus (SLE), ‘SLE-related APS’. APS may affect any organ system and displays a broad spectrum of thrombotic manifestations, ranging from isolated lower extremity deep vein thrombosis to the ‘thrombotic storm’ observed in catastrophic antiphospholipid syndrome. Less frequently, patients present with non-thrombotic manifestations (e.g. thrombocytopaenia, livedo reticularis, pulmonary hypertension, valvular heart disease, chorea, and recurrent fetal loss).The kidney is a major target organ in both primary and SLE-related APS. Renal involvement is typically caused by thrombosis occurring at any location within the renal vasculature, leading to diverse effects, depending on the size, type, and site of vessel involved. The renal manifestations of APS include renal artery stenosis and/or renovascular hypertension, renal infarction, APS nephropathy (APSN), renal vein thrombosis, allograft vasculopathy and vascular thrombosis, and thrombosis of dialysis access.Typical vascular lesions of APSN may be acute, the so-called thrombotic microangiopathy, and/or chronic, such as arteriosclerosis, fibrous intimal hyperplasia, tubular thyroidization, and focal cortical atrophy. The spectrum of renal lesions includes non-thrombotic conditions, such as glomerulonephritis. Furthermore, renal manifestations of APS may coexist with other pathologies, especially proliferative lupus nephritis.Early diagnosis of APS requires a high degree of clinical suspicion. The diagnosis requires one clinical (vascular thrombosis or pregnancy morbidity) and at least one laboratory (LA, aCL, and/or anti-β‎‎‎2GP1) criterion, positive on repeated testing.The aetiology of APS is not known. Although aPL are diagnostic of, and pathogenic in, APS, a ‘second hit’ (usually an inflammatory event) may trigger thrombosis in APS. The pathogenesis of the thrombotic tendency in APS remains to be elucidated, but may involve a combination of autoantibody-mediated dysregulation of coagulation, platelet activation, and endothelial injury.Treatment of APS remains centred on anticoagulation; however, it has also included the use of corticosteroids and other immunosuppressive therapy. The prognosis of patients with primary APS is variable and unpredictable. The presence of APS increases morbidity (renal and cerebral) and mortality of SLE patients.

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17

Drugs in Pregnancy and Lactation: A Reference Guide to Fetal and Neonatal Risk. 7th ed. Lippincott Williams & Wilkins, 2005.

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18

King, Carolyn, and David Forsyth, eds. Handbook of New Zealand Mammals. CSIRO Publishing, 2021. http://dx.doi.org/10.1071/9781486306299.

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The Handbook of New Zealand Mammals is the only definitive reference on all the land-breeding mammals recorded in the New Zealand region (including the New Zealand sector of Antarctica). It lists 65 species, including native and exotic, wild and feral, living and extinct, residents, vagrants and failed introductions. It describes their history, biology and ecology, and brings together comprehensive and detailed information gathered from widely scattered or previously unpublished sources. The description of each species is arranged under standardised headings for easy reference. Because the only native land-breeding mammals in New Zealand are bats and seals, the great majority of the modern mammal fauna comprises introduced species, whose arrival has had profound effects both for themselves and for the native fauna and flora. The book details changes in numbers and distribution for the native species, and for the arrivals it summarises changes in habitat, diet, numbers and size in comparison with their ancestral stocks, and some of the problems they present to resource managers. For this third edition, the text and references have been completely updated and reorganised into Family chapters. The colour section includes 14 pages of artwork showing all the species described and their main variations, plus two pages of maps.

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19

Drug-Induced Pathology. Springer, 2011.

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20

Barrach, H. J., H. V. Gärtner, M. Habs, E. Grundmann, and H. W. Altmann. Drug-Induced Pathology. Springer London, Limited, 2012.

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21

Goffin, Eric, Laura Labriola, and Michel Jadoul. Bacterial and fungal infections in patients on peritoneal dialysis. Edited by Jonathan Himmelfarb. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0270.

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Infections specifically related to peritoneal dialysis include peritonitis on the one hand, and exit-site and tunnel infections on the other hand.The diagnosis of peritonitis rests on the classical triad of cloudy dialysate, abdominal pain, and presence of < 100 white-cells (including < 50 % polymorphonuclear cells) within the dialysate effluent. Because peritonitis is associated with high mortality and morbidity rates, empiric antibiotics should be initiated without delay, covering both Gram-positive and Gram-negative organisms. Most regimens include vancomycin or a first-generation cephalosporin for the former, and a third-generation cephalosporin or an aminoglycoside for the latter. Antibiotics are usually administered via the intraperitoneal route. Prophylaxis with an anti-fungal agent has to be considered in diabetic patients and in those who just received prolonged antibiotic administration. Cure is obtained in up to 80 % of the cases ; treatment failure however may occur with refractory or relapsing peritonitis episodes. This is especially common in fungal or fecal associated peritonitis, and will require catheter withdrawal. The incidence of peritonitis has dramatically decreased in recent years with the advent of new connectology systems, and both adequate preventive measures and improved patients’ education. Still it is not clearly documented that new biocompatible dialysate fluids have a favorable effect on peritonitis incidence.Exit-site and tunnel infections are defined by the presence of a purulent discharge around the catheter and by erythema, oedema and tenderness of the subcutaneous pathway of the catheter, respectively. Antibiotics are recommended in case of documented infection. Cuff shaving may sometimes be required, as well as catheter removal in case of unfavourable evolution.

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22

S, Zagon Ian, and Slotkin Theodore A, eds. Maternal substance abuse and the developing nervous system. San Diego: Academic Press, 1992.

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23

Zagon, Ian S., and Theodore A. Slotkin. Maternal Substance Abuse and the Developing Nervous System. Elsevier Science & Technology Books, 2012.

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24

J, Akhurst R., Kavlock Robert J, and Daston George P, eds. Drug toxicity in embryonic development: Advances in understanding mechanisms of birth defects. Berlin: Springer, 1997.

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25

Drug Toxicity in Embryonic Dev Ii: Adv Understanding Mechanisms of Birth Defects; Mechanistic, Etc. Springer-Verlag Telos, 1997.

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26

Drug toxicity in embryonic development I/II: Advances in understanding mechanisms of birth defects. Berlin: Springer, 1996.

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27

(Editor), R. J. Akhurst, George P. Daston (Editor), and Robert J. Kavlock (Editor), eds. Drug Toxicity in Embryonic Dev I: Adv Understanding Mechanisms of Birth Defects: Morphogenesis Etc. Springer-Verlag Telos, 1997.

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28

J, Kavlock Robert, and Daston George P, eds. Drug toxicity in embryonic development I: Advances in understanding mechanisms of birth defects : morphogenesis and processes at risk. Berlin: Springer, 1996.

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29

J, Kavlock Robert, and Daston George P, eds. Drug toxicity in embryonic development II: Advances in understanding mechanisms of birth defects : mechanistic understanding of human developmental toxicants. Berlin: Springer, 1996.

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30

Ried, Sibylle, Sibylle Ri, and Gertrud Beck-Managetta. Epilepsy, Pregnancy and the Child. Blackwell Science, 1997.

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31

Medications & Mothers' Milk: 2019. Springer Publishing Company, Incorporated, 2017.

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32

Drugs in Pregnancy and Lactation. Lippincott Williams & Wilkins, 2011.

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