Books on the topic 'Metabolic derangements'
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1
Hormonal and Metabolic Derangements in Renal Failure. S. Karger AG (Switzerland), 1986.
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2
Dierdorf, Stephen F. Introduction to Metabolic and Endocrine Diseases. Edited by Matthew D. McEvoy and Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0024.
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Patients may have metabolic and endocrine dysfunction that is primary and results in surgical pathology, or the surgical condition can produce metabolic changes that influence the administration of anesthesia. These disorders can vary with incidence of occurrence from commonly encountered situations such as hyperkalemia, to more rare disorders such as the porphyrias. Knowledge of the metabolic/endocrine derangements can lead to treatment that can be life-saving during the perioperative period. While it is important to periodically review the new developments in metabolism and endocrinology disorders, it is also helpful to review the long standing accepted treatments of the more unusual disorders. This will help to improve the application of appropriate treatment steps in the perioperative care of the patient.
3
Cheng, Ning, Susan A. Masino, and Jong M. Rho. Metabolic Therapy for Autism Spectrum Disorder and Comorbidities. Edited by Jong M. Rho. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0014.
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Autism spectrum disorder (ASD) is a heretogenous developmental disorder characterized by deficits in sociability and communication and by repetitive and/or restrictive behaviors. Currently, only comorbid manifestations can be alleviated (such as seizures and sleep disturbance) not core behavioral symptoms. Recent studies have increasingly implicated mitochondrial dysfunction as a cause of ASD. Mitochondria play an integral role in many cellular functions and are susceptible to many pathophysiological insults. Derangements in mitochondrial structure and function provide a scientific rationale for experimental therapeutics. Meanwhile, the high-fat, low-carbohydrate ketogenic diet (KD) has been shown to enhance mitochondrial function through a multiplicity of mechanisms. Reviewed herein is clinical and basic laboratory evidence for the use of metabolism-based therapies such as the KD in the treatment of ASD, as well as emerging comorbid models of epilepsy and autism. Future research directions aimed at validating such therapeutic approaches and identifying novel mechanistic targets are discussed.
4
Jordan, Nerissa. Non-metastatic neurological manifestations of malignancy. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0238.
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Neurological complications of systemic malignancy are frequent. They may reflect direct local effects of the tumour; CNS infection; side effects of chemotherapy or radiotherapy; nutritional or metabolic derangements; or a paraneoplastic syndrome. The paraneoplastic neurological syndromes are a group of disorders associated with a malignancy outside the nervous system. The pathophysiology is immune-mediated, with the tumour’s expression of neuronal proteins invoking antibody formation, which in turn results in neurological symptoms. This chapter will mainly focus on these syndromes.
5
Franzese, Adriana, Enza Mozzillo, and Francesco Maria Rosanio. Glucose Metabolism Derangements in Pediatric Age. Cambridge Scholars Publishing, 2022.
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6
Meier, Petra M., and Thomas O. Erb. Craniosynostosis and Apert Syndrome. Edited by Kirk Lalwani, Ira Todd Cohen, Ellen Y. Choi, and Vidya T. Raman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190685157.003.0021.
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Apert syndrome is a complex, progressive multisystem condition of the craniosynostosis spectrum originating from a fibroblast growth factor receptor disorder. Multidisciplinary treatment teams may include craniofacial surgery, neurosurgery, otolaryngology, ophthalmology, oro-maxillofacial surgery, and pediatric intensive care. Secondary to midface hypoplasia, children often present with a compromised airway and have a high incidence of sleep disorders. Anesthetic considerations include difficult airway assessment, the presence of obstructive sleep apnea syndrome, and increased intracranial pressure. Extensive remodeling procedures can be associated with massive hemorrhage (e.g., venous sinus bleeding) and venous air embolism. Transfusion-related complications include coagulopathy, metabolic derangements, and primarily noninfectious hazards such as transfusion-related acute lung injury and transfusion-related immunomodulation. Multimodal blood management should focus on a combination of appropriate surgical techniques and blood conservation, along with guidance from point-of-care testing (including coagulation).
7
Nelson, Jonathon, and Franklyn P. Cladis. Pediatric Liver Transplantation. Edited by Kirk Lalwani, Ira Todd Cohen, Ellen Y. Choi, and Vidya T. Raman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190685157.003.0038.
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Liver transplantation has become a standard surgical treatment for pediatric patients with hepatic failure, tumors, and metabolic derangements. Liver transplantation in the pediatric population can be extremely challenging for the anesthesiologist due to multiple perioperative considerations. The first successful liver transplant was performed in a pediatric patient in the 1960s, and since then, there have been significant advances in immunosuppressant medications and preservation solutions which have led to improved survival. Nevertheless, the number of liver transplants continues to be limited by organ availability, although the pediatric donor pool has been increased by living related donors and split livers. The most common pediatric pathology that results in hepatic failure and transplantation is biliary atresia. This chapter covers the perioperative care of a pediatric patient undergoing a liver transplant, from the preoperative preparation to the intraoperative management, and discusses postoperative challenges which may be encountered while in the intensive care unit.
8
Ruskin, David N. Metabolic Therapy and Pain. Edited by Detlev Boison. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0022.
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Chronic pain is associated strongly with poor quality of life. Drug treatments for pain can be problematic; with the understanding that chronic pain syndromes often involve derangement of homeostasis, there is an increased interest in applying nonpharmacological metabolic therapies. This chapter surveys clinical and animal research into the effects of fasting, calorie restriction, ketogenic diet, and polyunsaturated fatty acid supplementation on pain. These dietary treatments can significantly ameliorate pain in inflammatory and neuropathic disorders. The choice among these treatments might depend on the specific pain syndrome and the tolerance of the patient for particular dietary modifications. Several possible mechanisms are discussed, some of which might be in common among these treatments, and some treatments might engage multiple mechanisms. Multiple mechanisms acting together could be ideal for restoring the disordered metabolism underlying some pain syndromes.
9
Taljanovic, Mihra S., Imran M. Omar, Kevin B. Hoover, and Tyson S. Chadaz, eds. Musculoskeletal Imaging Volume 1. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780190938161.001.0001.
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This volume meets the needs of radiology residents to become adept at interpreting musculoskeletal (MSK) imaging studies. It does so by presenting core knowledge and fundamentals that must be learned to accurately and effectively interpret MSK studies by the trainee and non-specialist. The goal is to impart to residents, as well as to refresh for practitioners, essential facts in a concise and readable format so the reader becomes conversant with all imaging modalities used and the essentials of interpretation and technique. Other resources are at too high a level for the resident in training or contain far more information than a resident can easily assimilate during a rotation. The book is part of the Rotations in Radiology series for residents, which defines and encapsulates core knowledge for areas within Radiology, offering a guided, structured approach to imaging diagnosis. It contains sections on 10 key topics in MSK radiology: trauma; arthritis; tumors and tumor-like conditions; metabolic, hematopoietic, endocrine, and deposition diseases; infectious diseases; arthrography; internal derangements of the joints; congenital diseases; and ultrasound. Each section begins with an overview chapter, orienting the reader to the specific concerns and issues related to imaging that anatomic region or category of problem. Each clinical problem or diagnosis is concisely covered to provide a targeted discussion and highlight salient points. For each topic, concise chunks of text will review: definition; clinical features; anatomy and physiology; how to appraoch the image; what not to miss; differential diagnosis; common variants if pertinent; clinical issues; key points; high yield references.
10
Taljanovic, Mihra S., Imran M. Omar, Kevin B. Hoover, and Tyson S. Chadaz, eds. Musculoskeletal Imaging Volume 2. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780190938178.001.0001.
Full textAbstract:
This volume meets the needs of radiology residents to become adept at interpreting musculoskeletal (MSK) imaging studies. It does so by presenting core knowledge and fundamentals that must be learned to accurately and effectively interpret MSK studies by the trainee and non-specialist. The goal is to impart to residents, as well as to refresh for practitioners, essential facts in a concise and readable format so the reader becomes conversant with all imaging modalities used and the essentials of interpretation and technique. Other resources are at too high a level for the resident in training or contain far more information than a resident can easily assimilate during a rotation. The book is part of the Rotations in Radiology series for residents, which defines and encapsulates core knowledge for areas within Radiology, offering a guided, structured approach to imaging diagnosis. It contains sections on 10 key topics in MSK radiology: trauma; arthritis; tumors and tumor-like conditions; metabolic, hematopoietic, endocrine, and deposition diseases; infectious diseases; arthrography; internal derangements of the joints; congenital diseases; and ultrasound. Each section begins with an overview chapter, orienting the reader to the specific concerns and issues related to imaging that anatomic region or category of problem. Each clinical problem or diagnosis is concisely covered to provide a targeted discussion and highlight salient points. For each topic, concise chunks of text will review: definition; clinical features; anatomy and physiology; how to appraoch the image; what not to miss; differential diagnosis; common variants if pertinent; clinical issues; key points; high yield references.
11
Taljanovic, Mihra S., Imran M. Omar, Kevin B. Hoover, and Tyson S. Chadaz. Musculoskeletal Imaging Volume 2: Metabolic, Infectious, and Congenital Diseases; Internal Derangement of the Joints; and Arthrography and Ultrasound. Oxford University Press, Incorporated, 2019.
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12
Gaitanis, John, Phillip L. Pearl, and Howard Goodkin. The EEG in Degenerative Disorders of the Central Nervous System. Edited by Donald L. Schomer and Fernando H. Lopes da Silva. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190228484.003.0013.
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Nervous system alterations can occur at any stage of prenatal or postnatal development. Any of these derangements, whether environmental or genetic, will affect electrical transmission, causing electroencephalogram (EEG) alteration and possibly epilepsy. Genetic insults may be multisystemic (for example, neurocutaneous syndromes) or affect only the brain. Gene mutations account for inborn errors of metabolism, channelopathies, brain malformations, and impaired synaptogenesis. Inborn errors of metabolism cause seizures and EEG abnormalities through a variety of mechanisms, including disrupted energy metabolism (mitochondrial disorders, glucose transporter defect), neuronal toxicity (amino and organic acidopathies), impaired neuronal function (lysosomal and peroxisomal disorders), alteration of neurotransmitter systems (nonketotic hyperglycinemia), and vitamin and co-factor dependency (pyridoxine-dependent seizures). Environmental causes of perinatal brain injury often result in motor or intellectual impairment (cerebral palsy). Multiple proposed etiologies exist for autism, many focusing on synaptic development. This chapter reviews the EEG findings associated with this myriad of pathologies occurring in childhood.
13
Manners, Jody, Kiruba Dharaneeswaran, and Ruchira Jha. Approach to Acute Altered Mental Status and Seizures (DRAFT). Edited by Raghavan Murugan and Joseph M. Darby. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190612474.003.0007.
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Altered mental status (AMS) is a common presenting symptom or complication in hospitalized patients. The etiology of AMS includes potential primary neurologic entities as well as systemic disturbances such as infection, intoxication, or metabolic derangement. A systematic and rapid evaluation of potentially life threatening conditions is necessary to guide appropriate management. Seizures (particularly non-convulsive episodes) are an important cause of AMS frequently encountered in acutely ill patients with multiple medical comorbidities and need to be recognized and treated early to minimize morbidity and mortality. This chapter outlines an approach to the evaluation of acute altered mental status with an emphasis on seizure management.
14
Chakera, Aron, William G. Herrington, and Christopher A. O’Callaghan. Disorders of plasma phosphate. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0176.
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The commonest cause of sustained hyperphosphataemia is renal impairment, because the kidney normally excretes phosphate (note that phosphate levels normally rise following meals and that there is significant diurnal variation). A considerable phosphate load may also be provided by some medications, in particular, those used for bowel preparation. Hypophosphataemia may arise from reduced intake or absorption, increased renal excretion, or intracellular redistribution, particularly in response to carbohydrate loads with refeeding after starvation. Excessive renal phosphate loss can reflect tubular damage or inherited phosphate-wasting nephropathies. This chapter reviews the causes of derangements of phosphate metabolism and the clinical consequences.
15
Chakera, Aron, William G. Herrington, and Christopher A. O’Callaghan. Disorders of plasma magnesium. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0177.
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Normal serum magnesium levels are in the range of 0.7–1.0 mmol/l and, as for calcium, most of the total body magnesium is found in bone and soft tissues. Magnesium is essential for normal cell metabolism (as a cofactor for numerous enzymes) and for neuronal function, and regulates parathyroid hormone release. Alterations in serum magnesium levels are usually asymptomatic unless severe. As there are large tissue reserves of magnesium, hypomagnesaemia usually only develops with chronic gastrointestinal or renal losses, or prolonged dietary insufficiency. Hypermagnesaemia is almost always iatrogenic, due to excessive supplementation. This chapter reviews the causes and management of derangements of plasma magnesium.
16
Sprague, Stuart M., and Menaka Sarav. Chronic kidney disease-mineral and bone disorder. Edited by David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0115_update_001.
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The kidneys play a critical role in maintaining normal serum calcium and phosphorus concentrations, under the regulation of three main hormones: parathyroid hormone, calcitriol, and fibroblast growth factor 23. With the progression of chronic kidney disease (CKD), most patients develop CKD–mineral and bone disorder (CKD-MBD), which is a systemic disorder involving derangement in mineral metabolism, renal osteodystrophy, and extraskeletal calcification. Disturbances in mineral metabolism develop early in CKD and include phosphate retention, hypocalcaemia, vitamin D deficiency, and hyperparathyroidism. Renal osteodystrophy involves pathologic changes of bone morphology related to progressive CKD and is quantifiable by histomorphometry, based on bone biopsy. CKD-MBD is associated with significant morbidity, including bone loss, fractures, cardiovascular disease, immune suppression, as well as increased mortality. As the disorder begins early in the course of CKD, a proactive approach with intervention is important. Therapeutic strategies could then be employed to prevent and correct these disturbances, aiming to improve cardiovascular outcomes and survival. Current practice guidelines for CKD-MBD are based on insufficient data and high-quality studies are required before specific treatment can be advocated strongly.
17
Litell, John M., and Nathan I. Shapiro. Pathophysiology of septic shock. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0297.
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The pathophysiology of sepsis is the result of a dysregulated host response to infection. Interactions between conserved pathogenic signals and host recognition systems initiate a systemic reaction to local infection. Pro- and anti-inflammatory intermediates and associated coagulatory abnormalities lead to altered macrovascular, microvascular, and mitochondrial function. Uncorrected, these processes yield similar patterns of failure in multiple organ systems. Mortality increases with successive organ failures. Although commonly thought to be a manifestation of impaired renal circulation, septic acute kidney injury may be due primarily to non-haemodynamic factors. Pulmonary parenchymal dysfunction in sepsis also contributes to failures in other organ systems. Sepsis involves complex alterations in myocardial function, vascular tone, and capillary integrity, which are mediated by elevated concentrations of inflammatory cytokines, inducible nitric oxide, and reactive oxygen species, among others. Gut hypomotility and translocation of enteric flora likely contribute to a persistent inflammatory response. This perpetuates the pathophysiological pattern of sepsis, and can lead to the delayed onset of these features in patients with other types of critical illness. The neurological manifestations of sepsis include acquired delirium, which is also probably due to circulatory and inflammatory abnormalities, as well as alterations in cerebral amino acid metabolism. Critical illness-related corticosteroid insufficiency and derangements in glucose metabolism are among the endocrine abnormalities commonly seen in septic patients. Restoration of homeostasis requires early haemodynamic resuscitation and aggressive infectious source control.