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1
Lohrenz, Steven E. Primary production of particulate protien amino acids: Algal protein metabolism and its relationship to the composition of particulate organic matter. Woods Hole, Mass: Woods Hole Oceanographic Institution, 1985.
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2
Weissman, Jacqueline, and Lisa Emrick. Diseases of Mitochondrial Energy Metabolism. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0061.
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Mitochondrial disorders are a group of inherited diseases of energy metabolism caused by impairment of mitochondrial function-primarily disorders of the oxidative phosphorylation system but also the more recently described disorders of mitochondrial transport and fission. This review will focus on primary disorders of mitochondrial oxidative phosphorylation. The neurologic system is one of the most profoundly affected by mitochondrial dysfunction and the effects can be varied and widespread. This has led to these diseases being commonly called mitochondrial encephalomyopathies. The heterogeneity of clinical presentation, laboratory findings, neuroimaging findings, pathologic findings, and genetic findings in these diseases make diagnosis extremely difficult. Treatment for mitochondrial disorders is currently lacking a solid evidence base but this is a rapidly expanding area of research.
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Fraser, Jamie L., Frédéric Sedel, and Charles P. Vendetti. Disorders of Cobalamin and Folate Metabolism. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0027.
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Cobalamin C deficiency (cblC) and related disorders of intracellular cobalamin metabolism may present at any time from the prenatal period through adolescence/adulthood and are due to deficiency of the cobalamin cofactors adenosylcobalamin and methylcobalamin. Chronic complications of cblC depend on the age at presentation and may include poor growth, renal dysfunction, neuropsychiatric manifestations, intellectual disability, strokes, progressive leukoencephalopathy and spinal cord degeneration, psychiatric manifestations and executive function deficits, and optic nerve and retinal anomalies. While less common than in isolated MMA, acute metabolic decompensation may occur in cblC patients due to accumulation of methylmalonic acid and associate metabolites and should be managed as in isolated MMA in conjunction with a metabolic consultant. The most common inborn error of folate (vitamin B9) metabolism relevant for adult patients is methylenetetrahydrofolate reductase (MTHFR) deficiency. Manifestations are primarily neurological, but the disorder may present in a substantial number of adults with psychiatric symptoms. Early recognition with adequate treatment is crucial.
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Wiklund, Olov, and Jan Borén. Pathogenesis of atherosclerosis: lipid metabolism. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0011.
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Lipids are carried in plasma as microparticles, lipoproteins, composed of a core of hydrophobic lipids and a surface of amphipathic lipids. In addition, the particles carry proteins (i.e. apolipoproteins). The proteins have key functions in the metabolism as receptor ligands, enzymes or activators. Lipoproteins are classified based on density into: chylomicrons, VLDL, IDL, LDL, and HDL. Retention of apoB-containing lipoproteins (LDL, IDL, and VLDL) in the arterial intima is the initiating event in the development of atherosclerosis. Retention is mediated by binding of apoB to structural proteoglycans in the intima. Increased plasma concentration of apoB-containing lipoproteins is the main risk factor for atherosclerotic cardiovascular disease (CVD) and the causative role of LDL has been demonstrated in several studies. Lp(a) is a subclass of LDL and elevated Lp(a) is an independent risk-factor, primarily genetically mediated. Genetic data support that high Lp(a) causes atherosclerosis. Elevated triglycerides in plasma are associated with increased risk for CVD. Whether triglycerides directly induce atherogenesis is still unclear, but current data strongly support that remnant particles from triglyceride-rich lipoproteins are causal. HDL are lipoproteins that have been considered to be important for reversed cholesterol transport. Low HDL is a strong risk-factor for CVD. However, the causative role of HDL is debated and intervention studies to raise HDL have not been successful. Reduction of LDL is the main target for prevention and treatment, using drugs that inhibit the enzyme HMG-CoA reductase, i.e. statins. Other drugs for LDL reduction and to modify other lipoproteins may further reduce risk, and new therapeutic targets are explored.
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Hollak, Carla E. M. Approach to the Patient with Respiratory Signs and Symptoms. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0071.
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The respiratory system is frequently involved in inborn errors of metabolism, either primarily or secondary to severe systemic disease. In disorders with progressive neurological disease, recurrent chest infections are a result of aspiration. Patients with cachexia and muscle weakness can develop breathing difficulties. Metabolic acidosis causes tachypnea. These secondary problems, occurring in the context of a multisystem disease with prominent other features, are well covered elsewhere and are not discussed in this chapter. The focus of the current chapter is the adult patient who presents with respiratory symptoms or signs as a first manifestation of an inborn error of metabolism. In addition, disorders where respiratory problems are a major part of the adult disease spectrum are listed.
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Hollak, Carla E. M. Hematological Abnormalities. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0077.
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The respiratory system is frequently involved in inborn errors of metabolism, either primarily or secondary to severe systemic disease. In disorders with progressive neurological disease, recurrent chest infections are a result of aspiration. Patients with cachexia and muscle weakness can develop breathing difficulties. Metabolic acidosis causes tachypnea. These secondary problems, occurring in the context of a multisystem disease with prominent other features, are well covered elsewhere and are not discussed in this chapter. The focus of the current chapter is the adult patient who presents with respiratory symptoms or signs as a first manifestation of an inborn error of metabolism. In addition, disorders where respiratory problems are a major part of the adult disease spectrum are listed
7
Warwick, David, Roderick Dunn, Erman Melikyan, and Jane Vadher. Osteoarthritis of the hand. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199227235.003.0009.
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Introduction 254Digital joint replacement 256Scaphoid–trapezium–trapezioid joint 258Thumb CMCJ arthritis 260Non-operative treatment for thumb CMC OA 262Operative treatment for thumb CMCJ OA 264Finger carpometacarpal joint 269Metacarpophalangeal joint 270Proximal interphalangeal joint 272Distal interphalangeal joint 274Common disease of diarthrodial joints. Primary aetiology is characterized by progressive degeneration of articular cartilage: a manifestation of an abnormal state of chondrocyte metabolism, loss of certain tissue components, alterations in microstructure and changes in biomechanical properties....
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Jarnert, Christina, Linda Mellbin, Lars Rydén, and Jaakko Tuomilehto. Glucose intolerance and diabetes. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656653.003.0016.
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Diabetes dramatically increases the risk of cardiovascular diseases (CVD). Diabetes is defined by elevated glucose in blood circulation. The level of glycaemia has a graded relation with CVD risk and diabetes is very frequent in people with CVD. In the general population half of the people with type 2 diabetes are undiagnosed, yet efficient methods for population screening exist. Despite considerable improvements in the management of CVD, patients with disturbed glucose metabolism have not benefited to the same extent as those without diabetes. Primary and secondary prevention of CVD in people with diabetes and other disturbances in glucose metabolism must be multifactorial and treatment targets stricter than for patients without glucose aberrations. Increased collaboration between different therapeutic disciplines including diabetologists, cardiologists, general practitioners, and dieticians is key to improved management for this large and high-risk population. Some important aspects of these issues are presented in this chapter.
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Jarnert, Christina, Linda Mellbin, Lars Rydén, and Jaakko Tuomilehto. Glucose intolerance and diabetes. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199656653.003.0016_update_001.
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Diabetes dramatically increases the risk of cardiovascular diseases (CVD). Diabetes is defined by elevated glucose in blood circulation. The level of glycaemia has a graded relation with CVD risk and diabetes is very frequent in people with CVD. In the general population half of the people with type 2 diabetes are undiagnosed, yet efficient methods for population screening exist. Despite considerable improvements in the management of CVD, patients with disturbed glucose metabolism have not benefited to the same extent as those without diabetes. Primary and secondary prevention of CVD in people with diabetes and other disturbances in glucose metabolism must be multifactorial and treatment targets stricter than for patients without glucose aberrations. Increased collaboration between different therapeutic disciplines including diabetologists, cardiologists, general practitioners, and dieticians is key to improved management for this large and high-risk population. Some important aspects of these issues are presented in this chapter.
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Gutiérrez, Orlando M. Fibroblast growth factor 23, Klotho, and phosphorus metabolism in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0119.
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Fibroblast growth factor 23 (FGF23) and Klotho have emerged as major hormonal regulators of phosphorus (P) and vitamin D metabolism. FGF23 is secreted by bone cells and acts in the kidneys to increase urinary P excretion and inhibit the synthesis of 1,25 dihydroxyvitamin D (1,25(OH)2D) and in the parathyroid glands to inhibit the synthesis and secretion of parathyroid hormone. Phosphorus excess stimulates FGF23 secretion, likely as an appropriate physiological adaptation to maintain normal P homeostasis by enhancing urinary P excretion and diminishing intestinal P absorption via lower 1,25(OH)2D. The FGF23 concentrations are elevated early in the course of chronic kidney disease (CKD) and may be a primary initiating factor for the development of secondary hyperparathyroidism in this setting. Klotho exists in two forms: a transmembrane form and a secreted form, each with distinct functions. The transmembrane form acts as the key co-factor needed for FGF23 to bind to and activate its cognate receptor in the kidneys and the parathyroid glands. The secreted form of Klotho has FGF23-independent effects on renal P and calcium handling, insulin sensitivity, and endothelial function. Disturbances in the expression of Klotho may play a role in the development of altered bone and mineral metabolism in early CKD. In addition, abnormal circulating concentrations of both FGF23 and Klotho have been linked to excess cardiovascular disease, suggesting that both play an important role in maintaining cardiovascular health.
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Heales, Simon, Simon Pope, Viruna Neergheen, and Manju Kurian. Abnormalities of CSF Neurotransmitters/Folates. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0082.
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The term Neurotansmitter disorder, in the area of metabolic disease, focuses particularly on inborn errors affecting monoamine (dopamine & serotonin), pyridoxal phosphate (B6) and folate metabolism. Whilst there has been considerable focus on these disorders with regards to the paediatric population, it is clear that an increasing number of adult patients are being identified. Adult neurologists need to be aware of the clinical presentation of such patients and the appropriate tests that need to be requested to ensure a correct diagnosis is achieved. CSF profiling, by a specialist laboratory, is often required. This has the ability to very often identify the nature of a primary defect with regards to implementation of appropriate treatment. For some of these disorders, treatment can be effective. This may be in the form of monoamine/vitamin replacement. However there are exceptions, e.g. aromatic amino acid decarboxylase and dopamine transporter deficiencies. There also needs also to be an awareness of the growing list of secondary factors that can cause impaired dopamine and serotonin metabolism.
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Steinberg, Deborah. Zooplankton Biogeochemical Cycles. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780199233267.003.0006.
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The structure of planktonic communities profoundly affects particle export and sequestration of organic material (the biological pump) and the chemical cycling of nutrients. This chapter describes the integral and multifaceted role zooplankton (both protozoan and metazoan) play in the export and cycling of elements in the ocean, with an emphasis on the North Atlantic Ocean and adjacent seas. Zooplankton consume a significant proportion of primary production across the world's oceans, and their metabolism plays a key role in recycling carbon, nitrogen, and other elements. The chapter also addresses how human or climate-influenced changes in North Atlantic zooplankton populations may in turn drive changes in zooplankton-mediated biogeochemical cycling.
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Jolly, Elaine, Andrew Fry, and Afzal Chaudhry, eds. Endocrine. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199230457.003.0007.
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Chapter 7 covers the basic science and clinical topics relating to the endocrine system which trainees are required to learn as part of their basic training and demonstrate in the MRCP. It covers endocrine physiology, acid-base balance, thyrotoxicosis, hypothyroidism, goitre and thyroid nodule, Cushing syndrome, acromegaly, hyperprolactinaemia, hypopituitarism, diabetes insipidus, adrenal incidentaloma, primary hyperaldosteronism, adrenal insufficiency, phaeochromocytoma and paraganglioma , male hypogonadism and Gynaecomastia, menstrual disorders and anovulation, hirsutism and the polycystic ovarian syndrome, multiple endocrine neoplasia and other genetic endocrine tumour syndromes, neuroendocrine tumours, acid-base disorders, sodium disorders, potassium disorders, hypocalcaemia, hypercalcaemia, hyperparathyroidism, osteoporosis, osteomalacia, Paget disease, dyslipidaemia, porphyria, adult inborn errors of metabolism, and obesity.
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Hartman, Adam L. Amino Acids in the Treatment of Neurological Disorders. Edited by Dominic P. D’Agostino. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0035.
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Studies of metabolism- and diet-based therapies in epilepsy and neuroprotection have focused primarily on the quality and quantity of fat supplementation or carbohydrate restriction. However, protein is another key dietary component that has not been as thoroughly studied. A number of amino acids have been shown to stop, terminate, or prevent seizures. In addition, some have been shown to exert neuroprotective effects in other neurological disorders. Amino acids (and their metabolites) may exert their effects by acting at membrane or cytoplasmic receptors, serving as substrates for membrane transporters and as modulators of signaling pathway activity. This chapter highlights examples of each of these mechanisms of action in select nervous system disorders.
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Nicholson, Grainne, and George M. Hall. Neuroendocrine physiology in anaesthetic practice. Edited by Jonathan G. Hardman. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0008.
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This chapter describes the hormonal, metabolic, and inflammatory response to surgery—commonly known as the surgical stress response. The changes in protein, carbohydrate, and fat metabolism to provide fuel for oxidation are outlined as well as changes in salt and water metabolism. Psychological sequelae of fatigue and malaise are also common in patients undergoing surgery. Attenuating the metabolic and endocrine changes associated with surgery may reduce postoperative morbidity and expedite recovery; the choice of anaesthetic drugs and techniques (regional vs general anaesthesia) and the increasing use of laparoscopic surgery have all been used to try to achieve this objective. The most common metabolic disease which anaesthetists have to manage is diabetes mellitus (DM) and its pathophysiology and medical management, as well as that of the related metabolic syndrome are discussed. Adrenal tumours are rare but usually require surgical excision. Phaeochromocytomas present unique anaesthetic challenges, but pre-, intra-, and postoperatively in terms of fluid management and blood pressure control. Conn’s syndrome (primary hyperaldosteronism) can also result in hypertension and electrolyte disturbances. Cushing’s disease (glucocorticoid excess) presents with the clinical effects of steroid excess and many patients have concomitant DM. Finally, perioperative steroid supplementation for patients already taking steroids and undergoing surgery is discussed.
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Cozza, Kelly L., Rita Rein, Gary H. Wynn, and Eric G. Meyer. Psychopharmacology of Depression as a Systemic Illness for Primary and Specialty Care Clinicians. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603342.003.0010.
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There are nearly 4 million patients with depression followed by primary care in the United States, with nearly 80% of prescriptions for antidepressants written by non-psychiatrists (Mark et al. 2009). Understanding and utilizing psychopharmacology is a critical skill for primary care physicians, who are often initial or sole prescribers. Persons with medical illnesses and depression are often prescribed a multitude of medications, necessitating attention to pharmacodynamic, pharmacokinetics, and an understanding of intended effects, side effects, toxicities, and drug interactions. This chapter begins with a brief review of drug mechanisms of action, metabolism, and interaction principles; addressing the interplay between depression, the medications used to treat depression, co-prescribed medications, and medical illness. The chapter includes a discussion of drugs used to treat depression in text and table format, highlighted with case examples. Details about mechanism of action, common side effects and adverse reactions, drug interactions, and other clinical implications are provided.
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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.
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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.
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Gordon, David, Ahmad Khattab, and Magdalena Anitescu. Bupivacaine and Glucocorticoid-Induced Myonecrosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190271787.003.0035.
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The most frequently used medications for chronic pain are local anesthetics (LA) and glucocorticoids. Common adverse events from LA, such as seizures and cardiotoxicity, are well known. A lesser known side effect is local tissue reaction to the LA concentration. Myotoxicity is one of the common denominators of direct tissue reaction to LA; it results from the disruption of the mitochondria in the muscle cells. All LA produce some degree of myotoxicity; bupivacaine has the greatest effect and procaine the least. If LA is combined with glucocorticoid, muscle breakdown is even more extensive showing a synergistic effect. Myotoxicity depends primarily on LA concentration, is time dependent, and is enhanced by preexisting altered metabolism. It affects mostly young patients. Potential effects of long-term or repeated administration of the combination LA/glucocorticoids medications should always be considered and discussed with patients.
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Wordsworth, B. P. Skeletal dysplasias. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0150.
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Bone is metabolically active throughout life and metabolic disturbances may have wide-ranging consequences that are not restricted to altering its mechanics. The study of some genetic bone diseases has already provided remarkable insights into the normal regulation of bone metabolism. Skeletal dysplasias are developmental disorders of the chondro-osseous tissues commonly resulting in short stature, which is often disproportionate. The underlying mutations are often in the structural genes encoding components of the matrix but may also involve growth factors or cell signalling. In contrast, the dysostoses tend to affect single bones or groups of bones, reflecting the transient nature of the many different signalling factors to which they are responsive during development. Abnormalities of bone density (high or low) may be due to primary deficiency of bone matrix synthesis (e.g. osteogenesis imperfecta and hypophosphatasia) but may also reflect an imbalance between bone formation and resorption. This may be caused by abnormalities of bone formation (e.g. hyperostosis/sclerosteosis and osteoporosis pseudoglioma syndrome) or bone resorption (e.g. classic osteopetrosis and fibrous dysplasia).
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Nates, Joseph L., and Sharla K. Tajchman. Indirect calorimetry in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0205.
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Critically-ill patients have unpredictable and dynamic metabolic demands that are difficult to predict and quantify. Combined with the high incidence of pre-existing or development of malnutrition in the ICU, these metabolic demands have deleterious effects on outcomes when patients are provided with inadequate or inappropriate nutrition support. Providing adequate nutritional support that meets these varying metabolic demands is a long-standing challenge in the intensive care unit (ICU). Indirect calorimetry (ICal) is a tool that allows ICU practitioners to accurately assess energy expenditure (EE) in critically-ill patients with unpredictable metabolic demands to optimize nutrition support. ICal provides clinicians with a patient’s measured EE (MEE), a quantification of cellular metabolism, and respiratory quotient (RQ), a reflection of which substrates are primarily being utilized for fuel. Study results help clinicians target optimal nutritional goals and prevent adverse effects associated with both under- and overfeeding patients. Recent studies have suggested avoiding caloric deficits and providing tight caloric control may improve morbidity and mortality outcomes in critically-ill patients, though more studies are needed to verify this potential benefit. Currently, there are no specific guideline recommendations to help clinicians utilize ICal in the ICU. Although ICal is considered to be the gold standard for determining EE in critically-ill patients, its use remains limited by availability, cost, and the need for trained personnel for correct use.
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J, Wilkin Terence, and Voss Linda 1945-, eds. Adult obesity: A paediatric challenge. London: Taylor & Francis, 2003.
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