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1
Shid-Moosavi, S. Mostafa. Effect of renal perfusion pressure and nerves on renal function, renin release and renin and angiotensinogen gene expression. Birmingham: University of Birmingham, 1998.
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2
Bolton, Charles Francis. Neurological complications of renal disease. Boston: Butterworths, 1990.
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3
Meisel, Abigail. Investigating eating disorders (anorexia, bulimia, and binge eating): Real facts for real lives. Berkeley Heights, NJ: Enslow Publishers, 2011.
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5
Garfield, Johanna. The life of a real girl: An autobiography of anorexia and madness. London: Sidgwick & Jackson, 1986.
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7
Wang, Yutang, Kyungjoon Lim, and Kate M. Denton, eds. Function of Renal Sympathetic Nerves. Frontiers Media SA, 2017. http://dx.doi.org/10.3389/978-2-88945-295-8.
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Gonzalez-Albarrán, Olga, and Luis M. Ruilope. The kidney and control of blood pressure. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0210.
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The kidneys can be at the root of the development of arterial hypertension or they can participate in the maintenance of hypertension and its sequels. Renal alterations interfering with the regulation of sodium homeostasis or facilitating the generation of vasoconstrictors, particularly angiotensin II, are involved in the dysregulation of arterial blood pressure that underlies the development of arterial hypertension. The biology of angiotensin is described in detail.The kidneys are also the mediator of hypertension in such examples as renal ischaemia and hyperaldosteronism. The role of renal nerves, and renal depressor substances, are also described.Transplantation experiments in animals and observations in human transplantation, as well as some primary gene defects, show the importance of renal mechanisms in hypertension. Once kidneys have been damaged, they often contribute to an increase in arterial pressure. Salt sensitivity is probably a major part of the mechanism, but it is mediated by multiple pathways.
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Dussaule, Jean-Claude, Martin Flamant, and Christos Chatziantoniou. Function of the normal glomerulus. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0044_update_001.
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Glomerular filtration, the first step leading to the formation of primitive urine, is a passive phenomenon. The composition of this primitive urine is the consequence of the ultrafiltration of plasma depending on renal blood flow, on hydrostatic pressure of glomerular capillary, and on glomerular coefficient of ultrafiltration. Glomerular filtration rate (GFR) can be precisely measured by the calculation of the clearance of freely filtrated exogenous substances that are neither metabolized nor reabsorbed nor secreted by tubules: its mean value is 125 mL/min/1.73 m² in men and 110 mL/min/1.73 m² in women, which represents 20% of renal blood flow. In clinical practice, estimates of GFR are obtained by the measurement of creatininaemia followed by the application of various equations (MDRD or CKD-EPI) and more recently by the measurement of plasmatic C-cystatin. Under physiological conditions, GFR is a stable parameter that is regulated by the intrinsic vascular and tubular autoregulation, by the balance between paracrine and endocrine agents acting as vasoconstrictors and vasodilators, and by the effects of renal sympathetic nerves. The mechanisms controlling GFR regulation are complex. This is due to the variety of vasoactive agents and their targets, and multiple interactions between them. Nevertheless, the relative stability of GFR during important variations of systemic haemodynamics and volaemia is due to three major operating mechanisms: autoregulation of the afferent arteriolar resistance, local synthesis and action of angiotensin II, and the sensitivity of renal resistance vessels to respond to NO release.
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Shaw, Pamela, and David Hilton-Jones. The lower cranial nerves and dysphagia. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0429.
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Disorders affecting the lower cranial nerves – V (trigeminal), VII (facial), IX (glossopharyngeal), X (vagus), XI (accessory) and XII (hypoglossal) – are discussed in the first part of this chapter. The clinical neuroanatomy of each nerve is described in detail, as are disorders – often in the form of lesions – for each nerve.Trigeminal nerve function may be affected by supranuclear, nuclear, or peripheral lesions. Because of the wide anatomical distribution of the components of the trigeminal nerve, complete interruption of both the motor and sensory parts is rarely observed in practice. However, partial involvement of the trigeminal nerve, particularly the sensory component, is relatively common, the main symptoms being numbness and pain. Reactivation of herpes zoster in the trigeminal nerve (shingles) can cause pain and a rash. Trigeminal neuralgia and sensory neuropathy are also discussed.Other disorders of the lower cranial nerves include Bell’s palsy, hemifacial spasm and glossopharyngeal neuralgia. Cavernous sinus, Tolosa–Hunt syndrome, jugular foramen syndrome and polyneuritis cranialis are caused by the involvement of more than one lower cranial nerve.Difficulty in swallowing, or dysphagia, is a common neurological problem and the most important consequences include aspiration and malnutrition (Wiles 1991). The process of swallowing is a complex neuromuscular activity, which allows the safe transport of material from the mouth to the stomach for digestion, without compromising the airway. It involves the synergistic action of at least 32 pairs of muscles and depends on the integrity of sensory and motor pathways of several cranial nerves; V, VII, IX, X, and XII. In neurological practice dysphagia is most often seen in association with other, obvious, neurological problems. Apart from in oculopharyngeal muscular dystrophy, it is relatively rare as a sole presenting symptom although occasionally this is seen in motor neurone disease, myasthenia gravis, and inclusion body myositis. Conversely, in general medical practice, there are many mechanical or structural disorders which may have dysphagia as the presenting feature. In some of the disorders, notably motor neurone disease, both upper and lower motor neurone dysfunction may contribute to the dysphagia. Once dysphagia has been identified as a real or potential problem, the patient should undergo expert evaluation by a clinician and a speech therapist, prior to any attempt at feeding. Videofluoroscopy may be required. If there is any doubt it is best to achieve adequate nutrition through the use of a fine-bore nasogastric tube and to periodically reassess swallowing. Anticholinergic drugs may be helpful to reduce problems with excess saliva and drooling that occur in patients with neurological dysphagia, and a portable suction apparatus may be helpful. Difficulty in clearing secretions from the throat may be helped by the administration of a mucolytic agent such as carbocisteine or provision of a cough assist device.
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Berrill, Andrew, and Pawan Gupta. General principles of regional anaesthesia. Edited by Philip M. Hopkins. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0052.
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Regional anaesthesia is now extremely safe in experienced hands. The vast majority of upper and lower limb procedures can now be performed with either a peripheral regional block alone or in combination with a general anaesthetic. Neuraxial blocks can provide reliable postoperative pain relief for operations on the trunk and lower limbs. There is no consensus on the maximum safe dose of local anaesthetics. It is important therefore to use a minimum optimal dose of a local anaesthetic for any nerve block to reduce the risk of toxicity and to improve the success rate. Adjuncts, such as clonidine and dexamethasone, can prolong the duration of the block. Advances in nerve localization methods and block needles have further improved the safety of nerve blocks. There is increasing evidence to show that ultrasound is superior to peripheral nerve stimulation for identifying nerves. Ultrasound also helps in real-time visualization of the spread of the local anaesthetic. Consent, sedation, and support from non-anaesthetic staff play a key role in the success of regional anaesthesia, especially in awake patients. Although serious complications from nerve blocks are uncommon, direct nerve injury is perhaps the most serious complication. Fortunately, these symptoms in the overwhelming majority resolve within a year. This chapter covers the history, factors affecting local anaesthetics, role of adjuncts, nerve localization techniques, and complications of regional anaesthesia. Finally, some suggestions to improve the success and safety of peripheral nerve blocks are discussed.
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Narouze, Samer N. Cervical Transforaminal/Nerve Root Injections: Ultrasound. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199908004.003.0005.
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Ultrasound provides direct visualization and imaging of various soft tissues without radiation exposure. Thus, it is a very appealing modality in neck injections, with the magnitude of critical soft-tissue structures compacted in a very vascular area. Moreover, ultrasound imaging allows real-time needle advancement and monitoring the spread of injectate, which improves the accuracy of the block and minimizes the risk of intravascular injection. This chapter reviews the feasibility and safety of the ultrasound-guided approach. It also provides a new insight into the technique and why some practitioners prefer an “extraforaminal” nerve root approach rather than the traditional “transforaminal” epidural approach.
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Jamison, David, Indy Wilkinson, and Steven P. Cohen. Facet Joint Interventions: Fluoroscopy. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199908004.003.0019.
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This chapter reviews the diagnosis and treatment of facet joint pain. Fluoroscopic guidance is commonly used to optimize treatment outcomes. The only reliable way to identify a painful facet joint is with image-guided blockade of either the medial branch innervating the joint or the joint itself. Although computed tomography (CT) and ultrasound have been shown to provide reliable landmarks for accurate needle placement, these modalities have limitations. The risks of CT include increased radiation exposure, cost, and an inability to perform real-time contrast injection. While ultrasound provides a convenient and inexpensive way to anesthetize the facet joints or medial branch nerves innervating them, it is unreliable in obese patients, is not as sensitive for detecting intravascular uptake as digital substraction or real-time contrast injection under fluoroscopy, and cannot be reliably used to place an electrode parallel to the course of the nerve, which has been shown to enhance lesion size.
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Wolter, Tilman. Cervical Transforaminal/Nerve Root Injections: Computed Tomography. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199908004.003.0006.
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Computed tomography (CT)–guided selective cervical nerve root blocks, particularly in the dorsal/posterior access, are sensitive, specific, efficacious, and safe. If performed with a lateral/anterolateral access, the CT-fluoroscopic technique with real-time visualization should be chosen. In comparison to fluoroscopy-guided nerve root blocks, CT guidance offers a more precise visualization of the contrast agent. While the advantages of CT guidance seem to outweigh the slightly higher exposure to radiation, this specific topic is debatable and requires additional scientific inquiry. Comparative studies are needed to address the sensitivity, specificity, efficacy, complication rates, and radiation exposure of CT- and fluoroscopy-guided cervical nerve root blocks.
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Hundert, Joshua S., Rashmi Verma, Ritika Suri, Anika T. Singh, and Ajay Singh. Neurological Manifestations of Renal Disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0191.
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In the United Syates, chronic kidney disease (CKD) affects approximately 5% to 10% of the general population. It is estimated that about 20 million Americans have some degree of CKD. Central nervous system (CNS) abnormalities are common in patients with CKD, especially in those individuals with end stage renal disease (ESRD) who require renal replacement therapy, such as dialysis or transplant. Neurological symptoms in patients with CKD may range from mild altered sensorium and cognitive dysfunction to tremors and coma. By the time patients require renal replacement therapy, some patients may have uremia, a clinical syndrome with protean manifestations.
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Shorter, Edward. How Everyone Became Depressed. Oxford University Press, 2013. http://dx.doi.org/10.1093/oso/9780199948086.001.0001.
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About one American in five receives a diagnosis of major depression over the course of a lifetime. That's despite the fact that many such patients have no mood disorder; they're not sad, but suffer from anxiety, fatigue, insomnia, or a tendency to obsess about the whole business. "There is a term for what they have," writes Edward Shorter, "and it's a good old-fashioned term that has gone out of use. They have nerves." In How Everyone Became Depressed, Edward Shorter, a distinguished professor of psychiatry and the history of medicine argues for a return to the old fashioned concept of nervous illness. These are, he writes, diseases of the entire body, not the mind, and as was recognized as early as the 1600s. Shorter traces the evolution of the concept of "nerves" and the "nervous breakdown" in western medical thought. He points to a great paradigm shift in the first third of the twentieth century, driven especially by Freud, that transferred behavioral disorders from neurology to psychiatry, spotlighting the mind, not the body. The catch-all term "depression" now applies to virtually everything, "a jumble of non-disease entities, created by political infighting within psychiatry, by competitive struggles in the pharmaceutical industry, and by the whimsy of the regulators." Depression is a real and very serious illness, he argues; it should not be diagnosed so promiscuously, and certainly not without regard to the rest of the body. Meloncholia, he writes, "the quintessence of the nervous breakdown, reaches deep into the endocrine system, which governs the thyroid and adrenal glands among other organs." In a learned yet provocative challenge to psychiatry, Shorter argues that the continuing misuse of "depression" represents nothing less than "the failure of the scientific imagination."
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Arroyo, Vicente, Mónica Guevara, and Javier Fernández. Renal failure in cirrhosis. Edited by Norbert Lameire. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0247.
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A major event in liver cirrhosis is the development of a progressive deterioration of circulatory function due to splanchnic arterial vasodilation and impairment in cardiac function. This feature determines a homeostatic activation of the renin–angiotensin–aldosterone system, sympathetic nervous system, and antidiuretic hormone. The splanchnic microcirculation is resistant to the vasoconstrictor effect of these systems. Therefore, the homeostasis of arterial pressure in cirrhosis occurs in the extrasplanchnic, mainly renal circulation. The activation of these systems produces renal fluid retention, which accumulates as ascites, and water retention and dilutional hyponatraemia. In the latest phase of cirrhosis, when circulatory dysfunction is severe, renal vasoconstriction is intense and patients develop type 2 hepatorenal syndrome (HRS) and refractory ascites.Type 1 HRS is an acute and rapidly progressive renal failure that occurs in the setting of a precipitating event, commonly an infection. Patients with type 1 HRS also present with rapid deterioration of liver function (encephalopathy, jaundice) and relative adrenal insufficiency. The mechanism of this multiorgan failure is an acute deterioration in circulatory function due to both an accentuation of arterial vasodilation and of cardiac dysfunction.There is no specific test for the diagnosis of HRS. The most accepted diagnostic criteria are those proposed by the International Ascites Club which are based on the exclusion of other types of renal failure. The course of renal failure following treatment of the precipitating event of HRS is another important diagnostic feature.The treatment of choice of tense ascites in cirrhosis is paracentesis associated with intravenous albumin infusion. Moderate sodium restriction and diuretics (spironolactone alone or associated with furosemide) are subsequently given to prevent re-accumulation of ascites. Diuretics are the treatment of choice in patients with moderate ascites. Patients with type 2 HRS and refractory ascites (not responding to diuretics) could be treated by frequent paracentesis or by the insertion of a transjugular intrahepatic portosystemic shunt (TIPS).Terlipressin plus albumin is the treatment of choice in type 1 HRS
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Vester, Udo, and Stefanie Weber. Townes–Brocks syndrome. Edited by Adrian Woolf. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0359.
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Townes–Brocks syndrome (TBS) is an autosomal dominant disease with variable expression. Classical features are imperforate anus, dysplastic ears with congenital hearing deficit, and triphalangeal thumbs in most cases. A variety of other malformations (renal, genitourinary, heart, central nervous system, eyes) or hypothyroidism has been described. Mutations in SALL1 have been identified in patients with TBS and genetic testing allows confirmation of the diagnosis. Familiar and sporadic forms (caused by de novo mutations) seem to be equally distributed. Renal involvement in TBS is not uncommon and includes renal agenesis, hypo-/dysplasia, and renal cysts and may eventually lead to chronic renal failure. As renal function may not deteriorate before adulthood, renal function should be monitored in all patients. As cases with TBS can be oligosymptomatic, TBS should be suspected in every case with unexplained renal failure, minor abnormalities, or indicative family history. Genetic counselling is mandatory in identified cases.
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Watson, Max, Caroline Lucas, Andrew Hoy, and Jo Wells. Genitourinary problems. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780199234356.003.0018.
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This chapter focuses on the anatomy and physiology of the bladder and micturition. It covers bladder wall, sphincter active urethra, nerve supply, bladder pain and its treatment, blood supply of the bladder, urinary tract infection (UTI), renal pain, ureteric colic, pelvic pain, urinary retention, ureteric obstruction, urinary incontinence, haematuria, catheterization, genitourinary fistulae, vesicoenteric fistulae, vesicovaginal fistulae, and sexual health in advanced disease.
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Lucas, Joshua, Dawn Fishback, and Steven Giannotta. Skull Base Schwannoma. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190696696.003.0013.
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This chapter presents a case example of a patient with progressive unilateral hearing loss who was ultimately diagnosed with a skull base schwannoma. The workup and differential diagnosis are presented and options for treatment are reviewed based on published evidence. Treatment options include observation, stereotactic radiosurgery, and surgical resection. The objective status of a patient’s hearing as well as the patient’s age influence treatment recommendations and the surgical approach. Intraoperative neuromonitoring provides real-time assessment of facial nerve irritation as well as cochlear nerve function and is an important component of surgery. Complication avoidance and management are also discussed in this chapter.
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Waldek, Stephen. Fabry disease. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0337.
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Fabry disease is a rare X-linked lysosomal storage disorder in which deficiency of alpha-galactosidase A leads to accumulation of substrate, mostly globotriaosylceramide, which causes a progressive, multiorgan disease affecting predominantly the kidneys, skin, heart, and nervous system. Painful peripheral (‘acral’) neuropathy is characteristic.Key clinical signs are angiokeratoma found by close examination of skin; characteristic eye lesions may be seen; lipid deposits may be seen in urine. Renal biopsy appearances are characteristic and this is commonly where the diagnosis is first made. Increasingly, cardiologists are suspecting the condition in adults with echocardiographic appearances of left ventricular hypertrophy. Diagnosis in men is usually made by measurement of alpha-galactosidase in either white cells or plasma (or using blood spots). Unfortunately, many female patients can have normal enzyme levels so that genetic testing is the only way to confirm a diagnosis. Non-selective screening strategies (e.g. males on renal replacement therapy with uncertain renal diagnoses) have had low yields.
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Groothoff, Jaap W. Primary Hyperoxaluria. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0065.
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Primary hyperoxalurias (PH) are rare autosomal recessive metabolic disorders characterized by an increased endogenous oxalate production which leads to the development of urolithiasis, nephrocalcinosis, and ultimately to renal failure.PH patients with severe renal failure develop life-threatening systemic oxalosis, which affects many organs such as bone, skin, retina, myocardium, vessel walls, and the central nervous system. So far, combined or sequential liver-kidney transplantation is the only therapeutic option for patients with advanced disease. Contrary to the former impression of a relatively mild course of disease in patients diagnosed as adults, recent data have shown that patients diagnosed in adulthood mostly present with established ESRD and systemic oxalosis. The fact that some of these patients respond to pyridoxine therapy underlines the importance of early diagnosis and measures to prevent renal failure and systemic oxalosis. All children with stone disease or nephrocalcinosis and all adults with recurrent stone disease should therefore be screened for PH.
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Levtchenko, Elena N., and Mirian C. Janssen. Cystinosis. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0339_update_001.
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Cystinosis is a rare autosomal recessive disease caused by mutations in the lysosomal cystine transporter cystinosin encoded by the CTNS gene (17p.13.2). Cystinosis is characterized by lysosomal cystine accumulation throughout the body with renal Fanconi syndrome being the most common presenting symptom of a multisystem disorder. It must be distinguished from cystinuria in which formation of cystine stones is the core problem. When left untreated, kidney dysfunction gradually progresses towards end-stage renal failure during the first 10 years of life. The advent of renal replacement therapy allowed cystinosis patients to survive into adulthood, but revealed numerous extrarenal manifestations of the disease, affecting eyes, endocrine organs, gastrointestinal tract, muscles, and central and peripheral nervous systems. The disease mechanism of cystinosis is not fully understood. The administration of the cystine-depleting agent cysteamine slows down renal and extrarenal organ damage, pointing to the pivotal role of cystine accumulation in the disease pathogenesis. Treatment with cysteamine should be initiated as early as possible and continued lifelong, and also after kidney transplantation for protecting extrarenal organs. Cysteamine eye drops are an indispensable part of the treatment of corneal cystine accumulation. Life expectancy of cystinosis patients has substantially improved and is now above 50 years.
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Waldek, Stephen. Fabry disease. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0335_update_001.
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Fabry disease is a rare X-linked disorder of glycosphingolipid metabolism caused by a deficiency of the lysosomal acid hydrolase enzyme, alpha-galactosidase A. The resulting accumulation of substrate, mostly globotriaosylceramide, leads to a progressive, multiorgan disease affecting predominantly the kidneys, skin, heart, and nervous system. It is one of over 50 lysosomal storage diseases. It is typically diagnosed in young men after many years of ‘acral pain’ syndrome, when the diagnosis is made through identification of characteristic abnormalities of skin, kidney or heart, or of other organs. Renal failure has been a common outcome. Females may also develop manifestations, usually later in life. Renal biopsy shows vacuoles/deposits in podocytes and other renal cell types with progressive scarring. The diagnosis can be made by measuring enzyme levels in men, or by genetic testing. This latter is the more reliable test in women. Fabry disease can now be treated where affordable by regular (every 2 weeks) intravenous infusions of recombinant preparations of the deficient enzyme. These are burdensome and expensive, but are transforming the outlook for the condition.
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Waldek, Stephen. Fabry disease. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0338_update_001.
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Fabry disease is a rare X-linked lysosomal storage disorder in which deficiency of alpha-galactosidase A leads to accumulation of substrate, mostly globotriaosylceramide (Gb3), which causes a progressive, multiorgan disease affecting predominantly the kidneys, skin, heart, and nervous system. Painful peripheral (‘acral’) neuropathy is characteristic. Proteinuria and estimated glomerular filtration rate (eGFR) are strongly associated with risk of progression, but this may be reduced by treatment with angiotensin-converting enzyme inhibitors as well as by enzyme replacement therapy (ERT). ERT was approved in 2001; it improves pain and other neuropathic symptoms, and well-being, and has been proven to clear deposits of Gb3 from tissues, at variable speeds. There is limited randomized controlled trial data but protective effects have been proven for renal outcomes, death, and better outcomes in some other organ systems. Renal function may be protected if ERT is commenced before there is heavy proteinuria or substantial loss of GFR. It is recommended to start ERT as soon as the diagnosis is made in those with very low or absent enzyme. For those with intermediate levels it is recommended to commence treatment only when signs or symptoms appear. Proteinuria and eGFR give most information from a renal point of view, but renal biopsy is also useful for confirming the renal diagnosis and staging the disease as well as monitoring progress in selected cases. Management should include regular screening for complications including myocardial and neurological assessments. It is likely that registries will show progressive rises in median survival with this condition.
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Gluckman, Sir Peter, Mark Hanson, Chong Yap Seng, and Anne Bardsley. Potassium in pregnancy and breastfeeding. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198722700.003.0022.
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Potassium is an important electrolyte involved in transmission of electrical signals for muscle contraction, nerve impulse transmission, and cardiac function. The fetus accumulates potassium throughout gestation, but little is known about maternal potassium balance during pregnancy. Conditions associated with pregnancy, such as severe vomiting or morning sickness, can cause potassium loss. Caffeine increases the renal excretion of potassium, and cases of hypokalaemia in pregnancy have been observed in women with heavy caffeine/cola consumption, resulting in extreme muscle fatigue. To date there is insufficient evidence to suggest that the potassium requirement is increased during pregnancy, although a small increase in intake is needed for lactation. Reduction of cardiovascular risk factors and bone loss may be assisted by increasing potassium intake and/or by dietary sodium reduction.
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Matthews, Philippa C. Infections classified by organ system. Edited by Philippa C. Matthews. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198737773.003.0018.
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This chapter provides a page-per-topic view for clinical syndromes classified by organ system (central nervous system, cardiac, respiratory, gastrointestinal, renal and genitourinary, ocular, and cutaneous syndromes). Each page contains a tabulated list of organisms that may be responsible for causing pathology in this organ system, with a brief description of the likely nature of the clinical presentation. This aims to provide clinicians with a quick check-list of the potential aetiology underpinning any particular clinical presentation, as well as providing a summary of information presented on specific organisms in earlier chapters of the book.
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Prestel, Joseph Ben. Precarious Calm. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198797562.003.0006.
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In Berlin, the portrayals of the negative emotional effects of the city ushered in attempts at “reform.” Doctors, real estate developers, and city clerks in the German capital penned publications in which they praised the positive effects of suburbs and physical exercise. Berliners were advised that through activities like breathing fresh air, gardening, and exercising the body, they could strengthen their nerves and bring back calm, positive, and controllable emotions. This notion of emotional betterment drove the spread of several gymnastic and sport clubs, as well as the creation of a number of new suburbs that mushroomed along the fringes of the city. While these developments came with a universal promise of improving Berlin as a whole, a closer look at the practices of emotional reform shows that they often served to rearticulate dividing lines of class and gender.
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Waldek, Stephen. Fabry disease. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0336.
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Fabry disease is a rare X-linked lysosomal storage disorder in which deficiency of alpha-galactosidase A leads to accumulation of substrate, mostly globotriaosylceramide, which causes a progressive, multiorgan disease affecting predominantly the kidneys, skin, heart, gut, and nervous system. Painful peripheral (‘acral’) neuropathy is characteristic. The disease is commonly diagnosed in children and young men often after some years of usually neuropathic symptoms, with exacerbations (Fabry crises), that commonly elude diagnosis for a long time. These usually occur years in advance of overt involvement of other organs. Diagnosis may also be suspected from renal biopsy, echocardiographic evidence of cardiomyopathy commonly beginning as left ventricular hypertrophy, or characteristic angiokeratomas typically in ‘bathing trunk’ distribution on skin. Renal manifestations are of proteinuria leading to progressive chronic kidney disease associated with deposits in podocytes. Diarrhoea is common. Disordered sweating is typical. Corneal lesions are also typical and there may be tortuosity of retinal vessels. Strokes are increased in frequency, and sensorineural deafness may occur. Women have fewer and later overt manifestations but some develop severe disease.
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Connor, Thomas, and Patrick H. Maxwell. Von Hippel–Lindau disease. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0332.
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Von Hippel–Lindau (VHL) disease is a dominantly inherited familial cancer syndrome caused by germline mutations in the VHL tumour suppressor gene. The most frequent manifestations of VHL disease are retinal and central nervous system haemangioblastomas, clear cell renal cell carcinomas, and phaeochromocytomas. Genetic testing and active screening for clinical manifestations is now started in childhood and has greatly improved the prognosis for patients with VHL disease. The VHL protein plays a critical role in regulating the cellular response to changes in oxygen tension. Loss of VHL function results in constitutive activation of a range of angiogenic and metabolic pathways. New drug therapies have been developed that reverse some of the cellular consequences of VHL loss of function in kidney cancer.
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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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Deep: Real life with spinal cord injury. Ann Arbor: University of Michigan Press, 2006.
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Marcy, Epstein, and Pettway Travar, eds. Deep: Real life with spinal cord injury. Ann Arbor: University of Michigan Press, 2006.
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Marcy, Epstein, and Pettway Travar, eds. Deep: Real life with spinal cord injury. Ann Arbor: University of Michigan Press, 2006.
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Deep: Real life with spinal cord injury. Ann Arbor: University of Michigan Press, 2006.
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Epstein, Marcy Joy, and Travar Pettway. Deep: Real Life with Spinal Cord Injury. University of Michigan Press, 2007.
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39
Levy, Jerrold H., and David Faraoni. Pathophysiology and causes of severe hypertension. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0162.
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Hypertension affects multiple groups of patients characterized by different clinical presentations and a spectrum of potential causes. The pathophysiology is complex and multifactorial. Although most patients are labelled ‘essential hypertension’, multiple mechanisms are involved in blood pressure regulation. Factors that influence blood pressure homeostasis include endothelial function, the renin-angiotensin system, and the sympathetic nervous system. In elderly patients, hypertension is common as the vascular system and arterial stiffness also contribute. Other important factors include inflammatory processes as part of systemic diseases, including atherosclerosis,which may contribute to renal and vascular injury. Hypertension is also associated with metabolic disturbances including dyslipidaemia that manifests in obese patients who also have insulin resistance. These different pathways all represent potential targets for treatment, but also increase the challenge of multimodal pathophysiology.
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Scolding, Neil. Vasculitis and collagen vascular diseases. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0862.
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That part of the clinical interface between neurology and general medicine occupied by inflammatory and immunological diseases is neither small nor medically trivial. Neurologists readily accept the challenges of ‘primary’ immune diseases of the nervous system: these tend to be focussed on one particular target such as oligodendrocytes or the neuro-muscular junction present in predictable ways, and are amenable as a rule to rational, methodological diagnosis, and occasionally even treatment. This is proper neurology.‘Secondary’ neurological involvement in diseases mainly considered systemic inflammatory conditions—for example, SLE, sarcoidosis, vasculitis, and Behçet’s—is a rather different matter. It may be difficult enough to secure such a diagnosis even when systemic disease has previously been diagnosed and new neurological features need to be differentiated from iatrogenic disease, particularly drug side effects or the consequences of immune suppression. But all the diseases mentioned may present with and confine themselves wholly to the nervous system; they may mimic one another, and pursue erratic and unpredictable clinical courses. In central nervous system disease, diagnosis by tissue biopsy is potentially hazardous and unattractive. Few neurologists enjoy excesses of confidence or expertise when faced with such clinical problems: the cautious diagnostician is perplexed, and the evidence-based neuroprescriber confounded. Unsurprisingly, great variations in approaches to diagnosis and management are seen (Scolding et al. 2002b).But rheumatologically inclined general, renal or respiratory physicians, comfortable when managing inflammation affecting their system or indeed other parts of the body designed to support the nervous system, are generally also ill at ease when faced with neurological features whose differential diagnosis may be large, particularly given the near universal diagnostic non-specificity of either imaging or CSF analysis.Here then is the subject material for this chapter: the diagnosis and management of central nervous system involvement in inflammatory and immunological systemic diseases (Scolding 1999a). In not one of these neurological conditions has a single controlled therapeutic trial been reported, and much that is published on these conditions is misleading or inaccurate. And yet the frequency with which the diagnosis is only confirmed or even first emerges at autopsy bears stark witness to both the severity and evasiveness of these disorders.
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Ng, Dominic S. Familial Lecithin Cholesterol Acyl Transferase Deficiency Syndromes. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0034.
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Lecithin cholesterol ester transferase (LCAT) is the sole enzyme in the circulation that mediates the esterification of free cholesterol (FC) to cholesterol ester (CE) in lipoproteins. Mutations in the LCAT gene result in one of two clinical syndromes: complete LCAT deficiency syndrome, and “fish eye disease.” The former is characterized by a broad spectrum of clinical features, including profound high-density lipoprotein (HDL) deficiency, hypertriglyceridemia, corneal opacities, anemia, neuropathies, and nephropathy. In contrast, fish eye disease patients develop severe HDL deficiency and severe corneal opacities, but the nervous system and kidneys are typically unaffected. Whether there is a predisposition to accelerated coronary heart disease with LCAT deficiency remains controversial. Currently, severe corneal opacities may be treated with corneal transplant. Only anecdotal evidence is available for preventive measures of progressive renal complications. LCAT replacement therapies are under investigation.
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Oliver, Nora, and Elizabeth Chiao. Malignant Diseases in HIV. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190493097.003.0033.
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Malignancies were one of the earliest recognized manifestations that led to the eventual description of the AIDS epidemic. Kaposi’s sarcoma was one of the first entities described in association with AIDS. Subsequently, intermediate-grade and high-grade non-Hodgkin’s lymphoma, invasive cervical cancer, and primary central nervous system lymphoma were defined by the Centers for Disease Control and Prevention as “AIDS-defining conditions.” Since the advent of combination antiretroviral therapy, several other cancers that are not AIDS-defining have been found to have an increased incidence in patients with HIV. These include, but are not limited to, Hodgkin’s disease and anal, liver, lung, oropharyngeal, colorectal, and renal cancers. They are generally referred to as “non-AIDS-defining cancers.” The increasing longevity of persons living with HIV as well as concurrent modifiable risk factors such as tobacco use may also influence the epidemiology of these malignancies.
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Sudhansu, Chokroverty, ed. Magnetic stimulation in clinical neurophysiology. Boston: Butterworths, 1990.
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Forsyth, Rob, and Richard Newton. Clinical approach. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198784449.003.0001.
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This chapter addresses consultation management and clinical method. It describes how to put families at ease and enable them to get all they hope from the encounter. It suggests an approach and language to use in difficult situations: the dying child, giving bad news, and bereavement. It offers guidance on clinical examination of central and peripheral nervous systems in newborn and older children. A real-world approach to quick neurological examinations is given. It encourages a synthesis of historical and clinical findings into a differential diagnosis, first siting the lesion, then defining the cause. This promotes the formulation of efficient and effective investigation and treatment plans as the essence of the clinical process.
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Pollard, Brian J. Muscle relaxants in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0047.
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The place of neuromuscular blocking agents in the intensive care unit (ICU) has changed markedly over the last 20 years. Originally regarded as a mainstay of the process of ‘sedation’, they are now only used for specific indications. The principal disadvantage is probably the difficulty in neurological assessment when a muscle relaxant is used coupled with the increased risk of awareness, because inadequate sedation will be masked. Of the available agents, the intermediate acting ones are the most popular. The degree of relaxation can be readily controlled and they have few side effects. In the presence of renal and/or hepatic disease atracurium or cisatracurium are preferred. Succinylcholine is only used for securing the airway due to its very rapid onset of action. Rocuronium given in a higher dose also possesses a rapid onset in situations when succinylcholine might be contraindicated. When using a muscle relaxant, its effect should always be monitored with a simple train of four pattern of stimulation from a hand-held nerve stimulator. This will ensure that an adequate and not excessive block is secured. If a more rapid reversal is required then a dose of neostigmine with glycopyrrolate may be used. Alternatively, if rocuronium is the relaxant in use then the new agent sugammadex is effective.
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Condon, Marie, Philippa Dodd, and Liz Lightstone. The patient with systemic lupus erythematosus. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0162.
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AbstractSystemic lupus erythematosus (SLE) is a chronic, relapsing, inflammatory, often febrile multisystemic disorder, characterized by involvement of the skin, joints, visceral organs, and serosal membranes. Symptoms and manifestations vary widely over an unpredictable relapsing and remitting course.The presentation of SLE can range from mild forms to severe disease requiring hospitalization. Most commonly it manifests as a combination of constitutional symptoms, particularly fatigue and fever, with cutaneous, musculoskeletal, mild haematological, and serological involvement; however, when renal, haematological or central nervous system disease predominate it can be more severe, even life-threatening. There is a tendency for the disease pattern present at the time of onset to prevail during subsequent exacerbations.Investigating SLE depends to an extent on the presentation of the individual. However a number of haematological, biochemical and immunological investigations provide useful diagnostic information, either for the disease itself or in context of organ system involvement, and should be performed routinely.The presence of lupus nephritis should be considered in any lupus patient with impaired kidney function, proteinuria, hypertension, or an active urine sediment; the gold standard investigation in this context is a kidney biopsy. Glomerular immune complex deposition is the hallmark of lupus nephritis and underpins the International society of Nephrology/Renal Pathology Society classification of lupus nephritis.The diagnosis of SLE is based upon the presence of clinical and/or laboratory features and immunological markers that meet the various published diagnostic criteria. In 2012, lupus nephritis identified on kidney biopsy became an independent diagnostic criterion.This chapter goes through the clinical manifestations, investigations (including a detailed look at the kidney biopsy) and a review of the latest published diagnostic criteria.
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Benjamin, Mike, Dennis McGonagle, Maribel I. Miguel, David A. Bong, and Ingrid Möller. Limb anatomy and medical imaging. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0065.
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This chapter provides a generalized framework for helping the clinician to understand basic principles of functional anatomy in the limbs in relation to medical imaging, particularly ultrasonography (US). Certain basic design principles that are evident in the limbs are explained: for example, that larger muscles lie proximally, and that tendons are more numerous and longer distally. While the upper limb is ultimately geared to moving the hand with ease and precision in three-dimensional space, the lower limb is both an organ of propulsion and a column supporting body weight. It is important to note that when the foot is on the ground this has an important influence on muscle function. Fundamental principles of muscle design and action are explained, including the distinction between prime movers, antagonists, synergists, and fixators; the fact that movements and not muscles are represented in the cerebral cortex; the all-or-nothing principle of fibre contraction; the modifying influence of gravity on muscle action; and issues relating to fibre architecture. The less appreciated functions of tendons are included and the difference between an enthesis and an enthesis organ is explained. The similar appearance of nerves and tendons in dissections and even in MRI and US images is explained and the importance of fascia is highlighted—particularly its role as an 'ectoskeleton'. Brief mention is made of adipose tissue and blood vessels, and planes of movement between adjacent structures are described in order to inform the ultrasonographer who deals with structures in real time.
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Grant, Robert. Neurocutaneous syndromes. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0235.
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This chapter describes several neurocutaneous syndromes, including tuberous sclerosis, neurofibromatosis, Sturge–Weber syndrome, Von-Hippel–Lindau disease and ataxia telangiectasia amongst others.Tuberous sclerosis, also known as Epiloia or Bournville’s Disease, is an autosomal dominant multisystem disease it usually presents in childhood with a characteristic facial rash, adenoma sebaceum, seizures, and sometimes learning difficulties. Central nervous system lesions in tuberous sclerosis are due to a developmental disorder of neurogenesis and neuronal migration. Other organs such as the heart and kidney are less commonly involved. The condition has very variable clinical expression and two-thirds of cases are thought to be new mutations, therefore it is important to examine and screen relatives. Management may involve many specialists and close co-operation between specialists is essential.The neurofibromatoses are autosomal-dominant neurocutaneous disorders that can be divided into ‘peripheral’ and ‘central’ types, although there is significant overlap. The characteristic features of neurofibromatosis type 1 are café au lait spots, neurofibromas, Lisch nodules, osseous lesions, macrocephaly, short stature and mental retardation, axillary freckling, and associations with several different types of tumours.Sturge–Weber syndrome involves a characteristic ‘port-wine’ facial naevus or angioma associated with an underlying leptomeningeal angioma or other vascular anomaly. It affects approximately 1/20 000 people. There can be seizures, low IQ, and underlying cerebral hemisphere atrophy as a result of chronic state of reduced perfusion and increased oxygen extraction. Patients may present with focal seizures which are generally resistant to anticonvulsant medication and can develop glaucoma.Von-Hippel– Lindau disease is one of the most common autosomal-dominant inherited genetic diseases that are associated with familial cancers. Von-Hippel–Lindau disease is characterized by certain types of central nervous system tumours, cerebellar and spinal haemangioblastomas, and retinal angiomas, in conjunction with bilateral renal cysts carcinomas or phaechromocytoma, or pancreatic cysts/islet cell tumours (Neumann and Wiestler 1991).Other neurocutaneous syndromes discussed include Hypomelanosis of Ito, Gorlin syndrome, Sjogren–Larsson syndrome, Proteus syndrome, Hemiatrophy and hemihypertrophy, Menke’s syndrome, Xeroderma pigmentosum and Cockayne’s syndrome.
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Hunter, Jennifer M., and Thomas Fuchs-Buder. Neuromuscular blockade and reversal. Edited by Michel M. R. F. Struys. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0016.
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Over the past 70 years since the introduction of d-tubocurarine, the search for an ideal neuromuscular blocking agent has led to the development of the depolarizing drug, succinylcholine (suxamethonium), with its rapid onset of action and plasma metabolism, and a series of non-depolarizing agents of which there are two groups: benzylisoquinoliniums (e.g. atracurium, cisatracurium and mivacurium) and aminosteroidal agents (e.g. pancuronium, vecuronium and rocuronium). The need to monitor neuromuscular block perioperatively to ensure the appropriate dose of any neuromuscular blocking drug is given has led to the development of several nerve stimulation techniques. Particularly useful clinically are the train-of-four twitch response, double-burst stimulation, and the post-tetanic count. Their benefits and limitations are considered in this chapter. The most suitable equipment to monitor neuromuscular block and the appropriate anatomical sites for stimulation are discussed. To prevent residual block with its pathophysiological consequences such as upper airway and pharyngeal dysfunction and potential respiratory failure at the end of surgery, antagonizing agents are used. These are of two types: anticholinesterases such as neostigmine and edrophonium, and the γ-cyclodextrin, sugammadex. The pharmacodynamics and pharmacokinetics of neuromuscular blocking drugs and their antagonists are altered by the extremes of age, obesity, and several disease states including renal and hepatic failure, neuromuscular disorders, and critical illness. The altered response to all these drugs in these pathologies, which is related to their metabolism and excretion, is considered in detail, together with their other side-effects including the particular disadvantages to the use of succinylcholine.
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Kaye, Alan, and Richard Urman, eds. Obstetric Anesthesia Practice. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780190099824.001.0001.
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Obstetrical Anesthesia Procedures provides timely updates in the field of obstetrical anesthesia and provides a concise, up-to-date, evidence-based and richly illustrated book for students, trainees, and practicing clinicians. The book comprehensively covers a robust list of topics focused to improve understanding in the field with emphasis on recent developments in clinical practices, technology, and procedures. This book describes all the essential topics that are required for the practitioner to quickly assess the patient and risk stratify them, decide on the type of analgesic and anesthetic plan that is most appropriate for the patient, its feasibility and safety, provide expert consultation to the other members of the obstetric team, manage anesthesia care and complications, and arrange for advanced care if needed. There are special considerations for pregnant patients undergoing non-obstetric surgery, anesthesia for assisted reproductive technologies, and anesthetic management of operations on placental support. It is also important to develop the skills needed to perform antenatal evaluation of high-risk parturients and understand the physiology of pregnancy and peripartum anesthetic implications of co-existing conditions involving hematologic, cardiac, neurological, renal, endocrine and pulmonary systems. There are also special considerations for parturients with pregnancy-induced hypertension, multiple gestations, abnormal fetal presentation, preterm labor, obstetric hemorrhage, and trauma in pregnancy. There are pharmacologic and non-pharmacologic pain management options for labor, caesarean delivery, and postoperative pain. This includes management of intravenous and oral analgesics, understanding of drug pharmacology and its effect on the mother and the baby, neuraxial techniques (spinal, epidural, combined spinal-epidural) and peripheral nerve blocks.