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1
Murtagh, Fliss E. M. End-stage kidney disease. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0156.
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End-stage kidney disease (ESKD) accounts for 1-2% of all deaths. Ageing populations means that this proportion will grow steadily over the coming years. Symptom burden in ESKD exceeds advanced cancer, with added renal-specific symptoms, such as itch and restless legs. Pain and depression are also more prevalent. Many renal symptoms go under-recognized and under-treated, especially as they arise from co-morbid conditions, rather than the renal disease itself. The most useful intervention to address symptoms is regular assessment of symptoms, using a valid and reliable global symptom score. Pharmacological interventions to alleviate symptoms need to take account of the severe constraints on using renally cleared drugs, and the high risk of toxicity from accumulation of parent compound or metabolites. The population with ESKD has extensive palliative care needs, and need significant medical, nursing, psychological, and social care to address these as their illness advances towards the end of life.
2
Brouwers, Martijn C. G. J. Approach to the Patient with General Symptoms. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0073.
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Fatigue and fever of unknown origin are frequently encountered symptoms at the general internal medicine outpatient clinic. Careful history taking and physical examination are essential in the detection of an inherited metabolic disease, since biomarkers, such as plasma lactate and creatine kinase levels, have low positive predictive values. Absence of any specific symptom or sign of an inherited metabolic disease do not advocate additional investigations.
3
Keshav, Satish, and Alexandra Kent. Alcoholic liver disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0211.
Full textAbstract:
Alcoholic liver disease develops in excessive drinkers and can manifest in three forms: alcoholic fatty liver (steatosis; >80%), alcoholic hepatitis (10%–35%), and cirrhosis (10%). The more alcohol consumed, the greater the risk of alcoholic liver disease, although other factors may also be involved. Alcohol can cause significant damage without producing any symptoms, and many patients will only have liver dysfunction detected on routine blood tests. Many patients report non-specific symptoms, such as anorexia, morning nausea, diarrhoea, and vague right upper quadrant abdominal pain. The underlying pathogenesis of alcohol-induced injury is not fully understood but is thought to involve various mechanisms. This chapter discusses alcoholic liver disease, focusing on its etiology, symptoms, demographics, natural history, complications, diagnosis, prognosis, and treatment.
4
Wijdicks, Eelco F. M., and Sarah L. Clark. Treatment of Brain Injury-Associated Symptoms and Signs. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190684747.003.0019.
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Acute neurologic disease results in a myriad of minor and major symptoms, some of which are partly specific to the nature of the illness. Symptom relief for acutely ill neurologic patients requires medication orders. Treatment of these symptoms is not without adverse effects, and regular use of opioids to treat severe headaches may very often lead to opioid-induced constipation, which may progress to adynamic ileus. This chapter focuses on, nausea and vomiting, hiccups, secretion control, constipation, fever and shivering, and rhabdomyolysis. Large volumes of emesis or secretions can easily cause aspiration and mucus plugging of large bronchial branches. Drug regimens are discussed in detail.
5
Chan, Kin-Sang, Doris M. W. Tse, and Michael M. K. Sham. Dyspnoea and other respiratory symptoms in palliative care. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0082.
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Dyspnoea is prevalent among palliative care patients with increased severity over time. There are two patterns of dyspnoea-breakthrough dyspnoea and constant dyspnoea-and three separate qualities of dyspnoea-air hunger, work or effort, and tightness. The measurement of dyspnoea includes three domains: sensory-perceptual experience, affective distress, and symptom impact. The management of dyspnoea includes specific disease management, non-pharmacological intervention, pharmacological treatment, and palliative non-invasive ventilation. Cough is prevalent and disturbing in patients with cancer and chronic lung diseases, and is often associated with airway hypersecretion and impaired mucociliary clearance. Management includes specific treatments for underlying non-cancer and cancer-related causes, symptomatic treatment by antitussives, mucoactive agents, and airway clearance techniques for expectoration and reduction in mucus production. Anticholinergics may be indicated for death rattles to facilitate a peaceful death. Haemoptysis occurs in 30-60% of lung cancer patients and initial management of haemoptysis includes airway protection and volume resuscitation. Localization of the site and source of bleeding may determine the choice of treatment. If a life-threatening haemoptysis occurs, sedation should be given as soon as possible. Support should be given to the family, and debriefing provided to team members.
6
Venuto, Charles S., and Karl Kieburtz. Huntington Disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0008.
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The clinical management of Huntington’s disease entails pharmacologic interventions and nonpharmacologic supportive therapy. There are no treatments that can halt or alter the progression of disease, therefore the goal is to maximize function and optimize quality of life. Tetrabenazine is the only pharmacologic agent with regulatory approval for Huntington’s disease chorea; however, off-label use of antidopaminergic agents is common. Treatment of behavioral disturbances can be tailored to the specific symptoms by using antidepressant, antipsychotic, and anxiolytic agents. Clinical trials testing therapeutic strategies for motor, behavioral, and cognitive aspects of disease and delaying progression are ongoing.
7
Kipps, Christopher, and John Hodges. Clinical cognitive assessment. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199644957.003.0010.
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Cognitive symptoms arise from the location of brain dysfunction and are not linked directly to any particular pathology. In the early stages of disease, symptoms may be non-specific, and while certain symptom clusters are commonly seen in particular disorders, atypical presentations are not infrequent. For example, in Alzheimer’s disease, patients may present with a focal language syndrome instead of the more commonly appreciated autobiographical memory disturbance despite identical pathology. In our approach to the cognitive assessment, we maintain a symptom oriented approach. This facilitates the localisation of pathology and subsequent clinical diagnosis, which may then be supplemented by associated neurological signs, imaging or other investigations.
8
Chneiweiss, Hervé. Anticipating a therapeutically elusive neurodegenerative condition: Ethical considerations for the preclinical detection of Alzheimer’s disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198786832.003.0016.
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Among neurodegenerative disorders, Alzheimer’s disease has held a special position during the last 40 years. It represents a huge burden of disease with more than 40 million people affected worldwide. The economic effect it has on society is enormous, and the specific challenges of dementia are tremendous. Now that science has demonstrated that the disease starts two or three decades before any symptoms occur, possibilities exist for diagnosis or testing increasingly early through the capabilities of predictive medicine. The related ethical debate is on the multiple meanings and the impact of preclinical diagnosis of Alzheimer’s disease before the onset of symptoms. To guide this discussion, this chapter draws upon lessons from other fields of medicine and the identification of high-risk individuals bearing pathogenic genetic mutations that predispose them to the disease. It concludes with thoughts on value and choice in the complex, fine balance between anticipating, knowing, and doing.
9
Unger, Philippe, and Gerald Maurer. Heart valve disease: mixed valve disease, multiple valve disease, and others. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0039.
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Multiple and mixed heart valve disease are highly prevalent. Echocardiography is the cornerstone technique for imaging these patients. As with patients with single-valve stenosis or regurgitation, one should aim to evaluate the aetiology, the mechanism(s) of dysfunction, as well as the consequences and the possibility of repair. There are, however, specific issues, which include the followings: (1) the lack of published data; (2) most indices of valvular regurgitation and of stenosis severity have been validated in patients with single-valve/single-lesion disease; and (3) the haemodynamic interactions that may affect the severity and the diagnosis of these lesions. A global assessment of the consequences of the lesions is of the utmost importance in the decision-making process: whereas only severe regurgitation or stenosis is usually considered for surgery by current guidelines in a single-valve lesion, the combination of two or more less-than-severe lesions causing symptoms, left ventricular dysfunction, and/or pulmonary pressure increase may warrant surgery. This chapter focuses on the echocardiographic assessment of these sometimes complex lesions, emphasizing some pitfalls and tips to take into account when managing these patients.
10
Sutor, Bruce. Psychiatry. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0603.
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An understanding of psychiatric illness is critical to the practice of internal medicine. Since 30% to 40% of ambulatory primary care visits have a psychiatric component to the chief complaint, successful disease management often hinges on successful treatment of comorbid psychiatric illness. A comprehensive psychiatric evaluation is essential because many psychiatric symptoms are nonspecific. This situation is analogous to a patient presenting in general internal medicine with fever or nausea. The presence of a single symptom (eg, depressed mood) is never pathognomonic for a specific disorder. For patients with psychiatric symptoms, the biopsychosocial model is widely used. With this approach, the biologic, psychologic, and social factors contributing to the patient's clinical presentation are evaluated. Some psychiatric symptoms indicate severe disease, whereas others may be less problematic and may not be clinically relevant.
11
Waldemar, Gunhild. Diagnosing Alzheimer’s disease in clinical practice. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198779803.003.0006.
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The diagnostic evaluation in a patient with cognitive impairment suspected of having Alzheimer’s disease (AD) should include investigations aimed at 1) confirming and characterizing the cognitive impairment using cognitive tests with particular attention to typical (episodic memory impairment) and atypical presentations of AD; 2) checking the diagnostic criteria for AD and considering biomarkers to document AD pathology; and 3) differential diagnosis: ruling out other conditions which could cause cognitive impairment. With the advent of CSF and imaging biomarkers for AD, it may be possible to establish an early specific diagnosis, or to confirm an increased risk of progressing to AD dementia, in patients with mild cognitive symptoms. In such cases pre-biomarker counselling and patient consent is essential.
12
Cui, Zhao, Neil Turner, and Ming-hui Zhao. Antiglomerular basement membrane disease. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0074_update_001.
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Individuals appear to be predisposed to antiglomerular basement membrane (anti-GBM) disease by carrying a predisposing human leucocyte antigen type, DRB1*1501 being identified as the highest risk factor, and there are likely to be other predisposing genes or influences on top of which a relatively rare ‘second hit’ leads to the development of autoimmunity. In anti-GBM disease this appears to have a self-perpetuating, accelerating component, that may be to do with antibodies and altered antigen presentation. Lymphocyte depletion may also predispose to the disease. A number of second hits have been identified and they seem to share a theme of damage to the glomerulus. There may be a prolonged (months to years) and usually subclinical phase in anti-GBM disease in which usually relatively low level antibody titres are associated with variable haematuria, sometimes minor pulmonary haemorrhage, but often no symptoms. Damage to the lung seems to determine whether there is a pulmonary component to the disease. Without pulmonary damage caused typically by smoking, inhalation of other fumes, and potentially infection or oxygen toxicity, the disease remains an isolated kidney disease. Antibodies appear to be an important component of the disease, but cell-mediated immunity is also critical to the clinical picture. In animal models, cell-mediated immunity triggered by the GBM antigen can cause severe renal damage in the absence of pathogenic antibody. The development of specific antibody also requires T-cell sensitization and help, and suppressing the response is likely to require suppressing both antibody and cell-mediated immunity. Antibodies recognize one major and some other epitopes, which are now well described. T-cell epitopes are becoming better understood. Evidence from animal models also suggests that the damage in anti-GBM disease is dependent on complement, macrophages, and neutrophils.
13
Hollak, Carla E. M. Skeletal Abnormalities. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0072.
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The skeleton is frequently involved in inborn error of metabolism as part of a chronic, multisystem disease. Several disorders in adulthood may present with skeletal symptoms as a first sign of an underlying metabolic disease. Examples are Gaucher disease, alkaptonuria, hypofosfatasia or hereditary hypophosphatemic rickets. In addition, secondary skeletal problems, specifically osteoporosis, is a frequent complication of a wide range of inborn errors of metabolism. The presence of additional symptoms, specific radiographical appearance and/or biochemical abnormalities can assist in making the appropriate diagnosis.
14
Puntis, John. Growth faltering (failure to thrive). Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198759928.003.0008.
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Growth faltering or ‘failure to thrive’ is a descriptive term implying failure not only of growth, but also impairment of other aspects of a child’s well-being. Weight crossing down over two major centiles is often taken as an indication for referral to a paediatrician. In the absence of specific symptoms or physical findings (other than poor growth) an underlying illness is unlikely. Few investigations may be needed, and should be guided by symptoms and any clinical findings. Coeliac disease and occasionally Crohn’s disease may present as growth faltering in the absence of symptoms. For some children, multidisciplinary assessment is appropriate; home visits at meal times can be particularly instructive.
15
King, Daniel. Aretaios of Kappodokia. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198810513.003.0003.
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This chapter turns to the neglected author, Aretaios of Kappodokia, and his nosological writings. Aretaios develops an anatomically informed vision of pain perception which employs Aristotelian ideas about perception; he describes these symptoms in a manner which combines specific and formal medical terminology with more quotidian language and metaphors for various pain symptoms. This combination of linguistic registers helps provide a structure for the recognition and diagnosis of different symptoms and their conditions. Aretaios combines these two aspects of his nosology with a vision of the patient and his interaction with them that emphasizes their joint, heroic confrontation of pain and disease. Aretaios stresses, ultimately, the patient’s and doctor’s joint or combined confrontation of pain and disease.
16
Cassidy, Jim, Donald Bissett, Roy A. J. Spence OBE, Miranda Payne, Gareth Morris-Stiff, and Madhumita Bhattacharyya. Breast cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199689842.003.0014_update_001.
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Thoracic cancer examines the epidemiology, aetiology, and role of screening and prevention in the reduction of deaths from lung cancer, the majority caused by cigarette smoking. The pathology and genetics of lung cancer, with particular note of the driver mutations, are followed by the symptoms and signs of the disease. Appropriate investigations are described to stage the tumour. The optimum treatment for localised non-small cell lung cancer (NSCLC) is surgical resection, followed in some cases by adjuvant chemotherapy. However, most cases present with disease too advanced for surgery, and for these chemotherapy and radiotherapy are appropriate. Metastatic NSCLC can be treated with platinum based doublet chemotherapy with modest palliative benefits. Metastatic NSCLC with specific driver mutations are amenable to control by targeted therapy. Locally advanced NSCLC is often treated with similar chemotherapy and radiotherapy, ideally administered concurrently, to achieve symptom relief but also improved survival rates. Short course simple radiotherapy offers symptom relief in patients not fit for chemotherapy. Patients with localised NSCLC who are not fit for surgery, may benefit from radical radiotherapy, particularly stereotactic radiotherapy. Small cell lung cancer (SCLC) is characterised by almost universal systemic spread, so that surgery is rarely appropriate. Staging is similar to NSCLC, and chemotherapy is the mainstay of treatment, usually cisplatin or carboplatin combined with etoposide. When possible, this is combined with concurrent thoracic irradiation covering all radiological sites of disease. Prophylactic cranial irradiation reduces the risk of CNS disease. Malignant pleural mesothelioma is caused by occupational asbestos exposure. Symptoms and signs, investigation and staging, and management are discussed. Thymic tumours, their pathology, presenting symptoms including paraneoplastic syndromes, investigation, staging and treatment are reviewed.
17
Gatto, Maria, Patricia Thomas, and Ann Berger. Anxiety. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190204709.003.0006.
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Anxiety is an inherent aspect of human existence. Anxiety and chronic diseases are interchangeable in their causal relationship: chronic diseases can exacerbate symptoms of anxiety, and anxiety disorders can lead to chronic diseases. Anxiety is a specific symptom emphasized in the National Consensus Project for Quality Palliative Care Clinical Practice Guidelines. Assessment is interdisciplinary and must address both the psychological and psychiatric aspects of care. To assure appropriate management, an understanding of etiologies for anxiety across populations and disease states is essential. Treatment relies on evidence-based pharmacological and nonpharmacological strategies to maximize patient and family coping and quality of life.
18
Jones, Roy W. Pharmacological treatment of dementia. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199644957.003.0038.
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This chapter summarises the available clinical evidence for specific pharmacological treatments for dementia with a particular emphasis on practical considerations and realistic expectations of currently available anti-dementia drugs. It covers the treatment of both cognitive and non-cognitive symptoms. The search for specific treatments for dementia has inevitably concentrated on Alzheimer’s disease (AD), partly because it is the commonest cause of dementia and partly because scientific progress has provided more potential therapeutic targets for AD than other dementias. AD is treated with AChEIs (donepezil, galantamine or rivastigmine) and the goals of treatment should be explained at the commencement of treatment. For DLB use AChEI, especially for hallucinations and other behavioural disturbance and consider memantine or increasing dose if BPSD symptoms persist. For VaD look for sources of emboli (e.g. carotid disease) and consider anticoagulation for atrial fibrillation and low dose aspirin. Ensure other relevant conditions (e.g. hypertension and diabetes) are being managed appropriately.
19
Schofield, C. J. American trypanosomosis (Chagas disease). Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0050.
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American trypanosomosis is due to infection with Trypanosoma cruzi (Protozoa, Kinetoplastidae). This is a widespread parasite of small mammals and marsupials throughout most of the Americas, roughly from the Great Lakes of North America (approx. 42 ° N) to southern Argentina (approx. 46 ° S). It is mainly transmitted by blood-sucking bugs of the subfamily Triatominae (Hemiptera, Reduviidae) which are widespread in the Americas, but rare in the Old World. Except in some research laboratories, and infected immigrants from Latin America, T.cruzi has not been reported from the Old World, although closely-related trypanosome species are commonly found in Old and New World bats.Human infection with T.cruzi is generally known as Chagas disease, taking the name of Brasilian clinician Carlos Justiniano das Chagas who first described it from patients in central Brasil (Chagas 1909). Chagas isolated and described the parasite, correctly deduced most of its life-cycle and clinical symptoms associated with the infection, identified the insect vectors and some of the reservoir hosts, and also trialed initial attempts to control it. He was nominated at least twice for the Nobel prize in medicine (Coutinho and Dias 2000; Lewinsohn 2003).Although difficult to treat, Chagas disease can be controlled by measures to halt transmission, primarily by eliminating domestic populations of the insect vectors, together with serological screening to avoid transmission by blood donation from infected donors. Since 1991, a series of multinational initiatives have used this approach to halt transmission over vast regions of the areas previously endemic for the human infection. Estimated prevalence of the human infection has declined from the 1990 estimate of 16–18 million people infected, to the current estimate of just over 7 million infected (OPS 2006; Schofield & Kabayo 2008). Prevalence is expected to decline further, and control strategies are now being adjusted to develop a sustainable system of disease surveillance, focal vector control, and specific treatment for any new cases (Schofield et al. 2006; WHO 2007). Guidance for diagnosis and treatment is also required for non-endemic countries, where recent years have seen increasing migration from Latin America such that cases of chronic Chagas disease have now been reported from amongst Latin American migrants in Europe, USA and Canada, and Japan, together with some congenital cases and transmission from infected blood donors and by organ transplant.
20
Voltz, Raymond, Stefan Lorenzl, and Georg Nübling. Neurological disorders other than dementia. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0155.
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The significance of a palliative care approach for patients with neurological disorders other than dementia is increasingly recognized. Whereas the care for these patients, for example, those with amyotrophic lateral sclerosis (ALS) or motor neuron disease, had been incorporated in the initial concept by Dame Cicely Saunders, recent scientific evidence supports this position. The need for palliative care in these patients is underpinned by their frequent wish for hastening death. This chapter describes palliative care approaches for a number of neurological disorders other than dementia. For ALS, palliative care management including specific issues such as respiratory insufficiency or malnutrition are fairly well established. Also, in parkinsonian syndromes, a lot of palliative care needs can be recognized and managed effectively. For patients with multiple sclerosis, the first randomized controlled trial showed clearly positive effects on symptoms as well as usage of health-care resources. The chapter also summarizes the drug use for specific symptom management, accounting for alternative application routes.
21
Ullman, Dana, and Karen Allen. Homeopathy in the Prevention and Treatment of Sexual Problems (DRAFT). Edited by Madeleine M. Castellanos. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190225889.003.0019.
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Homeopathic medicine is a specialized form of pharmacology used throughout the world by physicians and other health and medical care providers. Nanodoses of plants, mineral, animal, chemical, or pathogens are prescribed based on their ability to cause in overdose specific syndromes in patients. Because symptoms are considered adaptations of the human body to fight infection and/or to adapt to stress, using nanodoses of substances that could cause similar symptoms that patients experience is one way to influence gene expression, immunological development, and the genitourinary microbiome to initiate a healing process. The homeopathic approach to the prevention and treatment of sexual problems requires analysis of a person’s overall syndrome, not simply local disease. This chapter provides specific homeopathic medicines with abbreviated summaries of their indications in (a) genitourinary dysbiosis, (b) sexual trauma and psychosexual conflict, and (c) sexual pain and functional limitation.
22
Kölker, Stefan, Johannes Häberle, and Valerie Walker. Urea Cycle Disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0017.
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The urea cycle is the final pathway for removal of surplus nitrogen from the body, the major route in humans for irreversible detoxification of ammonia and a source of arginine.2,3 Patients with adult-onset urea cycle disorders present with clinical symptoms that have a broad differential diagnosis (e.g., protein aversion, inappetence, cyclic vomiting, epilepsy, psychiatric disease, migraine, liver dysfunction). Unlike infants and children some adult-onset patients may never develop acute hyperammonemic crises. Since symptoms are often fluctuating and the diagnosis can only be made if specific tests are made, the diagnosis is often delayed or missed. Earlier detection and intervention would improve the patients’ outcome, which currently is poor.
23
Keshav, Satish, and Alexandra Kent. Chronic abdominal pain. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0024.
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Separating chronic and acute abdominal pain is often difficult, and an arbitrary time limit of 4 weeks is often used. However, many chronic conditions (e.g. chronic pancreatitis) can cause relapsing symptoms, which may be acute during each episode. Pain receptors in the abdomen respond to chemical and mechanical stimuli. Stretch is the commonest mechanical stimulus to the viscera, although distension, torsion, and contraction are also sensed. Chemical receptors are stimulated by inflammation and infection, and this stimulation leads to the production of various substances, including serotonin, bradykinin, substance P, prostaglandins, and histamine. There are inter-individual differences in pain perception, with some people (e.g. patients with irritable bowel syndrome) being more sensitive to painful stimuli. Chronic abdominal pain occurs in 9%–15% of all children, and is present on questioning in 75% of adolescents and 50% of adults who are otherwise healthy. It is often a non-specific symptom that alone has a poor sensitivity for organic disease. Usually, it is the associated symptoms, and/or abnormal blood tests, that direct the doctor to a diagnosis. This chapter covers the approach to the diagnosis of chronic abdominal pain, key diagnostic tests, therapies, prognosis, and dealing with uncertainty.
24
Padilla, Claudia R., and Mario F. Mendez. Neuropsychiatric Features Across Neurodegenerative Diseases. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0006.
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Neuropsychiatric symptoms (NPS) are a major manifestation of neurodegenerative diseases(NDDs) including Alzheimer’s disease (AD), Dementia with Lewy Bodies (DLB) and frontotemporal dementia (FTD). NPS symptoms are a determining factor impacting economic and psychological costs for both the patient and their caregivers in these devastating illness. Recent developments in neuroscience have clarified the relationship of NPS with changes in brain structures, alterations in neural circuits and networks, and their neurotransmitter systems. It is increasingly recognized that NPS shared across different NDDs might have shared alterations in neural circuits and networks, and their neurotransmitter systems and ways to modulate them theraputcally. This chapter focuses on the more common NPS and their links to causative neurodegenerative processes that transcend specific diseases.
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Ahlskog, J. Eric. Dementia with Lewy Body and Parkinson's Disease Patients. Oxford University Press, 2013. http://dx.doi.org/10.1093/oso/9780199977567.001.0001.
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Patients, spouses, families, and caregivers dealing with dementia face a host of complex issues, particularly when they must confront Dementia with Lewy Bodies or Parkinson's Disease. Until now there has been no guidebook for the general public to help navigate these challenging disorders. In Dementia with Lewy Bodies and Parkinson's Disease Dementia, Dr. J. Eric Ahlskog draws on 30 years of clinical and research work at Mayo Clinic to arm patients and families with crucial information that will enable them to work in tandem with their doctors. A diagnosis of dementia can be devastating, leaving families and caregivers struggling with a loved one's radically-impaired thinking and memory. When dementia is coupled with Parkinson's, which will develop in Parkinson's patients that live long enough, or with Lewy Bodies, which is the second leading cause of dementia behind Alzheimer's, the difficulties become even more daunting. And while these disorders are all too common, most people have little solid information about them. Too often doctors cannot spend the necessary time answering questions or discussing the specific challenges and treatments for these kinds of dementia during office visits. Arriving for a doctor appointment knowing the issues and treatment options beforehand gives patients and families an important head start. Dr. Ahlskog clearly explains all aspects of these disorders, their causes, symptoms, most effective drug treatments, proper doses, and which medications to avoid. He also discusses the complications that can arise in treating these conditions, given the variety of available medications and their possible side effects and interactions. While a cure does not yet exist, in this accessible, highly informative guidebook, Dr. Ahlskog shows that optimal medical treatment can markedly improve the quality of life for both patients and family.
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Fox, Susan H. Twists and Turns. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190607555.003.0020.
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Focal dystonia is the most common clinical manifestation of primary dystonia. The focal and sometimes task-specific nature of the symptoms makes daily drug therapy less attractive due to a requirement for exposure to high doses of anticholinergic agents that are typically only minimally effective. Botulinum toxin therapy can be targeted to a specific muscle group that is judged to be most active, providing relief for 3 months although not necessarily modifying the underlying disease pathophysiology, which remains uncertain. Deep-brain stimulation is currently reserved for the most resistant cases in which the disability or pain derived from the dystonia justifies consideration of neurosurgery.
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Javaid, Kassim. Osteomalacia. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0273.
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Osteomalacia is a disorder of bone mineralization and is due to a lack of vitamin D. Vitamin D is a prohormone formed by the action of UV radiation on the vitamin’s precursor (7-dehydrocholesterol) in the skin. It undergoes two hydroxylation steps to become an active hormone. The commonest cause of osteomalacia is vitamin D deficiency due to a lack of UVB skin exposure. Other causes include malabsorption (coeliac disease and pancreatic insufficiency), obesity, and chronic kidney disease. The typical symptoms of osteomalacia are non-specific bone pain, proximal myopathy, fatigue, and polyarthralgia. This chapter addresses the causes, diagnosis, and management of osteomalacia.
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Introne, Wendy J. Alkaptonuria. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0015.
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Alkaptonuria is an autosomal recessive disorder with an incidence of 1:250,000 to 1:500,000. Aside from urine that darkens, the disease is relatively asymptomatic in childhood. As a result, the diagnosis is often overlooked early in life and not considered in many patients until they begin to manifest symptoms as adults. Features include pigment deposition (ochronosis) on the eyes, ears, and hands; early-onset, progressive arthritis, particularly of the spine and large joints; valvular heart disease; and renal and prostate stones. Management continues to be symptomatic, but specific treatment with nitisinone appears promising with additional clinical trials being planned.
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Donaldson, Katelyn, and Ahmet Höke. Animal Models of Peripheral Neuropathy and Neuropathic Pain. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0119.
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There are numerous types of peripheral neuropathies and conditions that cause neuropathic pain with varying symptoms and different mechanisms of pathogenesis. Therefore, it is not surprising that many different animal models of peripheral neuropathies and neuropathic pain have been developed with varying degrees of fidelity to recapitulate the human disease. Nevertheless, these models are useful in a deconstructive manner to examine role of specific molecular pathways in pathogenesis of different types of peripheral neuropathies and test potential new drugs.
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Cutter, David, and Martin Scott-Brown. Presentations in suspected cancer. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0323.
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Malignant neoplastic disease includes a vast range of conditions that can originate from and can directly or indirectly affect virtually every organ system of the body. As a consequence of this, the presentation of malignancy can be similarly varied. While a diagnosis of malignancy may be clinically obvious in some cases, in others diagnosis and investigation may be delayed due to non-specific presentations and the attribution of symptoms to non-malignant conditions. Early diagnosis of cancer has an impact on the success of subsequent treatment and overall survival. It is therefore vital to maintain an appropriate level of clinical suspicion when deciding whether and how much to investigate patients with symptoms that could be secondary to an underlying malignancy.
31
Levine, Michael S., Elizabeth A. Wang, Jane Y. Chen, Carlos Cepeda, and Véronique M. André. Altered Neuronal Circuitry. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199929146.003.0010.
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In mouse models of Huntington’s disease (HD), synaptic alterations in the cerebral cortex and striatum are present before overt behavioral symptoms and cell death. Similarly, in HD patients, it is now widely accepted that early deficits can occur in the absence of neural atrophy or overt motor symptoms. In addition, hyperkinetic movements seen in early stages are followed by hypokinesis in the late stages, indicating that different processes may be affected. In mouse models, such behavioral alterations parallel complex biphasic changes in glutamate-mediated excitatory, γ-aminobutyric acid (GABA)-mediated inhibitory synaptic transmission and dopamine modulation in medium spiny neurons of the striatum as well as in cortical pyramidal neurons. The progressive electrophysiologic changes in synaptic communication that occur with disease stage in the cortical and basal ganglia circuits of HD mouse models strongly indicate that therapeutic interventions and strategies in human HD must be targeted to different mechanisms in each stage and to specific subclasses of neurons.
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Federico, Antonio, and Silvia Palmeri. Oligosaccharidoses. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0057.
Full textAbstract:
Oligosaccharidoses are a group of lysosomal diseases, also called glycoproteinoses, biochemically characterized by storage of protein-bound oligosaccharides within lysosomes and excretion with urine of corresponding sugars. Storage of oligosaccharides results from absence or defective function of a specific lysosomal enzyme. Classification includes α and β mannosidosis, fucosidosis, sialidosis types I and II, Schindler disease, and aspartylglycosaminuria. Galactosialidosis characterized by deficiency of β-galactosidase and α-neuraminidase with presence in patient urine of oligosaccharides has been included among oligosaccharidoses but may be better classified as a lysosomal enzyme protection defect disease in relation to its primary defect of cathepsine A-protective protein. The clinical spectrum of the diseases vary widely, as is common in lysosomal storage disorders. Patients frequently have neurological symptoms, but in rare cases presenting in adulthood symptoms may be very subtle. Psychiatric presentations have been described in adults. For adult cases, no treatments are available except for supportive care.
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Pahuja, Meera, Jessica S. Merlin, and Peter A. Selwyn. HIV/AIDS. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0151.
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In less than two decades, AIDS has been transformed from a rapidly fatal, untreatable illness to a manageable chronic disease. Early in the AIDS epidemic, HIV care and palliative care were inseparable; over time, these two treatment paradigms diverged. In the developed world, and to a lesser but increasing extent in the developing world, decreasing mortality rates have resulted in growing numbers of HIV-infected patients living with the disease for many years. As this long-surviving population increases, the challenges of chronic disease management, an expanding range of co-morbidities, and a process that has been described as ‘accelerated ageing’, have all emerged to present new needs and opportunities for palliative care expertise. Earlier in the epidemic, palliative care for AIDS focused primarily on end-of-life care and pain and symptom management related to the manifestations of AIDS-specific opportunistic infections and malignancies. Currently, pain and symptoms may be related to these as well as other co-morbid chronic diseases which commonly occur in HIV-infected patients, including cardiovascular, pulmonary, renal, hepatic, metabolic, and neurocognitive complications. Attention to these symptoms, quality of life issues, and psychosocial problems in long-surviving patients over many years will be increasingly important to support engagement with care and effective adherence with antiretroviral therapy over time. End-of-life care, while less frequent, also remains important, as patients may still die from AIDS, or even more commonly, from end-organ failure, non-AIDS defining malignancies, and/or other complications of ageing and chronic co-morbid disease. All these converging factors have now resulted in a new need for the re-integration of HIV care and palliative care, both to help HIV-infected patients live better and longer, as well as manage late-stage and end-of-life issues when they emerge.
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Zetterberg, Henrik, and Jonathan M. Schott. Fluid Biomarkers Indicative of Neurodegenerative Diseases. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0008.
Full textAbstract:
A major unifying feature of neurodegenerative diseases (NDDs) is excessive neuronal loss. Depending on when and where this occurs, patients may express distinct neurological and psychiatric symptoms. Neurodegeneration is accompanied by protein aggregation, inflammation, and microglial activation that may be drivers of the disease or in some circumstances may be protective reactions to the neurodegenerative process. A key development over the past decade has been our ability to leverage these accompanying central nervous system changes to develop clinically impactful biomarkers of specific NDDs. This has been crucial in helping us develop an understanding the time line of progression of these diseases, in their early diagnosis and to help target patients appropriately in therapeutic clinical trials, This chapter gives an overview of both established and novel fluid biomarkers for neurodegeneration, protein accumulation, inflammation, and microglial activation across different neurodegenerative diseases. Common as well as disease-specific biomarker changes in cerebrospinal fluid and blood are emphasized.
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Orellana, Renán A., and Jorge A. Coss-Bu. Nutrition and Gastrointestinal Emergencies. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199918027.003.0014.
Full textAbstract:
Appropriate nutrition must be tailored to the specific needs of individual patients. Needs depend on the child’s baseline nutritional status, the severity of disease, and specific organ dysfunction. Enteral nutrition is preferable whenever possible. Parenteral nutrition may be necessary when efforts to supply adequate nutrition enterally are contraindicated or unsuccessful. Patients with symptoms of acute abdomen require prompt recognition of surgical and nonsurgical disorders. Upper gastrointestinal hemorrhage may require transfusion of blood products, vasoactive drug infusion to minimize ongoing losses, and endoscopy following stabilization. Pancreatitis typically requires an orogastric/nasogastric tube for decompression, aggressive pain management, and radiological evaluations. Abdominal compartment syndrome needs to be recognized promptly to avoid further injury. Acute liver failure commonly leads to multiorgan system dysfunction and death. Specific therapy is available only in a minority of cases, and outcome depends on excellent supportive care, prompt evaluation by a pediatric gastroenterologist, and referral to a transplant center.
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Keshav, Satish, and Alexandra Kent. Gastrointestinal tumours. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0204.
Full textAbstract:
Gastrointestinal (GI) tumours can affect any part of the GI tract, and colorectal cancer is the most common. Throughout the GI tract, chronic inflammation seems to promote the development of neoplasia: for example, chronic reflux oesophagitis is linked to oesophageal adenocarcinoma; chronic Helicobacter pylori infection is linked to gastric cancer; chronic pancreatitis is linked to pancreatic cancer; cirrhosis is linked to hepatocellular cancer; chronic biliary inflammation is linked to cholangiocarcinoma; untreated coeliac disease is linked to intestinal lymphoma; and chronic inflammatory bowel disease is linked to colorectal cancer. Symptoms depend on the location of the tumour, and occur as a result of local anatomical disruption, with consequent functional consequences and, less frequently, as a result of hormonal, metabolic, and immune effects. Weight loss is a common symptom seen in the gastroenterology outpatient clinic, given the high overall incidence of GI tumours. Often, the associated symptoms will direct the doctor to the site of a possible underlying cancer. Anaemia is another non-specific finding with a strong association with luminal cancers. Patients with anaemia with or without weight loss will normally undergo upper and lower GI investigations, usually via oesophagogastroduodenoscopy and colonoscopy (either CT or endoscopic colonoscopy). In tumours that are difficult to identify or assess the malignant potential, PET scanning can provide a large amount of information. PET scanning is a nuclear medicine scanning technique that utilizes 18F-fluorodeoxyglucose (FDG), which is taken up by metabolically active tissue. When combined with CT scanning it can provide information about both anatomical and metabolic activity. FDG is rapidly taken up by malignant tumours and, as a result, is often used for diagnosing, staging, and monitoring response in cancers.
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Schreiber, Benjamin E., Gregory J. Keir, and J. Gerry Coghlan. Cardiopulmonary investigations. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0073.
Full textAbstract:
Cardiopulmonary investigations are growing in number and complexity, but are crucial in management of patients with multisystem disease. Patients with rheumatological conditions are frequently at increased risk of a wide range of cardiac and pulmonary complications. Cardiac complications include accelerated atherosclerosis, valvular dysfunction, and pericardial, myocardial and endocardial involvement. Pulmonary complications include airways disease, interstitial lung disease, pulmonary embolism, and pulmonary hypertension. We aim to present some practical frameworks for selecting the appropriate initial tests in different clinical situations. This chapter is in three sections. In the first section, we review the recommended investigations for common clinical symptoms: shortness of breath, cough, chest pain, and syncope. In the second section, we review the importance of cardiopulmonary investigations in specific rheumatological conditions. In the third section we review the unique characteristics of the cardiopulmonary tests, stressing their particular strengths and weaknesses and associated complications.
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Schreiber, Benjamin E., Gregory J. Keir, and J. Gerry Coghlan. Cardiopulmonary investigations. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0073_update_001.
Full textAbstract:
Cardiopulmonary investigations are growing in number and complexity, but are crucial in management of patients with multisystem disease. Patients with rheumatological conditions are frequently at increased risk of a wide range of cardiac and pulmonary complications. Cardiac complications include accelerated atherosclerosis, valvular dysfunction, and pericardial, myocardial and endocardial involvement. Pulmonary complications include airways disease, interstitial lung disease, pulmonary embolism, and pulmonary hypertension. We aim to present some practical frameworks for selecting the appropriate initial tests in different clinical situations. This chapter is in three sections. In the first section, we review the recommended investigations for common clinical symptoms: shortness of breath, cough, chest pain, and syncope. In the second section, we review the importance of cardiopulmonary investigations in specific rheumatological conditions. In the third section we review the unique characteristics of the cardiopulmonary tests, stressing their particular strengths and weaknesses and associated complications.
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Passaro, Antony, Foteini Christidi, Vasiliki Tsirka, and Andrew C. Papanicolaou. White Matter Connectivity. Edited by Andrew C. Papanicolaou. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199764228.013.5.
Full textAbstract:
The applications of diffusion tensor imaging (DTI) have increased considerably among both normal and diverse neuropsychiatric populations in recent years. In this chapter, the authors examine the contributions of DTI in identifying profiles of trait-specific connectivity in several groups defined in terms of gender, age, handedness, and general intelligence. Additionally, the DTI literature is reviewed across a range of neurodegenerative disorders including Alzheimer’s disease, mild cognitive impairment, frontotemporal dementia, Parkinson disease, multiple sclerosis, and acquired neurological disorders resulting from neuronal injury such as traumatic brain injury, aphasia, agnosia, amnesia, and apraxia. DTI metrics sensitive to psychiatric disorders encompassing obsessive-compulsive disorder, depression, bipolar disorder, schizophrenia, and alcoholism are reviewed. Future uses of DTI as a promising means of confirming diagnoses and identifying in vivo early microstructural changes of patients’ clinical symptoms are discussed.
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Eastman, Brad, and Larry Field. Opioid and Benzodiazepine Overdose. Edited by Matthew D. McEvoy and Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0092.
Full textAbstract:
This chapter, “Opioid and Benzodiazepine Overdose,” reviews the pathophysiology of disease state pertaining to overdose as well as the molecular mechanisms involved with drug receptor binding. It discusses common presenting signs and symptoms of opioid and benzodiazepine overdose in the context of a clinical scenario. It also discusses specific patient populations that are at increased risk of opioid and benzodiazepine overdose. Initial and subsequent treatment options are thoroughly examined while allowing the reader to engage in clinical discussions to open-ended questions provided throughout the chapter. The use of opioid and benzodiazepine antagonists as antidotes is reviewed in detail along with common doses and regimens.
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Schelenz, Silke. Fungal diseases of the gastrointestinal tract. Edited by Christopher C. Kibbler, Richard Barton, Neil A. R. Gow, Susan Howell, Donna M. MacCallum, and Rohini J. Manuel. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755388.003.0026.
Full textAbstract:
Fungal diseases of the gastrointestinal (GI) tract can occur because of an overgrowth of yeast in the gut, exposure to contaminated food and water, or as part of disseminated invasive fungal infections from other sites. The extent of the disease depends on the underlying risk factors, such as diabetes or immunosuppression, and ranges from colonization, localized infection, or fungaemia, to aggressive life-threatening GI tract infections. Candida spp. are the commonest cause of mucosal infection, although mould infections are increasingly reported. Serious invasive mould infections are difficult to diagnose as symptoms are often non-specific. Early recognition, prompt antifungal treatment, and surgical intervention can be lifesaving.
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Gelb, Douglas J. Introduction to Clinical Neurology. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190467197.001.0001.
Full textAbstract:
Newly updated to reflect recent discoveries, the fifth edition of Introduction to Clinical Neurology covers all the take home points beneficial to everyone who relies on this quick and handy guide. This book focuses on the "how" and "why" of clinical neurology. It includes extensive factual material about individual disease processes, but the emphasis is on information that is important for understanding why patients with neurologic conditions are managed the way they are. This book covers what clinicians need to know in order to assess and manage the patients they will encounter in general medical practice, including the application of a logical approach to diagnosis, neurologic examination and how to interpret the findings, and the management of specific disease categories and symptoms. A highly accessible and engaging text, this is the go-to in all things neurology.
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Compston, Alastair. Multiple sclerosis and other demyelinating diseases. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0871.
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The oligodendrocyte–myelin unit subserves saltatory conduction of the nerve impulse in the healthy central nervous system. At one time, many disease processes were thought exclusively to target the structure and function of myelin. Therefore, they were designated ‘demyelinating diseases’. But recent analyses, based mainly on pathological and imaging studies, (re)emphasize that axons are also directly involved in these disorders during both the acute and chronic phases. Another ambiguity is the extent to which these are inflammatory conditions. Here, distinctions should be made between inflammation, as a generic process, and autoimmunity in which rather a specific set of aetiological and mechanistic conditions pertain. And there are differences between disorders that are driven primarily by immune processes and those in which inflammation occurs in response to pre-existing tissue damage.With these provisos, the pathological processes of demyelination and associated axonal dysfunction often account for episodic neurological symptoms and signs referable to white matter tracts of the brain, optic nerves, or spinal cord when these occur in young people. This is the clinical context in which the possibility of ‘demyelinating disease’ is usually considered by physicians and, increasingly, the informed patient. Neurologists will, with appropriate cautions, also be prepared to diagnose demyelinating disease in older patients presenting with progressive symptoms implicating these same pathways even when there is no suggestive past history. Both in its typical and atypical forms multiple sclerosis remains by far the commonest demyelinating disease. But acute disseminated encephalomyelitis, the leucodystrophies, and central pontine myelinolysis also need to be considered in particular circumstances; and multiple sclerosis itself has a differential diagnosis in which the relapsing-remitting course is mimicked by conditions not associated with direct injury to the axon–glial unit. Since our understanding of the cause, pathogenesis and features of demyelinating disease remains incomplete, classification combines aspects of the aetiology, clinical features, pathology, and laboratory components. Whether the designation ‘multiple sclerosis’ encapsulates one or more conditions is now much debated. We anticipate that a major part of future studies in demyelinating disease will be further to resolve this question of disease heterogeneity leading to a new taxonomy based on mechanisms rather than clinical empiricism. But, for now, the variable ages of onset, unpredictable clinical course, protean clinical manifestations, and non-specific laboratory investigations continue to make demyelinating disease one of the more challenging diagnostic areas in clinical neurology.
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Bates, David. Spinal cord disorders. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0650.
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Non-traumatic spinal cord disease may be caused by compression due to tumour, infection or haematoma, inflammation, infection or post-infection, metabolic disturbances, infarction, and degeneration. The diagnosis is often made easier by the clinical assessment: the patient’s age, the speed of onset of the disease, severity of the deficits, the pattern of motor and sensory involvement, and presence of pain and sphincter symptoms are all important in making an assessment of the site and likely nature of the spinal disease.Investigations are obligatory to confirm a diagnosis and to direct therapy. MRI is the most useful investigation. It has largely replaced myelography which should now only be considered in patients with indwelling cardiac pacing wires. Additional investigations including examination of the cerebrospinal fluid, evoked potentials, and specific blood tests may be required and the value of plain X-rays, CT scan, and, in some instances, angiography should not be overlooked.The remainder of this chapter will consider specific disorders, identifying pathology, clinical presentation, investigation, and management. Acute and chronic conditions are considered separately and those affecting the cauda equina, spinal root, and sphincters are considered in Chapter 29.
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King, Daniel. Galen. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198810513.003.0004.
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Galen develops a robustly aetiological approach to diagnosis and therapy which centres on the differentiation of pain perceptions throughout the body. He develops a specific definition of pain as the perception of overwhelming and contrary-to-nature change which links the perception of pain with his understanding of disease. Throughout On Affected Parts, he argues for pain terminology and descriptions that facilitate the communication of experiences and perceptions between doctor and patient. Galen promotes, in this context, a type of ‘common language’ in which familiar terminology communicates effectively the common experiences of doctor and patient: modern categories of subjective and objective language are not effective tools to help understand this complex approach to pain description. Galen’s control of language in this context is mirrored by his attempts to control his patients’ narration of pain symptoms, which moulds their experiences to fit Galen’s understanding of pain, disease, and the body.
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Noordenbos, Troy, and Dominique Baeten. Immune mechanisms: innate immunity. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198734444.003.0007.
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Innate immune mechanisms are strongly implied in the pathophysiology of spondyloarthritis (SpA). This chapter discusses available data on the role of the innate immune system in relation to HLA-B27, genetic associations, and the cellular and molecular characteristics of disease target tissue. Regarding the linkage with MCH-class I molecule HLA-B27, the chapter discusses the arthritogenic peptide hypothesis and three popular antigen-independent theories. The genetic architecture of the disease argues against a role for the adaptive immune system and identifies cytokine pathways, such as IL-1, TNF, and IL-23/IL-17. In experimental as well as in human SpA, the importance of these cytokine pathways are confirmed by effective reduction of signs and symptoms upon blockade of specific molecules. In-depth cellular and molecular analysis of the target tissue identifies a contribution of cells with strong innate features, rather than cells of the adaptive immune system.
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Brinkman, Maree, and Maurice Zeegars. Screening for bladder cancer. Edited by James W. F. Catto. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0073.
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Bladder cancer (BC) is one of the most common urological malignancies and ranks ninth among all cancers worldwide. While screening has the potential to detect early cases of BC and reduce disease specific mortality, to date there are no routine screening programmes of asymptomatic individuals conducted anywhere in the world. There are however, a range of tests and procedures available for the detection and subsequent diagnosis of BC for select individuals presenting with urological symptoms and who are at increased risk of the disease.This chapter provides an overview of the traditional screening tools used for the detection of BC, such as urinalysis for haematuria and urinary cytology, as well as a brief description of follow-up procedures including cystoscopy, imaging, and treatment modalities.
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Toledano, Roulhac D. Physiological changes associated with pregnancy. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198713333.003.0002.
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Pregnant patients pose several challenges to anaesthetists and other healthcare providers. Significant systemic and organ-specific changes accompany each stage of pregnancy, culminating during labour and delivery and in the early postpartum period. While healthy parturients tolerate these physiological adaptations to pregnancy well, patients with coexisting disease or pregnancy-related medical conditions may experience acute decompensation, with potential long-term sequelae. Alternatively, symptoms of a disease state may be obscured by pregnancy or mistaken for physiological changes of pregnancy. Anaesthetic management of pregnant patients is further complicated by concerns regarding difficulty with airway management, aspiration of gastric contents, haemodynamic effects of aortocaval compression, maternal obesity, and the effects of volatile agents on uterine tone; reference ranges for laboratory results that differ from those of the non-pregnant population; fears of fetal exposure to antibiotics, analgesics, and anaesthetics; and concerns that more than one patient must be taken into consideration. This chapter reviews the systemic and organ-specific physiological changes that occur during different stages of pregnancy, with a focus on how these adaptations to pregnancy affect anaesthetic management. Familiarity with updated, evidence-based practices and a firm understanding of the physiological changes of pregnancy are essential components of the anaesthetic management of obstetric patients at any gestational age.
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Woldstad, Christopher, Michael Boska, and Howard E. Gendelman. Neurological Complications of HIV in The Central Nervous System. Edited by Mary Ann Cohen, Jack M. Gorman, Jeffrey M. Jacobson, Paul Volberding, and Scott Letendre. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199392742.003.0026.
Full textAbstract:
This chapter serves to highlight both the research advances made in understanding the effects of HIV on the nervous system and what lies ahead. Particular focus is given to both the effects HIV can play on the nervous system at the molecular and cellular levels and the comorbid conditions that affect neural function. Attention is also given to specific biomarkers to be used for increasing the effectiveness and availability of therapies. The pathogenesis of HIV-associated neurocognitive disorders (HAND) is comparable to that of several other neurodegenerative disorders, and their mechanistic similarities are also discussed in detail. With the introduction of antiretroviral therapy the life expectancy of persons with HIV has increased, with a concomitant decrease in the incidence of severe dementia. There has been a remarkable improvement in cognitive function with almost a complete reversal of associated symptoms of disease. Past and present disease manifestations and the implications for treatment are outlined in the chapter.
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Todd, Stacy, and Nick Beeching. Fungal infection. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0315.
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Fungi, comprising yeasts, moulds, and higher fungi, have a worldwide distribution and are uncommon causes of disease in healthy individuals. However, over the last 20 years, invasive fungal disease (IFD) has become an increasing cause of morbidity and mortality. This is probably due to the increasing numbers of patients with underlying host conditions, which predispose to opportunistic IFD (e.g. transplant and anti-tumour necrosis factor immunosuppression, HIV, or chronic lung disease), and to increased recognition of endemic IFD (e.g. histoplasmosis), which cause disease in both immunocompetent and immunocompromised hosts in selected geographic locations. Diagnosis of IFD remains a challenge. Symptoms are often non-specific, and a definite diagnosis requires invasive sampling with appropriate laboratory testing of these samples. Non-invasive tests are being developed, but their positive and negative predictive values still need validation. Diagnostic criteria (‘proven, probable, and possible’) established primarily for use in research and clinical trials can also prove useful in clinical environments. However, the most important step in identifying patients with IFD is to consider the diagnosis in those at risk. This chapter will focus on the commonest causes of IFD (Candida spp., Aspergillus spp., Cryptococcus spp., and histoplasmosis).