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Geschichte als Lernprozess?: Zur Pathogenese politischer Modernität in Deutschland. Frankfurt am Main: Suhrkamp, 1991.
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Geschichte als Lernprozess?: Zur Pathogenese politischer Modernität in Deutschland. Frankfurt am Main: Suhrkamp, 1985.
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Radzinskiy, Viktor, Alevtina Savicheva, Sergey Vorob'ev, Elena Spasibova, Kira Shalepo, Ol'ga Budilovskaya, Tat'yana Husnutdinova i in. Biocenosis of the vagina. Norm. Disruption. Restoration. ru: Publishing Center RIOR, 2023. http://dx.doi.org/10.29039/978-5-907218-72-7.
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A healthy reproductive system is inconceivable without normal vaginal microbiota, and full-fledged treatment cannot be carried out without detailed understanding of the arrangement and functions of the human microbiome. Today superbugs are a reality, and the role of such concepts as “microbiome” and “biofilms” is already undeniable in medical practice. Every doctor understands that it is necessary to choose antibacterial drugs based on practicability, global experience and evidence-based medicine. All this clearly demonstrates that there is a need to create an authoritative source of knowledge — a handbook for practitioners. Each chapter contains up-to-date information on the impact of female microbiota on the course and outcomes of pregnancy, on the etiology, pathogenesis and diagnostics of vaginal microbiocenosis disorders, and detailed treatment regimens. The work is intended for obstetrician-gynecologists and heads of women’s health clinics, perinatal centers, departments of general hospitals, fellows and heads of departments of obstetrics and gynecology, students of all forms of continuous medical education, graduate students and clinical residents, as well as students of medical schools.
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Harris, Brent T., Galam A. Khan i Saed Sadeghi. Amyotrophic Lateral Sclerosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0029.
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Although the basic gross and microscopic pathological changes in amyotrophic lateral sclerosis (ALS) have been known for more than 100 years, emerging technology and research into the cellular and molecular changes found in this disease are challenging our understanding about the pathogenesis and pathophysiology. All cell types of the CNS/PNS as well as circulating immune cells have been implicated in the pathology of ALS. Numerous genes, their proteins, and environmental factors have also been associated. However, we still do not understand the specific gene-environmental interactions that bring about and drive this devastating disease in most cases. This short chapter does not address the causal factors and molecular pathogeneses that have been hypothesized and actively researched in the pathology of ALS-as these are discussed in other sections of this text. Here, it shows and discusses the basic pathological changes at the tissue and cellular levels that help to establish the pathological diagnosis of ALS at autopsy.
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Ferraiuolo, Laura, i Stephen J. Kolb. Amyotrophic Lateral Sclerosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0026.
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An overriding mystery of ALS pathogenesis orbits around the molecular basis of selective motor neuron vulnerability and clouds our view. There are likely mechanisms involved in the initiation of motor neuron loss and mechanisms involved in the progression of motor neuron loss once initiated. Motor neuron vulnerability is likely related to the unique biological characteristics of these cells. This chapter introduces central molecular pathways that appear to be involved in the pathogenesis of ALS, and highlights why dysregulation of these mechanisms could lead to motor neuron death. Indeed, there are likely mechanisms involved in the initiation of motor neuron loss and mechanisms involved in the progression of motor neuron loss once initiated. Our task is to determine those mechanisms that are relevant to ALS pathogenesis that may be targeted therapeutically to prevent onset and/or halt progression.
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Vincent, Tonia L., i Linda Troeberg. Pathogenesis of osteoarthritis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0138.
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Understanding pathogenic mechanism in disease is critical for development of targeted therapeutic strategies. Although there are, at this time, only a handful of experimental approaches for treating osteoarthritis (OA), until 10 years ago this disease was almost universally considered an unmodifiable condition. Emerging data during this time, largely fuelled by studies in rodent models, has completely changed the paradigm of disease pathogenesis and has for the first time, generated novel, realistic targets for this highly prevalent and disabling condition. These targets include the aggrecanases, members of the ADAMTS family, and collagenases, which together are critical for the early breakdown of the extracellular matrix of cartilage. Some recent success has also been demonstrated by targeting bone in disease. Development of pain in OA is complex and likely arises from different tissues at different stages of disease. In the following section we describe the pathological features of OA, and discuss the evolution of theories of OA pathogenesis and factors that have limited mechanistic clarity in this disease. We summarize the molecular pathways that are now known to be active in disease, and consider how these identified molecular pathways could be linked to known epidemiological risk factors. We finish by discussing possible future therapeutic strategies that will emerge from these discoveries and the current limitations in implementing new therapies in OA.
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Bending, David, Kiran Nistala i Lucy R. Wedderburn. Pathogenesis of juvenile idiopathic arthritis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0060.
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Although the term juvenile idiopathic arthritis (JIA) encompasses a heterogeneous group of diseases, they all share a common pathological hallmark: inflammation of the synovium. Highly activated T cells, monocytes, and neutrophils are attracted to the joint and secrete mediators that not only perpetuate inflammation but also may attenuate immune regulation. In the oligoarticular and polyarticular forms of JIA, which are thought to be autoimmune conditions, dysregulated adaptive immunity is a likely factor in disease pathogenesis; the nature of the interactions between T effector (Teff) cells and T regulatory cells (Treg) is probably a key factor in controlling disease progression. Factors that affect the frequency and function of Tregs and/or the sensitivity of Teffs to mechanisms of immune suppression will therefore impact on the disease course. In the systemic form of JIA, however, dysregulation of innate immune pathways appears more central to disease pathogenesis resulting in augmented levels of interleukins IL-1β, IL-6, and IL-18. In the end, a final, common pathological pathway in JIA is the activation of monocytes and neutrophils, which are the principal mediators of joint inflammation and damage. This is supported by the fact that the therapies that have targeted innate cytokine pathways have shown greater success in the treatment of JIA.
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Pillai, Jagan A., i James B. Leverenz. Pathogenesis of Lewy Body Dementia. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0020.
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This chapter discusses the Pathogenesis of Lew Body Dementia. The Lewy body dementias (LBDs) are a spectrum of dementing neurodegenerative disorders underpinned by the pathological accumulation of α- synuclein protein in both intraneuronal inclusions, “Lewy bodies, ” and neuronal processes, “Lewy neurites”. The chapter concludes that, as with other forms of cognitive impairment in the aged, the pathophysiology of cognitive impairment in LBD is likely multifactorial. Although it appears that α- synuclein pathology, particularly in the limbic and neocortical regions are linked to cognitive changes, other pathologies such as AD likely also play a role. Emphasizing the complexity, a number of genetic factors have been implicated in the LBDs, some specifically with associations to the synucleinopathies and some with other pathophysiologic processes. This complexity will need to be considered as therapeutic interventions are evaluated for the LBD.
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Harms, Matthew B., i Timothy M. Miller. Amyotrophic Lateral Sclerosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0027.
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Recent advances in sequencing technologies have dramatically expanded the number of genes associated with amyotrophic lateral sclerosis, including rare but highly penetrant causative mutations as well as common risk alleles. This chapter discusses these gene discoveries and how they have implicated a diverse array of biological pathways essential for motor neuron health and have begun to inform our understanding of ALS pathogenesis as a heterogeneous and multistep process. Insights from these discoveries are leading to a new generation of targeted therapies directed at specific genes and are poised to inform how patients with amyotrophic lateral sclerosis are evaluated and treated in the clinic.
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Guzik, Tomasz J., i Rhian M. Touyz. Vascular pathophysiology of hypertension. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0019.
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Hypertension is a multifactorial disease, in which vascular dysfunction plays a prominent role. It occurs in over 30% of adults worldwide and an additional 30% are at high risk of developing the disease. Vascular pathology is both a cause of the disease and a key manifestation of hypertension-associated target-organ damage. It leads to clinical symptoms and is a key risk factor for cardiovascular disease. All layers of the vascular wall and the endothelium are involved in the pathogenesis of hypertension. Pathogenetic mechanisms, whereby vascular damage contributes to hypertension, are linked to increased peripheral vascular resistance. At the vascular level, processes leading to change sin peripheral resistance include hyper-contractility of vascular smooth muscle cells, endothelial dysfunction, and structural remodelling, due to aberrant vascular signalling, oxidative and inflammatory responses. Increased vascular stiffness due to vascular remodelling, adventitial fibrosis, and inflammation are key processes involved in sustained and established hypertension. These mechanisms are linked to vascular smooth muscle and fibroblast proliferation, migration, extracellular matrix remodelling, calcification, and inflammation. Apart from the key role in the pathogenesis of hypertension, hypertensive vasculopathy also predisposes to atherosclerosis, another risk factor for cardiovascular disease. This is linked to increased transmural pressure, blood flow, and shear stress alterations in hypertension, as well as endothelial dysfunction and vascular stiffness. Therefore, understanding the mechanisms and identifying potential novel treatments targeting hypertensive vasculopathy are of primary importance in vascular medicine.
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Niaudet, Patrick, i Alain Meyrier. Pathogenesis of proteinuria in minimal change disease and focal segmental glomerulosclerosis. Redaktor Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0059_update_001.
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It is now well established that the podocyte, and in particular the slit diaphragm structure, are critical to the barrier to serum albumin entering glomerular filtrate in large quantities. In minimal change disease there is proteinuria without podocyte death, whereas in focal segmental glomerulosclerosis there is not only podocyte dysfunction but also podocyte loss.
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Benedetto, Chiara, Ilaria Castagnoli Gabellari i Gianni Allais. Migraine and pregnancy-related hypertension. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198749547.003.0005.
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Migraine is one of the most common, disabling neurological disorders in women of reproductive age. It is a disabling condition that can lead to a compromised health-related quality of life. Often `migraineurs' are unable to carry out everyday tasks due to a reduction in functioning and productivity. This burden impacts not only at work, but also on social and family life. Migraine affects not only the physical but also mental and social health. Chapter 5 discusses the available evidence of a correlation between migraine and pre-eclampsia. Pre-eclampsia complicates 3-5% of all pregnancies and remains a leading cause of maternal and perinatal morbidity, and mortality. Although the primary mechanisms of both migraine and pre-eclampsia are not yet well understood, they do share some common pathogenetic aspects. However, studies investigating the clinical association between migraine and pre-eclampsia are sparse. The majority suggest a close association between headaches and hypertensive disorders of pregnancy: gestational hypertension, pre-eclampsia, and eclampsia. There also appears to be a significant increase in the incidence of severe pre-eclampsia in women suffering from migraine. Clinical manifestations of both migraine and pre-eclampsia appear to result from an interaction of the mind and body. A relation with stress has been identified. Further robust research is needed to elucidate the psychosomatic contributions to the pathogenesis of migraine and pre-eclampsia, and the clinical application of their relationship in improving materno-fetal health.
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Baker, Alastair. Alagille syndrome. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198759928.003.0056.
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The chapter on Alagille syndrome covers the genetics and pathogenesis as well as the features and clinical presentation of this syndrome. It also discusses the complications as well as the suggested medical and surgical management for this condition.
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Tombetti, Enrico, i Justin C. Mason. Pathophysiology of vasculitis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0017.
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Vasculitis represents a spectrum of disorders that are often divided on the basis of the predominant vessel size affected into large-, medium- and small-vessel vasculitides. This chapter will focus on the pathogenesis of the anti-neutrophil cytoplasmic antibody (ANCA)-associated medium- and small-vessel vasculitides (AAV), and large-vessel vasculitis, Takayasu arteritis, and giant cell arteritis. Underlying pathogenic mechanisms in vasculitis remain to be fully understood. In particular, the initiating event(s) are not known. A combination of infectious or other environmental triggers on a susceptible genetic background is currently favoured. In addition to the vessel size affected, the mechanisms of vascular injury vary. Moreover, extravascular granulomatosis may play an important role in disease manifestations. The innate and adaptive immune systems contribute to its pathogenesis. Although pathogenic antibodies have not been identified in large-vessel vasculitis, ANCA are directly implicated in small- and medium-vessel AAV. Disease manifestations are varied and diverse and may include arterial stenosis or aneurysms, glomerulonephritis and renal failure, gastro-intestinal, pulmonary, cutaneous, and neurological complications, visual disturbance, deafness, and nasal bridge collapse. Life-threatening cardiovascular disease is also seen, with myocarditis, pericarditis, valvular heart disease, thrombosis, systemic and pulmonary arterial hypertension, and accelerated coronary heart disease all reported. Despite this, the prognosis for patients with vasculitis has improved significantly in recent decades. Further understanding of the pathogenesis of vasculitis will lead to the discovery of further therapeutic targets and novel, safer biologic therapies.
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Pletnikov, Mikhail V., Guo-Li Ming i Christopher A. Ross. Animal and Cellular Models of Psychotic Disorders. Redaktorzy Dennis S. Charney, Eric J. Nestler, Pamela Sklar i Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0015.
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Animal and cell models are experimental systems developed to study particular aspects of a disease, as no model can accurately reflect all features of the disease. In this critical review we mention some of the nongenetic models but focus on genetic mouse models, evaluate their advantages and limitations, and comment on potential new prospects for the field. The ability to reprogram somatic cells from patients and unaffected donors to induced pluripotent stem cells (iPSCs) has the potential to substantially enhance our knowledge of normal cellular development and disease pathogenesis. The use of cell and animal models will help elucidate basic cellular and molecular mechanisms of pathogenesis, which will enable the development of targeted therapeutic approaches.
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Viscardi, Rose M., i Ken B. Waites. Ureaplasma urealyticum and Ureaplasma parvum. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190604813.003.0022.
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The Mycoplasma species Ureaplasma parvum and Ureaplasma urealyticum colonize the human adult urogenital tract and are not typically associated with disease. Perinatal transmission, however, has been implicated in the pathogenesis of preterm birth, chorioamnionitis, and other complications of extreme prematurity, including neonatal pneumonitis, bronchopulmonary dysplasia (BPD), meningitis, and necrotizing enterocolitis (NEC). This chapter reviews the biology of these organisms. Epidemiologic and experimental evidence supporting a role for ureaplasmas in the pathogenesis of neonatal disease, clinical manifestations of infection in the infant, current microbiologic diagnostic methods, and the present status of treatment options are reviewed. Macrolide antibiotic therapy is controversial for infected infants, and current concepts regarding candidates for treatment are discussed. Key unanswered questions that need to be addressed in future research studies are also suggested.
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Beattie, R. Mark, Anil Dhawan i John W.L. Puntis. Chronic constipation. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569862.003.0038.
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Pathogenesis 267Clinical assessment 269Investigation 270Practical management 271Outcome 276Indications to refer for specialist advice 276Chronic functional constipation is a common problem in childhood. Without early treatment the condition is likely to impact on all aspects of the child's life, including education and psychological well-being as well as physical growth and development....
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Török, M. Estée, Fiona J. Cooke i Ed Moran. Viruses. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199671328.003.0008.
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This chapter provides an overview of viruses, starting with the basics of virology, before moving on to a systematic overview of each virus, covering important aspects of epidemiology, pathogenesis, clinical features of infection, diagnosis, and treatment and prevention. This chapter also includes prion disease, even if the causative agent is not a virus.
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Accardo, Jennifer. Restless Legs Syndrome and Periodic Limb Movement Disorder. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0172.
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Restless legs syndrome (RLS), also known as Willis Ekbom disease (WED), is a sensory disorder with a circadian component. An irresistible urge to move the legs disrupts sleep onset and maintenance. Periodic limb movements in sleep, semirhythmic in nature, often overlap with RLS, though periodic limb movement disorder can be diagnosed in the absence of RLS’s distinctive sensory symptoms. Disruptions in dopaminergic pathways, iron metabolism, and the opioid system have all been implicated in pathogenesis, and there is a strong genetic component. RLS is common, affecting 5% to 10% of adults. Its best-known treatments are dopamine agonists; however, other treatments are effective.
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Chang, Yonmee, i Andrew J. Matisoff. Williams-Beuren Syndrome. Redaktorzy Kirk Lalwani, Ira Todd Cohen, Ellen Y. Choi i Vidya T. Raman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190685157.003.0011.
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Williams-Beuren syndrome, also known as Williams syndrome (WS) is a genetic disorder involving the elastin gene on chromosome 7q11.23. Elastin is important for elasticity of vascular walls, and its deficiency can lead to widespread arteriopathy, most notably supravalvar aortic stenosis of the ascending aorta and coronary artery stenosis. Because of these cardiac defects, patients with WS are at high risk for cardiac arrest under anesthesia with a documented incidence around 5%. Appropriate perioperative management of all anesthetics includes a multidisciplinary approach to risk stratification, precise anesthetic management, and disaster planning. This chapter reviews the etiology, pathogenesis, diagnosis, and manifestations of WS. The authors also discuss the preoperative workup and anesthetic implications of WS, as well as issues related to cardiac arrest and extracorporeal cardiopulmonary resuscitation.
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Gu, Wenduo, Yao Xie i Qingbo Xu. Animal models to study pathophysiology of the vasculature. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0005.
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Animal models are designed to be preliminary tools for a better understanding of the pathogenesis, improvement in diagnosis, prevention, and therapy of vascular diseases in humans. Animal models are easily manageable, as compounding effects of dietary and environmental factors can be controlled experimentally. Blood vessel samples can be taken for detailed experimental and biomolecular examination. A thorough understanding of the animal models used is necessary and complete analysis must be validated so that the data can be extrapolated to humans. There are several species that are used for studying vascular pathophysiology, including mice, rats, rabbits, and pigs. Attracted by the well-defined genetic systems, a number of investigators have begun to use the mouse as an experimental system for arteriosclerosis research. Because vascular disorder is a complicated disease, which includes spontaneous (native) atherosclerosis, transplant arteriosclerosis, vein graft atherosclerosis, and angioplasty-induced restenosis, several models for studying all types of vascular disease have recently been established. Using these animal models, much knowledge concerning the pathogenesis of the disease and therapeutic intervention has been gained. This chapter will not attempt to cover all aspects of animal models, but will rather focus on the major progress in understanding the pathophysiology of the vasculature, the (dis)advantages of a variety of models, and how specific models can be appropriately chosen for different purposes of study.
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Gilden, Don, Randall J. Cohrs, Ravi Mahalingam i Maria A. Nagel. Varicella Zoster Virus Infection of the Nervous System. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0149.
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Varicella zoster virus (VZV) is a human herpesvirus that causes varicella (chickenpox), after which virus becomes latent in ganglionic neurons along the entire neuraxis. Reactivation of VZV due to a decline in the cell-mediated immune response to VZV in elderly or immunocompromised individuals causes zoster (shingles), frequently complicated by chronic pain (postherpetic neuralgia) and serious neurological disease (meningoencephalitis, myelitis and VZV vasculopathy due to retrograde spread of virus after zoster. Here, we describe clinical, laboratory and pathological features of neurological complications of VZV reactivation, including diagnostic testing to verify VZV infection of the nervous system, since all neurological complications of zoster may occur without rash. We also discuss VZV latency, primate models to study varicella pathogenesis and immunity, and immunization of elderly individuals to prevent VZV reactivation.
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Gibbs, Kevin. Lung Abscess. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199976805.003.0025.
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Lung abscesses are intraparenchymal collections of purulent and necrotic tissue caused by infectious organisms that present with subacute pulmonary symptoms. Primary lung abscess is classically a disease of middle-aged men. Infection and subsequent abscess formation result from large-volume aspiration of oral secretions. Therefore, conditions that predispose to aspiration also predispose to lung abscess. Such conditions include all causes of depressed sensorium as well as both mechanical and neurologic causes of dysphagia. The burden of oral anaerobes also plays an important role in disease pathogenesis. It can be difficult to differentiate a lung abscess from pneumonia. Patients with lung abscess generally appear less acutely ill, and have fewer rigors or shaking chills. These infections are typically polymicrobial and difficult to accurately culture, requiring empiric therapy with antibiotics with broad anaerobic coverage. Most patients respond well to antimicrobials, but mortality remains high in the subset who fails medical therapy.
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Klingenberg, Roland, i Ulf Müller-Ladner. Mechanisms of inflammation. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0270.
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This chapter provides a brief summary of the immune pathogenesis of atherosclerosis, highlighting shared features with inflammatory pathways in rheumatoid arthritis (RA) described in detail in Chapter 25.4. RA constitutes a prototype autoimmune disease primarily affecting the joints but also the heart and vessels associated with increased cardiovascular mortality. Recent years have produced a wealth of novel insights into the diversity of immune cell types which either propagate or dampen inflammation in atherogenesis. Expansion of this inherent anti-inflammatory component carried by regulatory T cells may constitute a new therapeutic target to harness the progression of atherosclerotic cardiovascular disease. Among the various inflammatory mediators involved in RA pathology, cytokines (tumour necrosis factor-α and interleukin-6) have gained major interest as therapeutic targets with approved therapies available. In light of the many common features in the pathogenesis of RA and atherosclerosis, these biologics are currently being evaluated in cardiovascular patients. The recently published CANTOS trial showed that IL-1 inhibition reduced adverse cardiovascular events in patients with coronary artery disease demonstrating that inflammation is a genuine therapeutic target. The near future will provide more information whether inflammation is a bona fide cardiovascular risk factor based on completion of several clinical trials using anti-inflammatory approaches in patients with both cardiovascular disease and rheumatoid arthritis.
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Lafeber, Floris P. J. G., Nick J. Besselink i Simon C. Mastbergen. Synovium and capsule. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0006.
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Synovium is an integrated tissue of the diarthrodial joints that interacts with all the other joint tissues and specifically is important in nourishment and lubrication of the articular cartilage, removal of waste products, and immunological surveillance. Chronic as well as recurrent low-grade synovial inflammation definitely contributes to progression and symptoms of certain patients with osteoarthritis. Low-grade inflammation may even be causative in the disease. The challenge is that osteoarthritis is a heterogeneous disorder with inflammation not only of the synovial tissue but with its mediators also present in cartilage and bone. Therefore, despite the presence of inflammatory mediators, in some cases synovitis may be seen as a bystander and not as a driving force in pathogenesis. Future research must be directed toward defining the risk-to-benefit ratio for (systemic) anti-inflammatory therapy, especially when targeting mediators of low-grade inflammation.
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Carrero, Juan Jesús, i Peter Stenvinkel. The role of inflammation in chronic kidney disease. Redaktor David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0110.
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Low-grade persistent inflammation is a common feature of chronic kidney disease. This chapter provides an overview of the pathogenesis and clinical consequences of elevated pro-inflammatory cytokines in the uraemic milieu with an emphasis on dialysis stages. It reviews the multifactorial dialysis- and non-dialysis-related causes of inflammation and its purported role in the development of protein energy wasting, vascular calcification, endocrine disorders, and depression. The chapter also discusses the use and the need of monitoring C-reactive protein levels regularly in the clinical setting and comments on possible therapeutic approaches to reduce inflammation in these patients.
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Denninghoff, James S., i Frederick S. vom Saal. Sources of Contaminants in the Home. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190490911.003.0004.
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Exposure to contaminants in the home and all indoor spaces can cause disease, including chronic inflammation, allergy, and asthma. Controlling dust, which can contain mold spores, insect parts, fecal material, pet dander, skin fragments, packaging materials, dust mites, volatile cleaning agents, and carpet fragments, is essential for clean indoor air. Dust is a vector for chemical toxins and organic and inorganic materials, which are sources of inflammation. The triggered immune response plays a central role in the pathogenesis of asthma, allergy, and sinusitis. Controlling humidity is necessary to minimize mold and the infiltration of dust mites and other insects in the home.
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Lee, Angela, i Gebhard Wagener. Distributive Shock. Redaktorzy Matthew D. McEvoy i Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0011.
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The distributive shock chapter reviews the definition, classification, epidemiology, pathophysiology, clinical manifestations, and therapeutic goals of shock. It examines the cardiovascular factors and mechanisms leading to impaired oxygen delivery and its effect on the pathogenesis of shock. It reviews the compensatory mechanisms in shock that cause symptoms and organ manifestations in patients with acute circulatory failure. This chapter also discusses the limitations and benefits of different monitoring modalities during shock management including central venous pressure, mixed venous oxygen saturation, and echocardiography. Finally, it considers therapeutic goals and treatments to restore perfusion to reverse the shock state.
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Garcia-Marcinkiewicz, Annery, i John E. Fiadjoe. Laryngotracheal Reconstruction. Redaktorzy Kirk Lalwani, Ira Todd Cohen, Ellen Y. Choi i Vidya T. Raman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190685157.003.0022.
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This chapter on laryngotracheal reconstruction (LTR) describes and reviews the preoperative, intraoperative, and postoperative course of a virtual case of a patient undergoing double stage laryngotracheal reconstruction (ds-LTR). The discussion section reviews the etiology and pathogenesis of subglottic stenosis (SGS) and describes the Myer-Cotton classification system of SGS. The chapter also reviews the medical management of gastroesophageal reflux disease, endoscopic treatment of granulations, anterior cricoid split, LTR with cartilage augmentation (single and double stage), and cricotracheal resection. The differences in the technique and patient selection of single stage LTR (ss-LTR) and ds-LTR are reviewed. The intraoperative and postoperative complications of LTR and postoperative sedation management are also discussed.
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Dasgupta, Bhaskar. Polymyalgia rheumatica. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0134.
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This chapter reviews advances in pathogenesis; European League Against Rheumatism/American College of Rheumatology (EULAR/ACR) classification criteria with clinical, laboratory, and ultrasound criteria for classification as polymyalgia rheumatica (PMR); the heterogeneity and overlap between PMR, inflammatory arthritis, and large-vessel vasculitis as illustrated by representative cases; recent guidelines on early and correct recognition, investigations, and management of PMR; the scope of disease-modifying agents; socio-economic impact, outcomes, and patient experience in PMR. It also discusses areas for future research including clinical trials with biological agents and newer steroid formulations, standardized outcome assessments, and the search for better biomarkers in PMR. PMR is one of the common inflammatory rheumatic diseases of older people and represents a frequent indication for long-term glucocorticoid (GC) therapy. It is characterized by abrupt-onset pain and stiffness of the shoulder and pelvic girdle muscles. Its management is subject to wide variations of clinical practice and it is managed in primary or secondary care by general practitioners (GPs), rheumatologists, and non-rheumatologists. The evaluation of PMR can be challenging, as many clinical and laboratory features may also be present in other conditions, including other rheumatological diseases, infection, and neoplasia. PMR is usually diagnosed in the primary care setting, but standard clinical investigations and referral pathways for suspected PMR are unclear. The response to standardized therapy is heterogeneous, and a significant proportion of patients do not respond completely. There is also an overlap with inflammatory arthritis and large-vessel vasculitis for which adjuvant disease-modifying medications are often used. Prolonged corticosteroid therapy is associated with a variety of side effects, especially when high-dose glucocorticoid therapy is employed. Giant cell arteritis (GCA) is also often linked to PMR. It is a vasculitis of large- and medium-sized vessels causing critical ischaemia. GCA is a medical emergency because of the high incidence of neuro-ophthalmic complications. Both conditions are associated with a systemic inflammatory response and constitutional symptoms. The pathogenesis is unclear. The initiating step may be the recognition of an infectious agent by aberrantly activated dendritic cells. The key cell types involved are CD4+ T cells and macrophages giving rise to key cytokines such as interferon-γ (implicated in granuloma formation), PDGF (intimal hyperplasia), and interleukin (IL)-6 (key to the systemic response). The pathogenesis of PMR may be similar to that of GCA, although PMR exhibits less clinical vascular involvement. The mainstay of therapy is corticosteroids, and disease-modifying therapy is currently indicated in relapsing disease.
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Gaston, J. S. Hill. Reactive arthritis and enteropathic arthropathy. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0115.
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Reactive arthritis (ReA), and enteropathic arthritis secondary to inflammatory bowel disease, are forms of spondyloarthritis, all of which share an association with HLA B27 and can involve both axial and peripheral joints. Genetic studies strongly implicate the cytokines IL-17 and IL-23 in their pathogenesis, and evidence for autoimmunity is lacking. ReA is triggered by particular bacteria, mainly affecting the gut and genitourinary tract, though infections are sometimes asymptomatic. Classically an acute oligo- or monoarthritis with enthesitis occurs, often with inflammatory back pain, though mild polyarthritis can also occur. Septic and crystal-induced arthritis are the principal differential diagnoses. Extra-articular features may aid diagnosis, which otherwise requires laboratory evidence of preceding infection. Bacterial components traffic to the joint (which is nevertheless sterile), and elicit local proinflammatory immune responses. Most ReA is self-limiting, but persistent cases may require disease-modifying anti-rheumatic drugs or even biologics.
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Gaston, J. S. Hill. Reactive arthritis and enteropathic arthropathy. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0115_update_002.
Pełny tekst źródłaStreszczenie:
Reactive arthritis (ReA), and enteropathic arthritis secondary to inflammatory bowel disease, are forms of spondyloarthritis, all of which share an association with HLA B27 and can involve both axial and peripheral joints. Genetic studies strongly implicate the cytokines IL-17 and IL-23 in their pathogenesis, and evidence for autoimmunity is lacking. ReA is triggered by particular bacteria, mainly affecting the gut and genitourinary tract, though infections are sometimes asymptomatic. Classically an acute oligo- or monoarthritis with enthesitis occurs, often with inflammatory back pain, though mild polyarthritis can also occur. Septic and crystal-induced arthritis are the principal differential diagnoses. Extra-articular features may aid diagnosis, which otherwise requires laboratory evidence of preceding infection. Bacterial components traffic to the joint (which is nevertheless sterile), and elicit local pro-inflammatory immune responses. Most ReA is self-limiting, but persistent cases may require disease-modifying anti-rheumatic drugs or even biologics.
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Zaffran, Stéphane. Cardiac growth II: Cardiomyocyte polarization. Redaktorzy José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, José Luis de la Pompa, David Sedmera, Cristina Basso i Deborah Henderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0010.
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During vertebrate embryogenesis, the planar cell polarity (PCP) signalling pathway is responsible for cell movements essential for convergent extension during gastrulation, neural tube closure, neural crest cell migration, and heart morphogenesis. In the heart, the non-canonical Wnt/PCP pathway regulates cell polarity, cell shape, and cell dynamics during formation of the cardiac crescent and deployment of second heart field cardiac progenitors to the poles of the heart tube. PCP signalling is also essential for the establishment of left–right patterning in the early embryo. This chapter reviews our current understanding of PCP signalling in heart morphogenesis and how it affects the pathogenesis of congenital heart diseases.
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Singhi, Pratibha, Naveen Sankhyan i Sunit Singhi. Acute Bacterial Meningitis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0144.
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Bacterial meningitis is one of the severest infections in childhood. Neuronal damage in meningitis is largely due to the extensive inflammatory cascade induced by pathogenic bacteria. This chapter discusses the current understanding of the interaction of multitude of factors in the pathogenesis of bacterial meningitis. This includes the mechanisms involved in transcellular traversal of the bacteria, and induction and release of several inflammatory cytokines and chemokines. The management of a child with bacterial meningitis requires meticulous supportive care and timely, appropriate, and adequate antibiotic therapy. The chapter also reviews the current understanding of some important clinical aspects of care of a child with bacterial meningitis.
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Fiza, Babar, i Vivek Moitra. Introduction to Shock. Redaktorzy Matthew D. McEvoy i Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0009.
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The chapter “Introduction to Shock” reviews the definition, classification, epidemiology, pathophysiology, clinical manifestations, and therapeutic goals of shock. It examines the cardiovascular factors and mechanisms leading to impaired oxygen delivery and its effect on end organ perfusion and the pathogenesis of shock. This chapter reviews the compensatory mechanisms in shock that cause the signs and symptoms, along with organ manifestations, reported in patients with acute circulatory failure. This chapter also discusses the limitations and benefits of different monitoring modalities during shock management including central venous pressure, mixed venous oxygen saturation, and echocardiography. Finally, it considers therapeutic goals and treatments to restore perfusion and reverse the shock state.
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Dalbeth, Nicola. Basic calcium phosphate crystal deposition. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0053.
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Basic calcium phosphate (BCP) crystals deposit within periarticular and articular sites, leading to a variety of clinical presentations. The most well-recognized clinical syndromes associated with BCP crystal deposition are calcific tendinitis and BCP crystal-associated destructive arthritis such as Milwaukee shoulder syndrome. There is emerging evidence that BCP crystals also play a role in osteoarthritis pathogenesis. Within the joint, tissue responses to BCP crystals include induction of pro-catabolic and inflammatory pathways. Clinical management of BCP crystal-associated arthropathies is limited by the lack of reliable and feasible methods to detect crystals, and the current unavailability of systemic therapies that promote BCP crystal dissolution.
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Tatham, Andrew, i Peng Tee Khaw. Glaucoma. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199672516.003.0008.
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This chapter explores glaucoma. It starts off with an outline of optic nerve head anatomy and then describes aqueous fluid dynamics and the pathogenesis of glaucoma. It then goes on to discuss the clinical skill areas of optic nerve head assessment in glaucoma, glaucoma imaging devices, tonometry and tachymetry, gonioscopy, and perimetry. The chapter also details ocular hypertension, primary open-angle glaucoma, primary angle closure, and secondary angle closure. In addition, it discusses normal tension glaucoma, steroid-induced glaucoma, traumatic glaucoma, inflammatory glaucomas, pseudoexfoliative glaucoma, pigmentary glaucoma, and neovascular glaucoma. It then covers aqueous misdirection, iridocorneal endothelial syndrome and iridocorneal dysgenesis, ocular hypotensive agents, laser therapy for glaucoma, and glaucoma surgery.
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de Bie, Robertus M. A., i Susanne E. M. Ten Holter. Advanced Treatment for Dystonia. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190607555.003.0019.
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Deep-brain stimulation is a last resort for the management of dystonia or dystonic movement disorders when oral or injectable therapies do not provide adequate relief to allow an acceptable quality of life. The underlying pathogenesis of dystonia is less well understood than in Parkinson’s disease, in which deep-brain stimulation is generally expected to provide effective and long-lasting benefit. Furthermore, it is likely that dystonia represents a number of different basal ganglia pathologies. The response of dystonia to deep-brain stimulation is typically delayed for up to weeks or months following a change in stimulation parameters. All of these factors make it more difficult to predict outcomes in dystonia following deep-brain stimulation, thus making patient selection all the more important.
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Shakkottai, Vikram G. Ataxias. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0014.
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Autosomal recessive cerebellar ataxias are a group of inherited neurological disorders with progressive balance and gait difficulties. In these disorders, cerebellar ataxia is often accompanied by eye movement abnormalities and peripheral nervous system involvement. A unifying mechanism for disease pathogenesis that is common to all the recessive ataxias likely does not exist. Nevertheless, some pathophysiological pathways are common to several autosomal recessive cerebellar ataxias. Specific gene defects in each disorder are summarized in the chapter. The most common recessively inherited ataxias are Friedreich ataxia and Ataxia telangiectasia. A recessive ataxia must be considered for any individual with progressive cerebellar ataxia with onset less than 30 years. The treatment is primarily supportive, but some recessive ataxias have specific treatment.
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Mayr, Roman, i Maximilian Burger. Squamous cell bladder cancer. Redaktor James W. F. Catto. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0080.
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In the developed countries, over 90% of the bladder cancer cases are transitional cell carcinoma (TCC), with squamous cell carcinoma (SCC), adenocarcinomas, and rare types of bladder cancer comprising the remaining 10% of bladder cancer cases. In Western regions, pure SCC of the bladder constitutes 1.2–4.5% of all bladder tumours. SCC can occur in both non-bilharzial and bilharzial bladders; the two subtypes differ in epidemiology, pathogenesis, and clinical outcome. Squamous cell carcinoma in the bilharzial bladder is an endemic disease in many regions of the Middle East, Africa, Southeast Asia, and South America. The knowledge of SCC of the bladder is nevertheless important due to different aetiology, clinical pathways, and clinical outcome.
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Boehncke, Wolf-Henning, i Dafna D. Gladman. Extra-articular manifestations: psoriasis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198734444.003.0018.
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Psoriasis is a chronic, recurrent inflammatory skin disease, affecting about 2% of the world’s population. In 2014, the World Health Organization’s member states adopted a resolution on psoriasis, recognizing it as ‘a chronic, non-communicable, painful, disfiguring, and disabling disease for which there is no cure’. The resolution acknowledges the psychosocial burden of the disease and that many people with psoriasis suffer due to lack of awareness and access to sufficient treatment. Psoriasis is a multifaceted disease including not only a variety of skin lesions, but also joint manifestations and comorbidities. This chapter focuses on the clinical features of psoriasis of the skin and its underlying pathogenesis, taking into account the current status of genetic research in the field. It also describes psoriatic arthritis, as well as the association of psoriasis with spondyloarthritis.
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Chiriac, Anca. Pediatric Dermatology. Volume II. ODO, 2022. http://dx.doi.org/10.7241/ourd.2022book.2.
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A consummate classic with a fresh approach to pediatric dermatology Childrens skin is different. Maturation affects the epidermal barrier, the cutaneous microbiome, adnexal structures, vasculature, and transcutaneous absorption of drugs. The immature skin is more susceptible to pathogens and environmental disruption. Many genetic disorders are either present at birth or manifest early in childhood. Skin diseases thus present differently in children than in adults. Pediatric dermatology has seen significant advances over the last decade, particularly in the field of molecular genetics research, which has furthered our understanding of the pathogenesis of many skin diseases and the development of new approaches to treatment. This first edition provides state-of-the-art information on all aspects of skin disease in children. It covers the diagnosis and treatment of all conditions.
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McKinlay Gardner, R. J., i David J. Amor. Down Syndrome, Other Full Aneuploidies, Polyploidy, and the Influence of Parental Age. Redaktorzy R. J. McKinlay Gardner i David J. Amor. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199329007.003.0013.
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This chapter reviews the archetypical chromosome disorder, namely Down syndrome (DS; trisomy 21), and the various different chromosomal forms that may be the basis of it: standard trisomy 21, translocation trisomy, both de novo and inherited, and other rare forms. The concept of dosage imbalance as the basis of the pathogenesis is reviewed, and the “DS critical region” on chromosome 21 is examined. Reproductive risks associated with each of these DS types are discussed. The chapter considers the other full autosomal trisomies, T13 and T18, and also (mosaic) T9. Triploidy, as the basis of hydatidiform mole, is reviewed. Also reviewed are the influence of parental, mostly maternal, age, in the genesis of these aneuploidies, and the effect of secular change on these observations. Tables provide precise age-related risk figures for recurrence risk of T21 and more general figures for other trisomies.
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Hughes, Alis, i Lesley Jones. Pathogenic Mechanisms. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199929146.003.0013.
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Huntington’s disease (HD) pathogenesis is complex. In the two decades since the gene and its mutation were discovered, there has been extensive exploration of how the expanded CAG repeat in HTT leads to neurodegeneration in HD. This chapter focuses on the mechanisms that potentially contribute to the dysfunction and death of cells in HD. These include repeat instability and RNA toxicity and the production, processing, modification, and degradation of mutant huntingtin. The effects of mutant HTT on cellular processes such as transcription, transport, neurotransmission, and protein clearance are also described. The interdependence and individual importance of these mechanisms in disease etiology remains to be clarified; however, consideration of each could be important for the development of therapeutic interventions in HD.
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Keshav, Satish, i Alexandra Kent. Alcoholic liver disease. Redaktorzy Patrick Davey i David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0211.
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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.
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Pereira, Luis F., Harold W. Goforth, Esteban Martínez, Joseph Z. Lux, Maria Ferrara i Michael P. Mullen. Cardiovascular Disease, Metabolic Complications and Lipodystrophy in Persons with HIV. Redaktorzy Mary Ann Cohen, Jack M. Gorman, Jeffrey M. Jacobson, Paul Volberding i Scott Letendre. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199392742.003.0046.
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The introduction of effective antiretroviral therapy has contributed to a dramatic reduction in HIV-related mortality. As patients live longer, evidence suggests an increased incidence of cardiovascular disease in persons with HIV over that among individuals who do not have HIV, thus early detection and treatment of multimorbidities and modifiable cardiovascular disease risk factors particularly in persons with HIV are needed. Several mechanisms have been proposed to explain the increased risk of cardiovascular disease, including the virus itself, antiretroviral therapy, and traditional risks factors. This chapter discusses detection and treatment of cardiovascular disease in persons with HIV, as well as metabolic complications involved, including dyslipidemia, insulin resistance, and lactic acidosis. The pathogenesis and management of HIV-associated lipodystrophy as well as its psychosocial impact are also addressed.
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O’Neal, M. Angela. Multiple Ovarian Cysts in a Woman with Epilepsy. Redaktor Angela O’Neal. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190609917.003.0007.
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This chapter explores how epilepsy can affect reproductive function. The National Institute of Health consensus definition of PCOS includes the presence of menstrual dysfunction, clinical evidence of hyperandrogenism, and exclusion of other endocrinopathies, such as Cushing’s syndrome and hypothyroidism. The etiology of PCOS is felt to be heterogenous, related to a complex interaction between both genetic and environmental factors. PCOS develops when the ovaries are stimulated to produce excessive testosterone. The diagnosis and pathogenesis of polycystic ovarian syndrome is explored; in particular, how valproate contributes to the condition in women with epilepsy. Valproate is the AED most associated with PCOS, as it can directly increase ovarian testosterone production. It can also cause weight gain leading to insulin resistance, another mechanism contributing to PCOS.
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Denton, Christopher P., i Pia Moinzadeh. Systemic sclerosis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0121.
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The term 'scleroderma' describes a group of conditions in which the development of thickened, fibrotic skin is a cardinal feature. This includes localized forms of scleroderma (e.g. morphoea) and also systemic forms of the disease that are more correctly termed systemic sclerosis. Systemic sclerosis (SSc) is a multiorgan, autoimmune disease that has a high clinical burden and mortality, due to affecting the skin as well as internal organs. As with other related diseases there is a female predominance and marked clinical diversity. The pathogenesis of SSc is not fully elucidated; it includes endothelial cell injury fibroblast activation and autoimmunity that lead to skin and internal organ manifestations. The majority of cases exhibit characteristic serum autoantibodies. Some of these antibodies are scleroderma-specific reactivities including anti-centromere (ACA), anti-topoisomerase-1 (ATA or Scl 70) or anti-RNA polymerase III antibodies. These anti-nuclear antibody (ANA) patterns are generally mutually exclusive and serve as useful clinical markers of disease subgroups. Additional subsetting of scleroderma cases, based on the extent of skin sclerosis, permits classification into limited and diffuse subsets. Because of the heterogeneity of the disease patients may suffer from different organ manifestations, such as lung fibrosis, hypertensive renal crisis, severe cardiac disease, gastrointestinal involvement, and pulmonary arterial hypertension. Although outcomes have improved recently, systemic sclerosis still has the highest case-specific mortality of any of the autoimmune rheumatic diseases and requires careful and systematic investigation, management and follow-up. Treatment includes symptomatic strategies with attention to each involved organ system; it is still an area where therapeutic progress and better understanding of pathogenesis is increasingly anticipated.
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Weiner, Howard, i Peter B. Crino. Familial tumour syndromes: tuberous sclerosis complex. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199651870.003.0017.
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Tuberous sclerosis complex (TSC) is a multisystem, genetic disorder that results from mutations in TSC1 or TSC2 genes. Neurological and neuropsychiatric disabilities include epilepsy, intellectual disability, autism, attention deficit disorder, and generalized anxiety. Cortical dysplasias (also known as tubers) are developmental abnormalities of the cerebral cortex that are believed to be responsible for seizures, cognitive disability, and autism. Subependymal giant cell astrocytomas (SEGAs) are intraventricular tumours that can cause hydrocephalus, increased intracranial pressure, and death. TSC results from hyperactivation of the mammalian target of rapamycin (mTOR) pathway in neurons in the brain. This chapter reviews the clinical presentations of TSC as well as diagnostic approaches for epilepsy and SEGAs. It discusses the genetics and cellular pathogenesis of TSC as well as reviewing the link to mTOR signalling. This chapter also presents evidence for different treatment modalities for seizures and SEGAs. It is written for qualified specialist physicians and caregivers.
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McCann, Shaun R. The role of technology in haematology. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198717607.003.0011.
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Various technologies have changed and improved the practice of haematology. Because it is possible to obtain blood cells so readily (via a simple venepuncture), haematology has been at the forefront of technological developments in medicine. The diagnosis of both malignant and benign haematological disorders has become more exact because of the technological advances outlined, and the understanding of the pathogenesis of many diseases has been advanced as a direct result of the application of technologies such as immunofluorescence, confocal and electron microscopy, automated cell counting, flow cytometry, digital cell morphology, advanced staining techniques, and PCR. However, it is important to stress that all technologies and ‘tests’ need to be cautiously interpreted, and a full history and physical examination should always be the first step in the investigation of patients.