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1
1943-, Greenwald Robert A., Golub Lorne M, and New York Academy of Sciences., eds. Inhibition of matrix metalloproteinases: Therapeutic potential. New York, N.Y: New York Academy of Sciences, 1994.
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2
Gregory, Bock, Marsh Joan, and Widdows Kate, eds. Polyfunctional cytokines: IL-6 and LIF. Chichester, Eng: Wiley, 1992.
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3
NATO Advanced Research Workshop on Regulation of Extravascular Fibrinolysis in Nervous System Development and Disease (1989 Maratea, Italy). Serine proteases and their serpin inhibitors in the nervous system: Regulation in development and in degenerative and malignant disease. Edited by Festoff Barry W, Hantaï Daniel, and North Atlantic Treaty Organization. Scientific Affairs Division. New York: Plenum Press, 1990.
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4
Takao, Kumazawa, Kruger Lawrence, and Mizumura Kazue, eds. The polymodal receptor: A gateway to pathological pain. Amsterdam: Elsevier, 1996.
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5
McMahon, Chris G. Ejaculatory disorders. Edited by David John Ralph. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0105.
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Ejaculatory/orgasmic disorders are common male sexual dysfunctions, and include premature ejaculation (PE), inhibited ejaculation, anejaculation, retrograde ejaculation, and anorgasmia.Premature ejaculation management is largely dependent upon aetiology. Life-long PE is best managed with PE pharmacotherapy (selective serotonin re-uptake inhibitor [SSRI] and/or topical anaesthetics). The management of acquired PE is aetiology-specific and may include erectile dysfunction (ED) pharmacotherapy in men with co-morbid ED. Behavioural therapy is indicated when psychogenic or relationship factors are present and is often best combined with PE pharmacotherapy in an integrated treatment programme. Delayed ejaculation, anejaculation, and/or anorgasmia may have a biogenic and/or psychogenic aetiology. Men with age-related penile hypoanesthesia should be educated, reassured, and instructed in revised sexual techniques which maximize arousal. No drugs have yet been approved by regulatory agencies for this purpose, and most drugs identified for potential use have limited efficacy, impart significant side effects, or are considered experimental in nature.
6
Tobon, Amalia Londono, and Hanna E. Stevens. Adolescents with SSRI-Resistant Depression. Edited by Ish P. Bhalla, Rajesh R. Tampi, Vinod H. Srihari, and Michael E. Hochman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190625085.003.0008.
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This chapter provides a summary of a landmark study in child and adolescent psychiatry addressing the common clinical experience of an adolescent that does not respond to initial antidepressant treatment. Should adolescents with selective serotonin reuptake inhibitor (SSRI) resistant depression be switched to another SSRI or to venlafaxine with or without cognitive behavioral therapy? Starting with that question, it describes the basics of the study, including funding, study locations, who was studied, how many patients, study design, study interventions, follow-up, endpoints, results, and criticism and limitations. This chapter also briefly reviews other relevant studies and information, discusses implications of the findings, and concludes with a relevant clinical case scenario and suggested management for the case.
7
Biotransformation Potential and Uncoupling Behavior of Common Benzotriazole-Based Corrosion Inhibitors. Storming Media, 2002.
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8
Jani, Suni, Ryan Herringa, and Derek Hursey. Pharmacologic Treatment of Children with Trauma- and Stressor-Related Disorders. Edited by Frederick J. Stoddard, David M. Benedek, Mohammed R. Milad, and Robert J. Ursano. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190457136.003.0023.
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This chapter reviews the principles of psychopharmacological treatment for trauma and stressor-related disorders in children. It will discuss emerging psychopharmacological treatments and theories of trauma- and stress-related disorders (TSRDs) common to childhood, reactive attachment disorder, and disinhibited social engagement disorder. Although there is limited literature on the role of pharmacotherapy in treating TSRDs in children, it has been recognized that α- and β-adrenergic blocking agents, novel antipsychotic agents, non-selective serotonin reuptake inhibitor antidepressants such as tricyclic antidepressants, and mood-stabilizing agents may be effective for children based on several open clinical trials. These trials, as well as existing promising clinical trials, are discussed in this chapter. It also provides an in-depth review of factors such as potential side effects, medication interactions, and black box warnings as they specifically apply to the pediatric population.
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Hopkins, Philip M. Adverse drug reactions in anaesthesia. Edited by Michel M. R. F. Struys. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0022.
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Adverse drug reactions are implicated in more than 40% of anaesthesia-related deaths. Undoubtedly, many more patients experience morbidity from adverse drug reactions. Widely cited definitions of adverse drug reactions encompass common side-effects but this chapter focuses on those that are unexpected reactions to drugs administered by anaesthetists and that occur at normal drug doses. The chapter includes a comprehensive account of malignant hyperthermia, which remains a major contributor to anaesthesia related to deaths. Malignant hyperthermia is a pharmacogenetic condition triggered by potent inhalational anaesthetics and possibly also suxamethonium. The genetic basis, pathophysiology, clinical presentations, and management of malignant hyperthermia are discussed. The chapter covers two other pharmacogenetic conditions: the acute porphyrias and butyrylcholinesterase (plasma cholinesterase) deficiency. Drug-induced anaphylaxis is another cause of perioperative morbidity and mortality. Recent data indicate that anaphylaxis during anaesthesia may be much more common than previously thought. The other type of adverse drug reaction covered in the chapter is serotonin syndrome. Perioperative serotonin syndrome is most likely to occur when patients who are already taking serotonergic drugs, such as selective serotonin reuptake inhibitor antidepressants or ‘triptan’ antimigraine treatments, are given a second drug with serotonergic properties, such as tramadol.
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Preusser, Matthias, Gabriele Schackert, and Brigitta G. Baumert. Metastatic brain tumours. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199651870.003.0019.
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Brain metastasis is a common clinical challenge in cancer patients, particularly those with lung cancer, breast cancer, and melanoma. The prognosis is poor, with median overall survival times measured in months for most patient populations. Established treatments include neurosurgical resection, radiotherapy (including stereotactic radiosurgery and stereotactic radiotherapy, whole-brain radiotherapy, and new radiation techniques), and supportive care measures. Recently, more and more targeted therapies such as EGFR inhibitors, HER2 antagonists, BRAF inhibitors, ALK inhibitors, and immune checkpoint inhibitors are demonstrating some efficacy in brain metastasis patients and should be considered in the clinical setting.
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Shah, Aali. Hypomagnesemia/Hypermagnesemia. Edited by Matthew D. McEvoy and Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0039.
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Hypomagnesemia is a relatively common electrolyte abnormality that may produce little to no significant clinical manifestations in patients. Commonly used medications such as proton-pump inhibitors and antidepressants can cause magnesium deficiency. The primary cardiac effect of hypomagnesemia is a prolongation of the Q-T interval. It is exposure to other drugs in the perioperative period and physiologic changes caused by anesthesia and surgery that can further alter cardiac electrophysiology and lead to serious ventricular dysrhythmias. Hypermagnesemia is generally iatrogenic from excessive ingestion, renal failure, or therapeutic administration for preeclampsia. Adverse effects of hypermagnesemia include somnolence, muscle weakness, and slowing of cardiac conduction.
12
Chong, Ji Y., and Michael P. Lerario. Forget About It. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190495541.003.0037.
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Cognitive impairment is common following stroke. The clinical course and presentation are variable in vascular dementia, but the diagnosis can often be tied to recent vascular events or to progressive white matter lesions on MRI. Because there is considerable overlap between patients with vascular and Alzheimer’s type dementia, both acetylcholinesterase inhibitors and memantine have been tried off-label to treat the cognitive symptoms of vascular dementia with mixed results.
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Waldmann, Carl, Neil Soni, and Andrew Rhodes. Cardiovascular drugs. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199229581.003.0011.
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β-Adrenergic agonists 166Phosphodiesterase inhibitors 168Vasodilators 170Vasopressors 174Antiarrhythmic agents 176Chronotropes 178Antianginal agents 182Antiplatelet agents 184Diuretics and the critically ill 186Levosimendan 190β-Adrenergic agents are used commonly for cardiovascular support in critical care to increase cardiac output via ...
14
Schneier, Franklin R., Hilary B. Vidair, Leslie R. Vogel, and Philip R. Muskin. Anxiety, Obsessive-Compulsive, and Stress Disorders. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199326075.003.0006.
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Patients with generalized anxiety disorder experience anxiety related to multiple areas, such as work, finances, and illness. Discrete, unexpected panic attacks and anticipatory anxiety characterize patients with panic disorder. Patients with social anxiety disorder have fear of embarrassment in social situations. Patients with obsessive-compulsive disorder are preoccupied with and distressed by inappropriate thoughts, urges, and images. The four cardinal features of posttraumatic stress disorder are intrusive reexperiencing of the initial trauma, avoidance, persistent negative alterations in cognitions and mood, and alterations in arousal and activity. One element common to patients suffering from most of the anxiety disorders is an elevated sensitivity to threat, which appears to involve brain systems identified to mediate “fear” responses, including the amygdala. The selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs) are the first-line pharmacotherapy treatment for obsessive-compulsive disorder and most of the anxiety and stress disorders. Cognitive-behavioral therapy for anxiety, obsessive-compulsive, and stress disorders is an empirically validated time-limited treatment.
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Bowker, Lesley K., James D. Price, Ku Shah, and Sarah C. Smith. Psychiatry. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198738381.003.0009.
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This chapter provides information on cognitive ageing, impairments in cognitive function without dementia, overview of dementia, assessment of dementia, dementia and common diseases, dementia and parkinsonism, normal pressure hydrocephalus, dementia and less common diseases, general management of dementia, risk management and abuse in dementia, prevention of dementia, use of acetylcholinesterase inhibitors in dementia, other drug treatments for dementia, managing behavioural problems in dementia, compulsory detention and treatment, psychosis, diagnosis of delirium, causes of delirium, clinical assessment of delirium, treatment issues in delirium, non-drug management of delirium, drug treatments for delirium, confusion and alcohol, squalor syndrome, presentation of depression, clinical features of depression, non-drug management of depression, drug treatments for depression, and suicide and attempted suicide.
16
Hill, Juniper. Becoming Creative. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780199365173.001.0001.
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How are an individual’s ability and motivation to be creative shaped by the world around her? Why does creativity seem to flourish in some environments, while in others it is stifled? Many societies value creativity as an abstract concept and many, perhaps even most, individuals feel an internal drive to be creative; however, tremendous social pressures restrict development of creative skill sets, engagement in creative activities, and willingness to take creative risks. Becoming Creative explores how social and cultural factors enable or inhibit creativity in music. The book integrates perspectives from ethnomusicology, education, sociology, psychology, and performance studies, prioritizing the voices of practicing musicians and music educators. Insights are drawn from ethnographic research and in-depth interviews with classical, jazz, and traditional musicians in South Africa, Finland, and the United States. By comparing and analyzing these musicians’ personal experiences, Becoming Creative deepens our understanding of the development and practice of musical creativity, the external factors that influence it, and strategies for enhancing it. The book reveals the common components of how musical creativity is experienced across these cultures and explains why creativity might not always be considered socially desirable. It identifies ideal creativity-enabling criteria—specific skill sets, certain psychological traits and states, and access to opportunities and authority—and illustrates how these enablers of creativity are fostered or thwarted by a variety of beliefs, learning methods, social relationships, institutions, and social inequalities. Becoming Creative further demonstrates formal and informal strategies for overcoming inhibitors of creativity.
17
O’Neal, M. Angela. Acute Headache in Pregnancy. Edited by Angela O’Neal. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190609917.003.0020.
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The case illustrates the characteristics of pituitary apoplexy. This anatomy of the pituitary, which predisposes to the condition, is described. The most common clinical feature is headache. Visual disturbance related to optic chiasm or optic nerve involvement is also common. Pituitary apoplexy is a neuroendocrine emergency. The most important hormone involved is adrenocorticotropic hormone, ACTH. However, there are often multiple hormonal deficiencies: growth hormone, hypothyroidism, and hypogonadotropic deficiency. A high prolactin level may reflect a prolactinoma or be due to hypothalamic inhibition. Diabetes insipidus (DI) is also common. The most urgent issue in treating pituitary apoplexy is prompt assessment of fluid and electrolyte imbalance and the replacement of corticosteroids.
18
Deramecourt, Vincent, Florence Lebert, and Florence Pasquier. Frontotemporal dementia. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199644957.003.0036.
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Frontotemporal dementia (FTD) is the second most common form of dementia in persons younger than 65 years after Alzheimer’s disease. The FTD spectrum is characterized by clinical, molecular and genetic heterogeneity. Core features of FTD are behavioural and language manifestations and the clinical spectrum of FTD currently includes a behavioural variant, progressive nonfluent aphasia and semantic dementia. The most common behavioural features are disinhibition, apathy, loss of empathy, hyperorality and perseveration. Neuroimaging usually demonstrates focal atrophy and hypometabolism in the anterior part of the frontal and temporal lobes. A careful history and neuropsychological examination, and judicious use of neuroimaging, can help distinguish FTD from other common forms of dementia, especially Alzheimer’s disease, vascular dementia, and dementia with Lewy bodies. Although no specific pharmacological treatments for FTD exists, symptom management with serotonin reuptake inhibitors and non pharmacological interventions have been shown to be beneficial.
19
Thornton, Kevin, and Michael Gropper. Diagnosis, assessment, and management of hyperthermic crises. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0247.
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Malignant hyperthermia, the neuroleptic malignant syndrome (NMS), and the serotonin syndrome are the principal disorders associated with life-threatening hyperthermia in the intensive care unit. While each is a clinically unique entity, all can progress to multisystem organ dysfunction with acidosis, shock, and death. MH usually results from exposure to halogenated volatile anaesthetics and/or succinylcholine and symptoms of increased CO2 production and respiratory acidosis progress rapidly without prompt intervention, including the administration of dantrolene. NMS is a syndrome of rigidity and altered mental status seen most commonly in patients being treated with antipsychotic medications. The serotonin syndrome is seen in patients treated with serotonergic agents including selective serotonin reuptake or monoamine oxidase inhibitors and tricyclic antidepressants. The salient clinical finding is clonus, but agitation, altered mental status and autonomic dysfunction are common. Recognizing the non-specific features of these syndromes presents a challenge as they are life-threatening if not treated promptly and correctly with specific therapies.
20
Woywodt, Alexander, and Diana Chiu. Drug-induced and toxic glomerulopathies. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0082.
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Glomerulopathies induced by particular exogenous compounds or molecules include those attributable to toxicity, and those caused by inducing an immune or autoimmune response. Tubules are more commonly the target of toxicity as they absorb and concentrate components of filtrate. Damage to endothelial cells may account for thrombotic microangiopathy in response to calcineurin inhibitors. Endothelial cells are also likely to be the target in drug-induced small vessel vasculitis. Toxicity to podocytes accounts for focal segmental glomerulosclerosis caused by pamidronate and other agents. Chloroquine can cause a remarkable pseudo-storage disorder with inclusions in podocytes that resemble those seen in Fabry disease. The mechanism by which drugs cause minimal change disease, another podocyte disorder, is not known. Membranous nephropathy may be caused by exposure to gold, mercury, and some other drugs; this is antibody mediated and presumably the targets are altered podocyte surface molecules. Inhibitors of the mammalian target of rapamycin (mTOR) cause proteinuria, possibly through effects on vascular endothelial growth factor, inhibitors of which are associated with not only proteinuria (an expected podocyte effect) but also thrombotic microangiopathy (endothelial cell effect). This latter may be through disturbing podocyte-endothelium cross-signaling.
21
Hart, Ashley S., and Martha A. Niemiec. Comorbidity and Personality in Body Dysmorphic Disorder. Edited by Katharine A. Phillips. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190254131.003.0011.
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Comorbidity is common in body dysmorphic disorder (BDD). Major depressive disorder, social anxiety disorder (social phobia), obsessive-compulsive disorder, and substance use disorders are the most frequently co-occurring Axis I conditions. Except for eating disorders (more common in women) and substance use disorders (more common in men), Axis I comorbidity rates in BDD appear similar across genders. Axis I comorbidity is associated with greater functional impairment and morbidity. Rates of comorbid personality disorders in BDD are high. Disorders from cluster C occur most frequently, with avoidant personality disorder the most common. Associated traits include low self-esteem and high levels of neuroticism, introversion, unassertiveness, social anxiety and inhibition, rejection sensitivity, and perfectionism. Research is needed on the relationship between BDD and psychiatric comorbidity, the causes and consequences of comorbidity in BDD, and the relationship between BDD and associated personality traits.
22
(Editor), Robert A. Greenwald, New York Academy of Sciences (Corporate Author), and Lorne M. Golub (Editor), eds. Inhibition of Matrix Metalloproteinases: Therapeutic Potential (Annals of the New York Academy of Sciences). New York Academy of Sciences, 1994.
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23
Chakera, Aron, William G. Herrington, and Christopher A. O’Callaghan. Disorders of plasma potassium. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0173.
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Potassium is the major intracellular cation, and maintenance of potassium homeostasis is critical for normal cellular function. Serum potassium levels usually range from 3.5–4.5 mmol/l (compared with intracellular levels of ~150 mmol/l). Hypokalaemia is defined as a serum potassium level <3.5 mmol/l, and hyperkalaemia as a serum potassium level >4.5 mmol/l. Hyperkalaemia occurs in over 5% of hospitalized patients, and is most common in older age groups, where it is associated with renal impairment and medication use. Medications that block the renin–angiotensin system, such as angiotensin-converting-enzyme inhibitors and angiotensin receptor blockers, are often responsible. Hypokalaemia is also common, affecting over 15% of hospitalized patients, and is usually related to diuretic use, gastrointestinal losses, or inadequate potassium in the diet. This chapter reviews the causes and management of derangements of plasma potassium.
24
Burger, John. Side Effects of Medications and Mitigation Strategies. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190461508.003.0009.
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Sexual dysfunction is a common side effect of many common medications, including the first-line agents for treating post-traumatic stress disorder (PTSD), traumatic brain injury (TBI), and attention-deficit hyperactivity disorder (ADHD). Selective serotonin and norepinephrine reuptake inhibitors have been especially well studied. This chapter reviews the different classes of medications used to treat PTSD, TBI, and ADHD that can cause sexual side effects as well as several strategies important in understanding the source of sexual symptoms. Specific mitigation strategies are then reviewed, including changing the dose, switching within a class, switching to a different class, adding an augmenting agent, watching and waiting, and taking drug holidays. Key research supporting each strategy is presented and discussed with consideration for the typical responses of both men and women. Strength of research is also weighed. Finally, some considerations for future treatment strategies are considered.
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Newell-Price, John, Alia Munir, and Miguel Debono. Primary hyperparathyroidism. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0187.
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Primary hyperparathyroidism is a disorder of bone mineralization and renal physiology due to excess parathyroid hormone secretion. Parathyroid hormone (PTH) is produced and released by the parathyroid chief cells, under regulation of the G- protein-coupled calcium-sensing receptor. Primary hyperparathyroidism occurs when there is a loss of the inhibitory feedback of PTH release by extracellular calcium. The rise in PTH levels is initially associated with a normal serum calcium, and then over time with hypercalcaemia. The most common cause of primary hyperparathyroidism is a benign solitary adenoma (80%). Other causes include multiple adenomas and hyperplasia. This chapter reviews the causes, clinical features, and management of primary hyperparathyroidism.
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(Editor), Robert A. Greenwald, New York Academy of Sciences (Corporate Author), and Lorne M. Golub (Editor), eds. Inhibition of Matrix Metalloproteinases: Therapeutic Potential (Annals of the New York Academy of Sciences, Vol 732). New York Academy of Sciences, 1994.
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27
Odlaug, Brian L., and Jon E. Grant. Phenomenology and Epidemiology of Pathological Skin Picking. Edited by Jon E. Grant and Marc N. Potenza. Oxford University Press, 2012. http://dx.doi.org/10.1093/oxfordhb/9780195389715.013.0070.
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Pathological skin picking (PSP), or neurotic excoriation, is characterized by the repetitive and compulsive picking of skin, causing tissue damage. It appears to have a prevalence rate of 1.4%–5.4% in the general population and is seen predominantly in females in clinical settings. Individuals with PSP may pick for hours each day, resulting in significant scarring, infections, and medical complications. Although PSP is common, most individuals with this disorder are unaware of treatment options and thus often do not seek treatment. Co-occurring psychiatric conditions are common in PSP, with depressive, anxiety, and obsessive-compulsive disorders presenting as the most prevalent conditions. Significant psychosocial impairment and activity avoidance due to shame and embarrassment are frequent. Neurocognitive research has recently shown that individuals with PSP have deficits in inhibitory control, a finding similar to that found in trichotillomania. From a public health perspective, concurrent collaboration between dermatology and the behavioral sciences is imperative for future advances in the understanding and treatment of PSP.
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D’Mello, Ajay. Mitochondrial Disease. Edited by Kirk Lalwani, Ira Todd Cohen, Ellen Y. Choi, and Vidya T. Raman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190685157.003.0047.
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Mitochondrial disease is now considered to be an important cause for a diverse range of neurological, muscular, cardiac and endocrine disorders. Initially thought to be a rare group of disorders, it is now increasingly common for children with mitochondrial disease to present for a surgical procedure. While the mitochondrial respiratory chain is the essential finally common pathway for aerobic metabolism, mitochondria also play a role in a several important cellular processes. A variety of anesthetic techniques have been successfully used for this group of patients. However, the possibility of complications due to inhibition of mitochondrial function by anesthetic agents and surgical stress is a worry for the physician managing these patients. Anesthetic management focuses on disease symptoms at presentation, maintaining normoglycemia, while preventing further metabolic stress and complications that worsen lactic acidosis.
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Fomberstein, Kenneth, Marissa Rubin, Dipan Patel, John-Paul Sara, and Abhishek Gupta. Perioperative Opioid Analgesics of Use in Pain Management for Spine Surgery. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190626761.003.0004.
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This chapter compares the basic properties of several opioid analgesics and explores their applications in perioperative pain control in spine surgery. Parenteral opioids have long been the cornerstone of treatment for postoperative pain; they work by inhibiting voltage-gated calcium channels and increasing potassium influx, which results in reduced neuronal excitability, thereby inhibiting the ascending transmission of painful stimuli and activating the descending inhibitory pathways. This chapter reviews concepts including opioid conversion and rotation, opioid tolerance, and opioid cross-tolerance. It discusses common opioid side effects, and it explores the perioperative use of several specific opioids including remifentanil, sufentanil, methadone, oxycodone, morphine, and tapentadol and discusses their use in spine surgery. Additionally, this chapter discusses patient-controlled analgesia (PCA) and its importance in postoperative pain control.
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Greenberg, Jennifer L., Alexandra Sullivan, and Sabine Wilhelm. Treating Children and Adolescents with Body Dysmorphic Disorder. Edited by Katharine A. Phillips. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190254131.003.0028.
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Body dysmorphic disorder (BDD) is a common and severe disorder that typically has its onset during adolescence. Youth with BDD appear more severely ill than adults in terms of having poorer insight and a higher likelihood of having attempted suicide. Despite BDD’s severity and early onset, there is only limited research on its treatment in youth. Cognitive-behavioral therapy (CBT) and serotonin reuptake inhibitors (SRIs) are the first-line treatments for BDD in adults and appear to be effective for adolescents with BDD. This chapter provides an overview of the treatment of BDD in youth, including cognitive-behavioral and pharmacologic approaches, and an illustrative case example. The chapter also addresses cosmetic treatment for BDD in children and adolescents, which appear to be ineffective.
31
Graham, Andrew, and Clare Galton. Nervous system. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0018.
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Rheumatological conditions may be complicated by a variety of both central and peripheral nervous system disorder. Common complications such as entrapment neuropathies are familiar to rheumatologists but accurate diagnosis of less common neurological disorders may be challenging; careful clinical reasoning is essential, supplemented where necessary by imaging, neurophysiology, and other special investigations including cerebrospinal fluid examination. Complications vary according to the nature of background condition. In rheumatoid arthritis, neurological involvement is typically related to the mechanical consequences of advancing disease; the commonest complications are carpal tunnel syndrome and cervical myelopathy due to atlantoaxial subluxation. By contrast, neurological involvement in systemic lupus erythematosus (SLE) tends to occur earlier in the disease course, with a much wider range of manifestations. The management of stroke or seizures in SLE is not necessarily any different from that in the general population, unless complicated by the antiphospholipid syndrome. However, less common neurological syndromes may demand more specific investigation and treatment. For example, longitudinally extensive transverse myelitis and recurrent optic neuritis (neuromyelitis optica, or Devic's disease) is frequently associated with antibodies to aquaporin-4, and is highly likely to relapse unless treated vigorously with humoral immunosuppression. Nervous system involvement in vasculitis is common. Finally, not all neurological disorder in rheumatological disease is necessarily due to the underlying condition; neurological complications of disease-modifying therapy are increasingly recognized, in particular central and peripheral nervous system demyelination associated with TNF-α inhibitors.
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Meyrier, Alain, and Patrick Niaudet. Primary focal segmental glomerulosclerosis. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0058_update_001.
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The proportion of cases of primary focal segmental glomerulosclerosis responsive to treatment with corticosteroids is variable and depends on histological type, patient age and duration, and dose of steroid treatment, but overall complete remission rate is estimated at 20–25% in white and Asian patients, and lower in black patients. Partial response dependent on a high dose of steroids is common. Despite anxieties about nephrotoxicity, there may be justification for adding calcineurin inhibitors to control nephrotic syndrome if it is severe. Data for additional agents is not very encouraging. Plasma exchange appears to remove a circulating factor that causes proteinuria in focal segmental glomerulosclerosis, as illustrated by responses to this treatment when proteinuria recurs acutely after kidney transplantation. This is rarely pursued clinically except after transplantation, in advance of severe glomerular injury.
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Beach, Scott R., and Theodore A. Stern. Antidepressants in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0044.
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Selective serotonin reuptake inhibitors (SSRIs), serotonin norepinephrine reuptake inhibitors (SNRIs), and atypical antidepressants are considered first-line agents for depression in the intensive care unit (ICU) setting, and are preferred over older antidepressants due to their more benign side effect profile and tolerability. This chapter reviews the literature on the use of antidepressants in the ICU. Common side effects of SSRIs include insomnia and gastrointestinal discomfort, while citalopram may uniquely cause prolongation of the QTc interval. All SSRIs carry a risk for the development of serotonin syndrome following overdose. SNRIs are similar to SSRIs in their side effect profile, although they are more likely to cause hypertension. Mirtazapine is strongly associated with sedation and weight gain. Stimulants may also be used to treat depression in the medically ill, and can be particularly effective in treating apathy, low energy, and loss of appetite. Monotherapy is typically the initial treatment strategy and low doses are generally recommended in the ICU setting. Efficacy may not be apparent for up to 8 weeks. Patients who have been taking an antidepressant prior to their arrival in the ICU should continue on the medication so as to prevent discontinuation syndrome. Delirium may warrant cessation of the antidepressant and potentially dangerous medication interactions also need to be evaluated. At present, there is no evidence to suggest that an antidepressant should be initiated after a significant physical or emotional trauma.
34
Lameire, Norbert. Prevention of acute kidney injury. Edited by Norbert Lameire. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0224_update_001.
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The prevention of acute kidney injury (AKI) should start with an assessment of the risk to develop AKI, by identification of co-morbidities, use of potentially nephrotoxic medications, and early recognition of acute reversible risk factors associated with AKI. This chapter discusses first the most relevant general risk factors for AKI and describes the recent introduction of several surveillance systems. In addition, some specific risk factors play a role in the pathogenesis of post-cardiac surgery AKI. Finally risks associated with commonly used drugs such as non-steroidal anti-inflammatory drugs, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, statins, and warfarin are considered.
35
Kortgen, Andreas, and Michael Bauer. The effect of acute hepatic failure on drug handling in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0197.
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Impaired hepatic function is a common event in intensive care unit patients and as the liver plays a central role in drug metabolism and excretion this may lead to profound changes in pharmacokinetics. Underlying mechanisms are altered enzyme function of phase I and phase II metabolism, altered transporter protein function together with cholestasis and hepatic perfusion disorders. Moreover, multidrug therapy may lead to induction and inhibition of these enzymes and transporter proteins. In addition, changes in plasma protein binding and volumes of distribution of drugs are common. Altogether, these changes may not only lead to sometimes unpredictable plasma levels of xenobiotics, but also to drug-induced liver injury when hepatocellular accumulation of noxious substances occurs. Concomitant renal dysfunction may further complicate this situation. Pharmacodynamic alterations might also occur. In conclusion, the clinician must carefully evaluate medication given to patients with hepatic failure. Therapeutic drug monitoring should be performed wherever available to guide therapy.
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Frawley, Geoff. Mucopolysaccharidoses. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199764495.003.0064.
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The mucopolysaccharidoses (MPS) are a group of seven chronic progressive diseases caused by deficiencies of 11 different lysosomal enzymes required for the catabolism of glycosaminoglycans (GAGs). Hurler syndrome (MPS IH) is an autosomal recessive storage disorder caused by a deficiency of α-L-iduronidase. Hunter syndrome (MPS II) is an X-linked recessive disorder of metabolism involving the enzyme iduronate-2-sulfatase. Many of the MPS clinical manifestations have potential anesthetic implications. Significant airway issues are particularly common due to thickening of the soft tissues, enlarged tongue, short immobile neck, and limited mobility of the cervical spine and temporomandibular joints. Spinal deformities, hepatosplenomegaly, airway granulomatous tissue, and recurrent lung infections may inhibit pulmonary function. Odontoid dysplasia and radiographic subluxation of C1 on C2 is common and may cause anterior dislocation of the atlas and spinal cord compression.
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Bleck, Thomas P. Pathophysiology and causes of seizures. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0231.
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Seizures result from imbalances between excitation and inhibition, and between neuronal synchrony and dyssynchrony. Current models implicate the cerebral cortex in the genesis of seizures, although thalamic mechanisms (particularly the thalamic reticular formation) are involved in the synchronization of cortical neurons. Often, the precipitants of a seizure in the critical care setting are pharmacological. Several mechanisms linked to critical illness can lead to seizures. Failure to remove glutamate and potassium from the extracellular space, functions performed predominantly by astrocytes, occurs in trauma, hypoxia, ischaemia, and hypoglycaemia. Loss of normal inhibition occurs during withdrawal from alcohol and other hypnosedative agents, or in the presence of GABA. Conditions such as cerebral trauma, haemorrhages, abscesses, and neoplasms all produce physical distortions of the adjacent neurons, astrocytes, and the extracellular space. Deposition of iron in the cortex from the breakdown of haemoglobin appears particularly epileptogenic. Although acute metabolic disturbances can commonly produce seizures in critically-ill patients, an underlying and potentially treatable structural lesion must always be considered and excluded.
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Buckholtz, Joshua W., and Andreas Meyer-Lindenberg. Genetic Perspectives on the Neurochemistry of Human Aggression and Violence. Edited by Turhan Canli. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199753888.013.009.
Full textAbstract:
Violence is a devastating social phenomenon that is costly both to affected individuals and to society at large. Pathological aggression, especially reactive/impulsive aggression, is a cardinal symptom common to several psychiatric disorders—including antisocial personality disorder, borderline personality disorder, and psychopathy—that are associated with risk for violence. Thus, understanding the factors that predispose people to impulsive violence represents a crucial goal for psychology, neuroscience, and psychiatry. Although we are far from a full understanding of the etiopathophysiology of violence, impulsive aggression is heritable, suggesting that genetic mechanisms may be important for determining individual variation in susceptibility. This chapter synthesizes available preclinical and human data to propose a compelling neurogenetic mechanism for violence, specifically arguing that a genetically determined excess in serotonin signaling during a critical developmental period leads to dysregulation within a key corticolimbic circuit for emotional arousal and regulation, inhibitory control, and social cognition.
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Tamimi, Rulla, Susan Hankinson, and Pagona Lagiou. Breast Cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190676827.003.0016.
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Most of the established reproductive risk factors for breast cancer, like age at menarche or parity, are not appropriate for public health intervention. Several lines of evidence, like the associations with birthweight and early exposure to radiation, support an important influence of early-life events on subsequent breast cancer risk. The best established modifiable risk factors for the disease include postmenopausal hormone use, moderate alcohol intake, and adult weight gain. More recently, we have come to appreciate that instead of a single disease, breast cancer is rather a heterogeneous group of subtypes with different etiologies. Yet the wealth of available epidemiologic information can be synthesized into a consistent and testable, albeit still hypothetical, causal model. With our increasing knowledge on the relation between endogenous hormones and breast cancer, and the development of selective estrogen receptor modulators, as well as aromatase inhibitors, chemoprevention will likely become more common in the future.
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Finnerup, Nanna Brix, and Troels Staehelin Jensen. Management issues in neuropathic pain. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0133.
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Neuropathic pain is a common complication to cancer, cancer treatment, HIV, and other conditions that may affect the somatosensory nervous system. Neuropathic pain may be present in up to 40% of cancer patients and may persist independently of the cancer and affect the quality of life in disease-free cancer survivors. Particular surgical treatment and chemotherapy may cause chronic persistent neuropathic pain in cancer survivors. The diagnosis of neuropathic pain can be challenging and requires documentation of a nervous system lesion and pain in areas of sensory changes. The pharmacological treatment may include tricyclic antidepressants, selective serotonin noradrenaline reuptake inhibitors (duloxetine or venlafaxine), calcium channel α2↓ agonists (gabapentin or pregabalin), and opioids. Topical lidocaine and capsaicin, NMDA antagonists, carbamazepine, oxcarbazepine, and cannabinoids may be indicated. Due to limited efficacy or intolerable side effects at maximal doses, combination therapy is often required and careful monitoring of effect and adverse reactions is important.
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Thiruchelvam, Nikesh. Benign prostatic hyperplasia. Edited by Christopher R. Chapple. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0057.
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Male lower urinary tract symptoms (LUTS) has a multifactorial aetiology and is not simply solely due to bladder outflow obstruction (BOO) from benign prostatic hyperplasia (BPH). Other causes of LUTS include bladder dysfunction, malignant prostatic disease, urethral disease, and medical conditions such as polyuria and sleep disorders. In an ageing population, LUTS and BPH will become more common. BOO can only be diagnosed by urodynamic evaluation, although treatment can be started before requiring this invasive investigation. Once considered the only treatment option for BOO, open prostatectomy has been surpassed by TURP and over the past few decades by medical therapy for BPH. α-blockers and 5-α reductase inhibitors improve LUTS and in combination, can reduce the progression of BPH. There are now many competing surgical options for TURP including a variety of laser ablating and enucleating techniques. To date, no one endourological option shows superiority on outcome and complication rates.
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Covic, Adrian, Mugurel Apetrii, Luminita Voroneanu, and David J. Goldsmith. Vascular calcification. Edited by David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0120_update_001.
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Vascular calcification (VC) is a common feature of patients with advanced CKD and it could be, at least in part, the cause of increased cardiovascular mortality in these patients. From a morphologic point of view, there are at least two types of pathologic calcium phosphate deposition in the arterial wall—namely, intima calcification (mostly associated with atherosclerotic plaques) and media calcification (associated with stiffening of the vasculature, resulting in significantly adverse cardiovascular outcomes). Although VC was viewed initially as a passive phenomenon, it appears to be a cell-mediated, dynamic, and actively regulated process that closely resembles the formation of normal bone tissue, as discovered recently. VC seems to be the result of the dysregulation of the equilibrium between promoters and inhibitors. The determinants are mostly represented by altered calcium and phosphorus metabolism, secondary hyperparathyroidism, vitamin D excess, high fibroblast growth factor 23, and high levels of indoxyl sulphate or leptin; meanwhile, the inhibitors are vitamin K, fetuin A, matrix G1a protein, osteoprotegerin, and pyrophosphate. A number of non-invasive imaging techniques are available to investigate cardiac and vascular calcification: plain X-rays, to identify macroscopic calcifications of the aorta and peripheral arteries; two-dimensional ultrasound for investigating the calcification of carotid arteries, femoral arteries, and aorta; echocardiography, for assessment of valvular calcification; and, of course, computed tomography technologies, which constitute the gold standard for quantification of coronary artery and aorta calcification. All these methods have a series of advantages and limitations. The treatment/ prevention of VC is currently mostly around calcium-mineral bone disease interventions, and unproven. There are interesting hypotheses around vitamin K, Magnesium, sodium thiosulphate and other potential agents.
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Krueger, Darcy A., and Jamie Capal. Familial CNS Tumor Syndromes. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0136.
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Tuberous sclerosis complex is an autosomal dominant multi-system disease that involves the skin, brain, heart, lungs, and kidneys and is associated with seizures including infantile spasms, intellectual disability, autism and pulmonary and heart disease. Skin lesions can be particularly disfiguring and infantile spasms can be associated with marked cognitive decline. The outlook for patients has improved markedly with the recognition that TSC is caused by upregulation of the mammalian target of rapamycin (mTOR) enzyme, which connects energy needs and supply with cellular and neuronal growth. mTOR is upregulated in TSC because of mutations in hamartin or tuberin, which normally serve as a brake on mTOR. The drug rapamycin is commonly used as an immunosuppressive for patients undergoing kidney transplants; it has also found a new use in patients with TSC. Although the drug is immunosuppressive for non-TSC patients, careful titration of the drug in TSC patients corrects its upregulation but is not particulary immunosuppressive. Additional mTOR inhibitors such as everolimus have been developed and have been shown to be effective for pulmonary disease associated with TSC. Rapamycin in ointment form is dramatically effective in suppressing skin lesions of TSC and studies are underway to test the effect of mTOR inhibitors on seizures, brain tubers, intellect, and features of autism. Infantile spasms associated with TSC are very responsive to vigabatrin.
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Dixon, Bradley P., J. Christopher Kingswood, and John J. Bissler. Tuberous sclerosis complex renal disease. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0330.
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Tuberous sclerosis complex (TSC) is an autosomal dominant genetic disorder affecting almost all organs. It has wider phenotypic variation than often appreciated, with less than half showing the combination of characteristic facial angiofibromas, epilepsy, and mental retardation. Renal angiomyolipomata or cysts are found in 90% and renal failure was historically a common mode of adult death from the disease. Pulmonary lymphangioleiomyomatosis is restricted to females. Angiomyolipomata or cystic disease, or both, may cause renal failure. Angiomyolipomata may also haemorrhage, especially from larger lesions. Manifestations of brain involvement substantially complicate management of many patients with TSC. The causative genes TSC1 and TSC2 encode tuberin and hamartin which are involved in control of the mammalian target of rapamycin pathway. Inhibitors of that pathway, such as sirolimus and everolimus, are therefore logical approaches to therapy and have been shown to be effective in reducing angiomyolipomata volume. It remains to be seen whether they can protect renal function.
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Kang, Duk-Hee, and Mehmet Kanbay. Urate nephropathy. Edited by Adrian Covic. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0092.
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Gout is a disorder of purine metabolism, characterized by hyperuricaemia and urate crystal deposition within and around the joints. The recognition of increased comorbidity burden in patients with gout rendered it as a systemic disorder rather than simply a musculoskeletal condition. Gout nephropathy (also known as chronic uric acid nephropathy or urate nephropathy) is a form of chronic tubulointerstitial nephritis, induced by deposition of monosodium urate crystals in the distal collecting ducts and the medullary interstitium, associated with a secondary inflammatory reaction. Other renal histologic changes include arteriolosclerosis, glomerulosclerosis, and tubulointerstitial fibrosis. In patients with urate nephropathy, hypertension is common, but usually there is only mild proteinuria and a slight increase in serum creatinine. The reduction of serum uric acid, using xanthine oxidase inhibitors and perhaps low-purine diet, is the mainstay of therapy. There is current research around the question of whether it is beneficial to lower serum uric acid in asymptomatic patients with renal disease or with cardiovascular risk factors.
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Cummings, Jeffrey L., and Kate Zhong. Clinical Trials and Drug Development in Neurodegenerative Diseases. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0018.
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This chapter describes the common therapeutic targets, approaches to clinical trial design, biomarkers, and therapeutic interventions across neurodegenerative disorders (NDDs). Each unique NDD-Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), etc.-has a unique phenotype associated with the regional cell population most affected. Each disease, however, is associated with protein misfolding, oxidation, inflammation, apoptosis, and cell death. If vulnerable cell populations include transmitter source nuclei, transmitter deficits also emerge (e.g. cholinergic abnormalities in AD and dopaminergic deficits in PD). Biomarkers show regionally appropriate brain atrophy or process-related cerebrospinal deficits. Clinical trial designs share features for symptomatic interventions (e.g. cholinesterase inhibitors in AD and dopamine agents in PD) and disease-modifying therapies. Biomarkers play similar roles in trials for NDD, including demonstrating target engagement and supporting disease modification. No disease-modifying therapies have been approved for any NDDs; all programs face similar pharmacokinetic, pharmacodynamic, and regulatory challenges in therapeutic development.
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Leung, Doris G. Other Proven and Putative Autoimmune Disorders of the Peripheral Nervous System. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0098.
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Myasthenia gravis is in most cases an autoimmune disorder of the neuromuscular junction in which antibodies are directed at nicotinic acetylcholine receptors or other synaptic proteins, such as the MusK protein that is involved in the formation of the formation and maturation of the motor endplate. Less commonly, myasthenia gravis can result from antibodies directed to presynaptic calcium channels as a side effect of paraneoplastic antibodies (Lambert-Eaton syndrome) or from a developmental paucity of acetylcholine receptors in the neonatal form of the disease. Treatment is usually a combination of aceetylcoholinesterase inhibitors such as pyridostigmine to prolong the life of acetylcholine released at the neuromuscular junction and/or drugs such as corticosteroids aimed at reducing inflammation.
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Groeneveld, A. B. J., and Alexandre Lima. Vasodilators in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0035.
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Vasodilators are commonly used in the intensive care unit (ICU) to control arterial blood pressure, unload the left or the right heart, control pulmonary artery pressure, and improve microcirculatory blood flow. Vasodilator refers to drugs acting directly on the smooth muscles of peripheral vessel walls and drugs are usually classified based on their mechanism (acting directly or indirectly) or site of action (arterial or venous vasodilator). Drugs that have a predominant effect on resistance vessels are arterial dilators and drugs that primarily affect venous capacitance vessels are venous dilators. Drugs that interfere with sympathetic nervous system, block renin-angiotensin system, phosphodiesterase inhibitors, and nitrates are some examples of drugs with indirect effect. Vasodilator drugs play a major therapeutic role in hypertensive emergencies, primary and secondary pulmonary hypertension, acute left heart, and circulatory shock. This review discusses the main types of vasodilators drugs commonly used in the ICU.
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Gill, Steven J., and Michael H. Nathanson. Central nervous system pathologies and anaesthesia. Edited by Philip M. Hopkins. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0081.
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Anaesthesia induces changes in many organ systems within the body, though clearly none more so than the central nervous system. The physiology of the normal central nervous system is complex and the addition of chronic pathology and polypharmacy creates a significant challenge for the anaesthetist. This chapter demonstrates a common approach for the anaesthetist and specific considerations for a wide range of neurological conditions. Detailed preoperative assessment is essential to gain understanding of the current symptomatology and neurological deficit, including at times restrictions on movement and position. Some conditions may pose challenges relating to communication, capacity, and consent. As part of the consent process, patients may worry that an anaesthetic may aggravate or worsen their neurological disease. There is little evidence to support this understandable concern; however, the risks and benefits must be considered on an individual patient basis. The conduct of anaesthesia may involve a preference for general or regional anaesthesia and requires careful consideration of the pharmacological and physiological impact on the patient and their disease. Interactions between regular medications and anaesthetic drugs are common. Chronically denervated muscle may induce hyperkalaemia after administration of succinylcholine. Other patients may have an altered response to non-depolarizing agents, such as those suffering from myasthenia gravis. The most common neurological condition encountered is epilepsy. This requires consideration of the patient’s antiepileptic drugs, often relating to hepatic enzyme induction or less commonly inhibition and competition for protein binding, and the effect of the anaesthetic technique and drugs on the patient’s seizure risk. Postoperative care may need to take place in a high dependency unit, especially in those with limited preoperative reserve or markers of frailty, and where the gastrointestinal tract has been compromised, alternative routes of drug delivery need to be considered. Overall, patients with chronic neurological conditions require careful assessment and preparation, a considered technique with attention to detail, and often higher levels of care during their immediate postoperative period.
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McCulloh, Russell J., and Steven M. Opal. Drug-induced depression of immunity in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0290.
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Immunosuppressive drugs are among the fastest-growing category of drugs in medicine today, both in terms of new medication development and in terms of use. Glucocorticoids, calcineurin inhibitors, and biological agents, among others, are used in a variety of diseases. . Although often of great benefit to patients, immunosuppressive agents also pose significant long-term risks for opportunistic infection. These drugs can also blunt normal host responses to infection, and patients receiving immunosuppressive medications are at high risk for severe illness, sepsis, and death from opportunistic infections. Knowledge of immunosuppressive agents, their mechanisms of action, effects on the immune system, and commonly-associated infectious complications plays an instrumental role in guiding appropriate diagnostic and treatment plans for immunosuppressed patients. This chapter reviews the most commonly-used immunosuppressive agents today, and provides the reader with the specific effects these medications can have on a patient’s immune system and the potential infectious agents of concern associated with their prolonged use.