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Books on the topic 'Multisystemic therapy'

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Author: Grafiati
Published: 4 June 2021
Last updated: 12 February 2022

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1

W, Henggeler Scott. Multisystemic therapy. Boulder, Colo: Center for the Study and Prevention of Violence, Institute of Behavioral Science, University of Colorado at Boulder, 1998.

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2

Multisystemic therapy and neighborhood partnerships: Reducing adolescent violence and substance abuse. New York: Guilford Press, 2009.

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3

M, Borduin Charles, ed. Family therapy and beyond: A multisystemic approach to treating the behavior problems of children and adolescents. Pacific Grove, Calif: Brooks/Cole, 1990.

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4

Black families in therapy: A multisystems approach. New York: Guilford Press, 1989.

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5

Kristi, Sayers L., and Torrey Carol C, eds. Pediatric adapted motor development and exercise: An innovative multisystem approach for professionals and families. Springfield, Ill: C.C. Thomas, 1998.

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6

Schoenwald, Sonja K. The Transport and Diffusion of Multisystemic Therapy. Oxford University Press, 2015. http://dx.doi.org/10.1093/med:psych/9780195389050.003.0012.

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Chapter 12 describes the many factors that have played a role in the diffusion and implementation of multisystemic therapy (MST), considering policy as well as service provision demands for the intervention, and the development and refinement of procedures to most effectively transport and maintain the adherent administration of this treatment.
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7

Serious Emotional Disturbance in Children and Adolescents: Multisystemic Therapy. The Guilford Press, 2002.

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8

1950-, Henggeler Scott W., ed. Multisystemic therapy for antisocial behavior in children and adolescents. 2nd ed. New York: Guilford Press, 2009.

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9

Henggeler, Scott W., Cynthia Cupit Swenson, Ida S. Taylor, and Oliver W. Addison. Multisystemic Therapy and Neighborhood Partnerships: Reducing Adolescent Violence and Substance Abuse. The Guilford Press, 2004.

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10

1950-, Henggeler Scott W., ed. Multisystemic treatment of antisocial behavior in children and adolescents. New York: Guilford Press, 1998.

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11

Kazdin, Alan E. Psychosocial Treatments for Conduct Disorder in Children and Adolescents. Oxford University Press, 2015. http://dx.doi.org/10.1093/med:psych/9780199342211.003.0005.

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Significant advances have been made in the treatment of antisocial and aggressive behavior (conduct disorder), a severe source of impairment among children and adolescents. Several psychosocial interventions with strong evidence in their behalf with children and adolescents are highlighted in the chapter. They include parent management training, multisystemic therapy, multidimensional treatment foster care, cognitively based treatments, functional family therapy, brief strategic family therapy, and the Good Behavior Game. The treatments have been very well studied, with multiple replications. There remain questions about the long-term impact of treatments, the persons for whom one or more of these treatments are well suited, and how to optimize therapeutic change.
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12

Vladimir, Kvetan, and Dantzker David R, eds. The critically ill cardiac patient: Multisystem dysfunction and management. Philadelphia: Lippincott-Raven, 1996.

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13

(Editor), Vladimir Kvetan, and David R. Dantzker (Editor), eds. The Critically Ill Cardiac Patient: Multisystem Dysfunction and Management. Lippincott Williams & Wilkins, 1996.

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14

Wiffen, Philip, Marc Mitchell, Melanie Snelling, and Nicola Stoner. Therapy-related issues: musculoskeletal diseases. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199603640.003.0025.

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Rheumatoid arthritis 548Gout 556Rheumatoid arthritis (RA) is an autoimmune disease which causes joints lined with synovium to become inflamed, swollen, stiff, and painful, and leads to joint erosion. It is a multisystem disorder which can affect many organs including the eyes, lungs, heart, and blood vessels. The aim of treatment is to decrease pain and inflammation, prevent joint damage, and ultimately induce remission of disease....
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15

Swales, Catherine. Inflammatory connective tissue disease. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199550647.003.010005.

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♦ Systemic lupus erythematosus (SLE) is the commonest multisystem connective tissue disease♦ All patients with SLE are antinuclear antibody (ANA) positive, but not all ANA-positive patients have SLE♦ Renal lupus carries a high mortality and requires aggressive immunosuppression♦ Dermatomyositis may be associated with malignancy in the elderly♦ The vasculitides are classified according to vessel size and ANCA (antineutrophil cytoplasmic antibody) profile♦ Therapy for vasculitis includes corticosteroids, steroid-sparing agents, and cytotoxics.
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16

Patterson, Marc C. Congenital Disorders of Glycosylation. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0066.

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Congenital disorders of glycosylation (CDG) comprise a family of multisystem diseases in which N- and O-linked glycosylation and glypiation of a variety of proteins and lipids is deficient. The hypoglycosylation of multiple glycoconjugates impairs normal development of the brain (and other organs), and is associated with both episodic and chronic organ dysfunction. Developmental disorders; seizures; strokelike episodes (and stroke); hearing and visual loss; peripheral neuropathy; coagulopathy; and immune, liver, endocrine, cardiac, and cutaneous manifestations may occur in varying combinations. Specific therapy is available for MPI-CDG and SLC35C2-CDG. Most forms of O-linked CDG affect muscle; these include congenital muscular dystrophies and limb girdle dystrophies.
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17

Krause, Andreas, and Volker Fingerle. Lyme borreliosis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0101.

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Lyme borreliosis (LB) is a multisystem infectious disease caused by the tick-borne spirochete Borrelia burgdorferi. The most frequent clinical manifestations include erythema migrans, meningoplyneuritis, and arthritis. Diagnosis of LB is made on clinical grounds and usually supported by a positive serology. Early diagnosis and treatment almost always leads to a rapid healing of the disease. However, in late manifestations gradual remission of symptoms may take several weeks to months. In rare cases, the pathogen can persist for many years or induce a persisting immunopathological response that may cause acrodermatitis chronica atrophicans, chronic neuroborreliosis of the central nervous system, or antibiotic resistant Lyme arthritis. However, even these chronic manifestations usually slowly regress after thorough antibiotic and symptomatic therapy, although in part with irreversible organ defects.
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18

Krause, Andreas, and Volker Fingerle. Lyme borreliosis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0101_update_001.

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Lyme borreliosis (LB) is a multisystem infectious disease caused by the tick-borne spirochete Borrelia burgdorferi. The most frequent clinical manifestations include erythema migrans, meningoplyneuritis, and arthritis. Diagnosis of LB is made on clinical grounds and usually supported by a positive serology. Early diagnosis and treatment almost always leads to a rapid healing of the disease. However, in late manifestations gradual remission of symptoms may take several weeks to months. In rare cases, the pathogen can persist for many years or induce a persisting immunopathological response that may cause acrodermatitis chronica atrophicans, chronic neuroborreliosis of the central nervous system, or antibiotic resistant Lyme arthritis. However, even these chronic manifestations usually slowly regress after thorough antibiotic and symptomatic therapy, although in part with irreversible organ defects.
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19

Fowler, Robert, and Abhijit Duggal. Management of pandemic critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0009.

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Adequate and appropriate provision of critical care services during pandemics may dramatically alter vital outcomes of patients who develop acute respiratory distress syndrome and critical illness. Specific anti-viral therapy, antibiotics directed towards probable secondary infections, supportive ventilation and oxygenation, and adherence to multisystem critical care ‘best practices’ can prevent substantial mortality and morbidity, and lessen the pandemic’s impact on global health. However, severe acute respiratory syndrome and the 2009 H1N1 pandemic also highlighted the limited capacity for increased provision of critical care, even in well-resourced settings, and the potential for dramatic differences in mortality in under-resourced settings. Pandemic preparedness hinges on the development of appropriately-trained staff with well-defined roles, and the ability to manage surge in the number of patients. A rigorous infection control programme, and triage protocols based on equitable distribution of resources and ethical principles of justice, beneficence and non-maleficence. Research preparedness, with approved protocols, electronic case report forms and harmonized clinical trials is necessary.
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20

Noori, Muna, and Catherine Nelson-Piercy. Pathophysiology and management of pre-eclampsia, eclampsia, and HELLP syndrome. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0366.

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Pre-eclampsia is a multisystem disorder of pregnancy, characterized by the gestational onset of hypertension and proteinuria, which presents as part of a spectrum of disease with potentially serious consequences for both mother and foetus. Pre-eclampsia is a syndrome with multiple aetiologies, which has made it difficult to develop adequate screening tests and treatments. Pre-eclampsia is likely to develop only in vulnerable women with a mix of genetic susceptibility, vascular, metabolic, and inflammatory dysfunction. A number of prepregnancy risk factors for pre-eclampsia have been identified. However, not all women with risk factors develop pre-eclampsia, while many women without do, making it a challenging condition to predict. As pre-eclampsia cannot be prevented, its management remains supportive, with close monitoring of clinical signs and symptoms, antihypertensive therapy, seizure prophylaxis, and ultimately delivery when necessary. This chapter outlines the pathophysiology, diagnosis, and sequelae of pre-eclampsia, and provides an overview of antenatal, intrapartum, and post-natal management of women with pre-eclampsia.
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21

Levtchenko, Elena N., and Mirian C. Janssen. Cystinosis. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0339_update_001.

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Cystinosis is a rare autosomal recessive disease caused by mutations in the lysosomal cystine transporter cystinosin encoded by the CTNS gene (17p.13.2). Cystinosis is characterized by lysosomal cystine accumulation throughout the body with renal Fanconi syndrome being the most common presenting symptom of a multisystem disorder. It must be distinguished from cystinuria in which formation of cystine stones is the core problem. When left untreated, kidney dysfunction gradually progresses towards end-stage renal failure during the first 10 years of life. The advent of renal replacement therapy allowed cystinosis patients to survive into adulthood, but revealed numerous extrarenal manifestations of the disease, affecting eyes, endocrine organs, gastrointestinal tract, muscles, and central and peripheral nervous systems. The disease mechanism of cystinosis is not fully understood. The administration of the cystine-depleting agent cysteamine slows down renal and extrarenal organ damage, pointing to the pivotal role of cystine accumulation in the disease pathogenesis. Treatment with cysteamine should be initiated as early as possible and continued lifelong, and also after kidney transplantation for protecting extrarenal organs. Cysteamine eye drops are an indispensable part of the treatment of corneal cystine accumulation. Life expectancy of cystinosis patients has substantially improved and is now above 50 years.
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22

Hall, Andrew, and Shamima Rahman. Mitochondrial diseases and the kidney. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0340.

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Mitochondrial disease can affect any organ in the body including the kidney. As increasing numbers of patients with mitochondrial disease are either surviving beyond childhood or being diagnosed in adulthood, it is important for all nephrologists to have some understanding of the common renal complications that can occur in these individuals. Mitochondrial proteins are encoded by either mitochondrial or nuclear DNA (mtDNA and nDNA, respectively); therefore, disease causing mutations may be inherited maternally (mtDNA) or autosomally (nDNA), or can arise spontaneously. The commonest renal phenotype in mitochondrial disease is proximal tubulopathy (Fanconi syndrome in the severest cases); however, as all regions of the nephron can be affected, from the glomerulus to the collecting duct, patients may also present with proteinuria, decreased glomerular filtration rate, nephrotic syndrome, water and electrolyte disorders, and renal tubular acidosis. Understanding of the relationship between underlying genotype and clinical phenotype remains incomplete in mitochondrial disease. Proximal tubulopathy typically occurs in children with severe multisystem disease due to mtDNA deletion or mutations in nDNA affecting mitochondrial function. In contrast, glomerular disease (focal segmental glomerulosclerosis) has been reported more commonly in adults, mainly in association with the m.3243A<G point mutation. Co-enzyme Q10 (CoQ10) deficiency has been particularly associated with podocyte dysfunction and nephrotic syndrome in children. Underlying mitochondrial disease should be considered as a potential cause of unexplained renal dysfunction; clinical clues include lack of response to conventional therapy, abnormal mitochondrial morphology on kidney biopsy, involvement of other organs (e.g. diabetes, cardiomyopathy, and deafness) and a maternal family history, although none of these features are specific. The diagnostic approach involves acquiring tissue (typically skeletal muscle) for histological analysis, mtDNA screening and oxidative phosphorylation (OXPHOS) complex function tests. A number of nDNA mutations causing mitochondrial disease have now been identified and can also be screened for if clinically indicated. Management of mitochondrial disease requires a multidisciplinary approach, and treatment is largely supportive as there are currently very few evidence-based interventions. Electrolyte deficiencies should be corrected in patients with urinary wasting due to tubulopathy, and CoQ10 supplementation may be of benefit in individuals with CoQ10 deficiency. Nephrotic syndrome in mitochondrial disease is not typically responsive to steroid therapy. Transplantation has been performed in patients with end-stage kidney disease; however, immunosuppressive agents such as steroids and tacrolimus should be used with care given the high incidence of diabetes in mitochondrial disease.
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