{"title":"Thrombotic Disorders","authors":"Lawrence L K Leung","doi":"10.2310/fm.1412","DOIUrl":"https://doi.org/10.2310/fm.1412","url":null,"abstract":"<jats:p />","PeriodicalId":10989,"journal":{"name":"DeckerMed Family Medicine","volume":"31 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-11-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88724885","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Chronic kidney disease (CKD) is a clinical syndrome arising from progressive kidney injury, formerly known as chronic renal failure, chronic renal disease, and chronic renal insufficiency. It is classified into five stages based primarily on glomerular filtration rate (GFR). This article discusses the epidemiology of CKD and end-stage renal disease (ESRD), as well as etiology and genetics, pathophysiology, and pathogenesis. The section on diagnosis looks at clinical manifestations and physical findings, laboratory (and other) tests, imaging studies, and biopsy. A short section on differential diagnosis is followed by a discussion of treatment, including hemodialysis and peritoneal dialysis. Long-term complications of patients on dialysis include cardiovascular disease, renal osteodystrophy, dialysis-related amyloidosis, and acquired cystic disease (renal cell carcinoma). The final section addresses prognosis and socioeconomic burden. Figures include the classification system for CKD, prevalence of CKD in the United States, rising prevalence, risk of, and leading causes of ESRD in the United States, plus the changing prevalence of ESRD over time, clinical manifestations of uremia, and an overview of hemodialysis circuit. Tables look at the burden of CKD relative to other chronic disorders, the specific hereditary causes of kidney disease, and situations when serum creatinine does not accurately predict GFR. Other tables list equations for estimating GFR, the causes of CKD without shrunken kidneys, and clinical features distinguishing chronic kidney disease from acute kidney injury. ESRD and indications for initiation of dialysis are presented, as well as typical composition of dialysate and reasons for failure of peritoneal dialysis. This chapter contains 8 figures, 17 tables and 77 references Keywords: Renal disease, chronic kidney disease, hemodialysis, peritoneal dialysis, end-stage renal disease, glomerular filtration rate, mineral bone disease
{"title":"Chronic Kidney Failure and Dialysis","authors":"R. Durvasula, J. Himmelfarb","doi":"10.2310/fm.1168","DOIUrl":"https://doi.org/10.2310/fm.1168","url":null,"abstract":"Chronic kidney disease (CKD) is a clinical syndrome arising from progressive kidney injury, formerly known as chronic renal failure, chronic renal disease, and chronic renal insufficiency. It is classified into five stages based primarily on glomerular filtration rate (GFR). This article discusses the epidemiology of CKD and end-stage renal disease (ESRD), as well as etiology and genetics, pathophysiology, and pathogenesis. The section on diagnosis looks at clinical manifestations and physical findings, laboratory (and other) tests, imaging studies, and biopsy. A short section on differential diagnosis is followed by a discussion of treatment, including hemodialysis and peritoneal dialysis. Long-term complications of patients on dialysis include cardiovascular disease, renal osteodystrophy, dialysis-related amyloidosis, and acquired cystic disease (renal cell carcinoma). The final section addresses prognosis and socioeconomic burden. Figures include the classification system for CKD, prevalence of CKD in the United States, rising prevalence, risk of, and leading causes of ESRD in the United States, plus the changing prevalence of ESRD over time, clinical manifestations of uremia, and an overview of hemodialysis circuit. Tables look at the burden of CKD relative to other chronic disorders, the specific hereditary causes of kidney disease, and situations when serum creatinine does not accurately predict GFR. Other tables list equations for estimating GFR, the causes of CKD without shrunken kidneys, and clinical features distinguishing chronic kidney disease from acute kidney injury. ESRD and indications for initiation of dialysis are presented, as well as typical composition of dialysate and reasons for failure of peritoneal dialysis.\u0000\u0000This chapter contains 8 figures, 17 tables and 77 references\u0000Keywords: Renal disease, chronic kidney disease, hemodialysis, peritoneal dialysis, end-stage renal disease, glomerular filtration rate, mineral bone disease\u0000","PeriodicalId":10989,"journal":{"name":"DeckerMed Family Medicine","volume":"121 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89629613","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The acute leukemias are malignant clonal disorders characterized by aberrant differentiation and proliferation of transformed hematopoietic progenitor cells. These cells accumulate within the bone marrow and lead to suppression of the production of normal blood cells, with resulting symptoms from varying degrees of anemia, neutropenia, and thrombocytopenia or from infiltration into tissues. They are currently classified by their presumed cell of origin, although the field is moving rapidly to genetic subclassification. This review covers epidemiology; etiology; classification of leukemia by morphology, immunophenotyping, and cytogenetic/molecular abnormalities; cytogenetics of acute leukemia; general principles of therapy; acute myeloid leukemia; acute lymphoblastic leukemia; and future possibilities. The figure shows the incidence of acute leukemias in the United States. Tables list World Health Organization (WHO) classification of acute myeloid leukemia and related neoplasms, expression of cell surface and cytoplasmic markers for the diagnosis of acute myeloid leukemia and mixed-phenotype acute leukemia, WHO classification of acute lymphoblastic leukemia, WHO classification of acute leukemias of ambiguous lineage, WHO classification of myelodysplastic syndromes, European LeukemiaNet cytogenetic and molecular genetic subsets in acute myeloid leukemia with prognostic importance, cytogenetic and molecular subtypes of acute lymphoblastic leukemia, terminology used in leukemia treatment, and treatment outcome for adults with acute leukemia. This review contains 2 figures, 15 tables, and 119 references. Keywords: Acute leukemia, acute myeloid leukemia, acute lymphoblastic leukemia, cancer, cytogenetics, chromosomal abnormality
{"title":"Acute Leukemia","authors":"R. Larson, R. Walter","doi":"10.2310/fm.1247","DOIUrl":"https://doi.org/10.2310/fm.1247","url":null,"abstract":"The acute leukemias are malignant clonal disorders characterized by aberrant differentiation and proliferation of transformed hematopoietic progenitor cells. These cells accumulate within the bone marrow and lead to suppression of the production of normal blood cells, with resulting symptoms from varying degrees of anemia, neutropenia, and thrombocytopenia or from infiltration into tissues. They are currently classified by their presumed cell of origin, although the field is moving rapidly to genetic subclassification. This review covers epidemiology; etiology; classification of leukemia by morphology, immunophenotyping, and cytogenetic/molecular abnormalities; cytogenetics of acute leukemia; general principles of therapy; acute myeloid leukemia; acute lymphoblastic leukemia; and future possibilities. The figure shows the incidence of acute leukemias in the United States. Tables list World Health Organization (WHO) classification of acute myeloid leukemia and related neoplasms, expression of cell surface and cytoplasmic markers for the diagnosis of acute myeloid leukemia and mixed-phenotype acute leukemia, WHO classification of acute lymphoblastic leukemia, WHO classification of acute leukemias of ambiguous lineage, WHO classification of myelodysplastic syndromes, European LeukemiaNet cytogenetic and molecular genetic subsets in acute myeloid leukemia with prognostic importance, cytogenetic and molecular subtypes of acute lymphoblastic leukemia, terminology used in leukemia treatment, and treatment outcome for adults with acute leukemia.\u0000This review contains 2 figures, 15 tables, and 119 references.\u0000Keywords: Acute leukemia, acute myeloid leukemia, acute lymphoblastic leukemia, cancer, cytogenetics, chromosomal abnormality","PeriodicalId":10989,"journal":{"name":"DeckerMed Family Medicine","volume":"78 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82842884","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
According to 2009 estimates from the American Cancer Society, cancers originating in the gastrointestinal tract rank second in both incidence and cancer-related deaths. One in four deaths in the United States is caused by cancer, with 25% of cancer-related deaths caused by gastrointestinal (GI) malignancies; more than 50% of these deaths are caused by cancer of the pancreas, stomach, esophagus, liver, or biliary tract. Recent advances in molecular biology, medical genetics, and imaging and endoscopic techniques, as well as the development of antitumor agents, have significantly altered the approaches to the prevention, diagnosis, and treatment of GI cancers. The chapter covers esophageal, gastric, pancreatic, hepatocellular, biliary tract, and anal cancers, as well as GI stromal tumors and gastric lymphoma. Coverage of all cancers includes diagnosis and treatment; various sections include information on epidemiology, etiology, risk factors, screening and prevention, molecular mutations, pathogenesis, and/or metastatic disease. Figures depict a barium esophagogram showing squamous cell carcinoma; imaging of esophageal cancer, gastric cancer, and pancreatic cancer; a pedigree of a family with inactivation of germline mutation of E-cadherin; hereditary gastric cancer; gastric cancer survival rates after gastrectomy; axial T1-weighted magnetic resonance imaging (MRI) showing cancer of the pancreatic head; and T1- and T2-weighted MRIs of intrahepatic bile duct carcinoma. Tables provide information on new cases and mortality from GI cancer in 2009; guidelines for diagnosis and surveillance of Barrett esophagus; the declining incidence of gastric cancer in Japan, Slovenia, and the United States; TNM staging of gastric cancer, pancreatic cancer, and hepatocellular carcinoma; the incidence of familial pancreatic carcinoma; molecular mutations involved in pancreatic cancer; staging of pancreatic intraepithelial neoplasia; and the Chinese University Prognostic Index. This review contains 9 figures, 39 tables, and 173 references. Keywords: biliary cancer, carcinoma, endoscopic, esophageal, gastric, hepatic, lesions, lymphoma, malignant, mutations
{"title":"Pancreatic, Gastric, and other Gastrointestinal Cancers","authors":"D. Sohal, Weijing Sun, D. Haller","doi":"10.2310/FM.1182","DOIUrl":"https://doi.org/10.2310/FM.1182","url":null,"abstract":"According to 2009 estimates from the American Cancer Society, cancers originating in the gastrointestinal tract rank second in both incidence and cancer-related deaths. One in four deaths in the United States is caused by cancer, with 25% of cancer-related deaths caused by gastrointestinal (GI) malignancies; more than 50% of these deaths are caused by cancer of the pancreas, stomach, esophagus, liver, or biliary tract. Recent advances in molecular biology, medical genetics, and imaging and endoscopic techniques, as well as the development of antitumor agents, have significantly altered the approaches to the prevention, diagnosis, and treatment of GI cancers. The chapter covers esophageal, gastric, pancreatic, hepatocellular, biliary tract, and anal cancers, as well as GI stromal tumors and gastric lymphoma. Coverage of all cancers includes diagnosis and treatment; various sections include information on epidemiology, etiology, risk factors, screening and prevention, molecular mutations, pathogenesis, and/or metastatic disease. Figures depict a barium esophagogram showing squamous cell carcinoma; imaging of esophageal cancer, gastric cancer, and pancreatic cancer; a pedigree of a family with inactivation of germline mutation of E-cadherin; hereditary gastric cancer; gastric cancer survival rates after gastrectomy; axial T1-weighted magnetic resonance imaging (MRI) showing cancer of the pancreatic head; and T1- and T2-weighted MRIs of intrahepatic bile duct carcinoma. Tables provide information on new cases and mortality from GI cancer in 2009; guidelines for diagnosis and surveillance of Barrett esophagus; the declining incidence of gastric cancer in Japan, Slovenia, and the United States; TNM staging of gastric cancer, pancreatic cancer, and hepatocellular carcinoma; the incidence of familial pancreatic carcinoma; molecular mutations involved in pancreatic cancer; staging of pancreatic intraepithelial neoplasia; and the Chinese University Prognostic Index.\u0000This review contains 9 figures, 39 tables, and 173 references.\u0000Keywords: biliary cancer, carcinoma, endoscopic, esophageal, gastric, hepatic, lesions, lymphoma, malignant, mutations","PeriodicalId":10989,"journal":{"name":"DeckerMed Family Medicine","volume":"56 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78826445","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Chronic infection with the hepatitis C virus (HCV) remains a significant global health issue, with more than 71 million infected worldwide and accounting for over 720,000 deaths annually in the United States alone. It can be associated with significant liver-related morbidity and mortality owing to complications from cirrhosis and end-stage liver disease. The aging HCV population, together with changing patterns of drug use, has seen an increase in these complications of HCV and an increase in the number of acute HCV infections. Screening and managing complications of chronic hepatitis C are an important consideration. The changing epidemiology, risk factors, transmission, diagnosis, natural history (including complications) and patient evaluation and education are discussed. This review contains 4 figures, 2 tables, and 70 references Key words: epidemiology, hepatitis C virus, transmission, risk factors, natural history, patient education, evaluation
{"title":"Viral Hepatitis C: Epidemiology, Pathogenesis, Transmission, And Natural History","authors":"R. Chung, A. Lidofsky, J. Holmes","doi":"10.2310/GASTRO.14070","DOIUrl":"https://doi.org/10.2310/GASTRO.14070","url":null,"abstract":"Chronic infection with the hepatitis C virus (HCV) remains a significant global health issue, with more than 71 million infected worldwide and accounting for over 720,000 deaths annually in the United States alone. It can be associated with significant liver-related morbidity and mortality owing to complications from cirrhosis and end-stage liver disease. The aging HCV population, together with changing patterns of drug use, has seen an increase in these complications of HCV and an increase in the number of acute HCV infections. Screening and managing complications of chronic hepatitis C are an important consideration. The changing epidemiology, risk factors, transmission, diagnosis, natural history (including complications) and patient evaluation and education are discussed.\u0000\u0000This review contains 4 figures, 2 tables, and 70 references\u0000Key words: epidemiology, hepatitis C virus, transmission, risk factors, natural history, patient education, evaluation\u0000 ","PeriodicalId":10989,"journal":{"name":"DeckerMed Family Medicine","volume":"65 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90906023","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Chronic hepatitis B virus (HBV) infection is a major health burden worldwide, with approximately 257 million people with chronic infection. HBV is a small partially double-stranded DNA virus that replicates within the nucleus of the hepatocyte and commonly leads to chronic infection. Chronic HBV infection can cause cirrhosis, hepatocellular carcinoma, and extrahepatic manifestations such as glomerulonephritis or vasculitis. The latter is due to deposition of circulating immune complex in the different tissues. The natural history of HBV infection can be conceptualized as a spectrum encompassing different phases, including immune tolerance, immune clearance, inactive carrier, and reactivation and resolution. The diagnosis of the different phases of chronic HBV infection relies on various HBV serologies, liver enzyme levels, and histology findings. There are currently eight therapies approved for the treatment of HBV. Tenofovir alafenamide was the most recently approved therapy with a better side effect profile compared with tenofovir disoproxil fumarate. With the recent advances in the basic research in hepatitis B, new treatment options may become available in the near-future. This review contains 9 figures, 11 tables and 80 references Key words: cirrhosis, entecavir, Hepadnaviridae, hepatitis B virus, hepatocellular carcinoma, precore mutation, tenofovir
{"title":"Hepatitis B Virus","authors":"M. Lin, A. Wall","doi":"10.2310/fm.5483","DOIUrl":"https://doi.org/10.2310/fm.5483","url":null,"abstract":"Chronic hepatitis B virus (HBV) infection is a major health burden worldwide, with approximately 257 million people with chronic infection. HBV is a small partially double-stranded DNA virus that replicates within the nucleus of the hepatocyte and commonly leads to chronic infection. Chronic HBV infection can cause cirrhosis, hepatocellular carcinoma, and extrahepatic manifestations such as glomerulonephritis or vasculitis. The latter is due to deposition of circulating immune complex in the different tissues. The natural history of HBV infection can be conceptualized as a spectrum encompassing different phases, including immune tolerance, immune clearance, inactive carrier, and reactivation and resolution. The diagnosis of the different phases of chronic HBV infection relies on various HBV serologies, liver enzyme levels, and histology findings. There are currently eight therapies approved for the treatment of HBV. Tenofovir alafenamide was the most recently approved therapy with a better side effect profile compared with tenofovir disoproxil fumarate. With the recent advances in the basic research in hepatitis B, new treatment options may become available in the near-future.\u0000This review contains 9 figures, 11 tables and 80 references\u0000Key words: cirrhosis, entecavir, Hepadnaviridae, hepatitis B virus, hepatocellular carcinoma, precore mutation, tenofovir","PeriodicalId":10989,"journal":{"name":"DeckerMed Family Medicine","volume":"42 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81001312","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Epidemics of infectious jaundice have been reported throughout recorded history. However, the proof that many of these outbreaks and individual cases of acute hepatitis were caused by a viral infection, the hepatitis A virus (HAV), did not appear until the 1960s. After the transmission of infection to marmosets and humans, the epidemiologic and virologic characteristics that differed between hepatitis A and hepatitis B virus infections were defined more clearly. After the development and licensure of hepatitis A vaccines in the 1990s, it became possible to implement an effective prevention program involving routine immunization of young children in the United States and several other Western countries. However, despite the dramatic efficacy of the childhood immunization program in reducing the incidence of acute hepatitis from HAV in the population, older children and adults remained susceptible. Significant morbidity continues to occur in the United States among international travelers, injection drug users, persons with underlying liver disease, and other high-risk populations. Since HAV is a global pathogen, the prevention of increasing morbidity from hepatitis A attributable to the incidence of clinically more severe disease increases in countries transitioning from high to intermediate or low endemic status is a major public health challenge. In this review, we discuss the epidemiology, virology, clinical characteristics, and prevention of hepatitis A infections. This review contains 8 figures, 3 tables and 89 references Key words: epidemiology, global impact, hepatitis A vaccine, hepatitis A virus, prevention, reservoirs, risk factors, treatment
{"title":"Viral Hepatitis A","authors":"K. Nelson, B. Kmush","doi":"10.2310/GASTRO.14068","DOIUrl":"https://doi.org/10.2310/GASTRO.14068","url":null,"abstract":"Epidemics of infectious jaundice have been reported throughout recorded history. However, the proof that many of these outbreaks and individual cases of acute hepatitis were caused by a viral infection, the hepatitis A virus (HAV), did not appear until the 1960s. After the transmission of infection to marmosets and humans, the epidemiologic and virologic characteristics that differed between hepatitis A and hepatitis B virus infections were defined more clearly. After the development and licensure of hepatitis A vaccines in the 1990s, it became possible to implement an effective prevention program involving routine immunization of young children in the United States and several other Western countries. However, despite the dramatic efficacy of the childhood immunization program in reducing the incidence of acute hepatitis from HAV in the population, older children and adults remained susceptible. Significant morbidity continues to occur in the United States among international travelers, injection drug users, persons with underlying liver disease, and other high-risk populations. Since HAV is a global pathogen, the prevention of increasing morbidity from hepatitis A attributable to the incidence of clinically more severe disease increases in countries transitioning from high to intermediate or low endemic status is a major public health challenge. In this review, we discuss the epidemiology, virology, clinical characteristics, and prevention of hepatitis A infections.\u0000This review contains 8 figures, 3 tables and 89 references\u0000Key words: epidemiology, global impact, hepatitis A vaccine, hepatitis A virus, prevention, reservoirs, risk factors, treatment","PeriodicalId":10989,"journal":{"name":"DeckerMed Family Medicine","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82151168","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Valvular heart disease is an important cause of cardiac morbidity in developed countries despite a decline in the prevalence of rheumatic disease in those countries. This chapter discusses the many etiologies of valvular heart disease and presents methods for assessment and management. Specific valvular lesions discussed include mitral stenosis, mitral regurgitation, mitral valve prolapse, aortic stenosis, aortic regurgitation, and tricuspid and pulmonary disease. The section on tricuspid disease includes a discussion of mechanical prostheses (ball-in-cage and tilting-disk) and biologic prostheses (xenografts, allografts, and autografts) and their complications. This review contains 6 figures, 13 tables, 69 references. Keywords: Valvular heart disease, stenosis, regurgitation, mitral regurgitation, mitral valve prolapse (MVP), aortic stenosis, congenital bicuspid valve, senile valvular calcification, aortic regurgitation, chordae or papillary muscles
{"title":"Valvular Heart Disease - Part I","authors":"M. Jacob, B. Griffin","doi":"10.2310/FM.1226","DOIUrl":"https://doi.org/10.2310/FM.1226","url":null,"abstract":"Valvular heart disease is an important cause of cardiac morbidity in developed countries despite a decline in the prevalence of rheumatic disease in those countries. This chapter discusses the many etiologies of valvular heart disease and presents methods for assessment and management. Specific valvular lesions discussed include mitral stenosis, mitral regurgitation, mitral valve prolapse, aortic stenosis, aortic regurgitation, and tricuspid and pulmonary disease. The section on tricuspid disease includes a discussion of mechanical prostheses (ball-in-cage and tilting-disk) and biologic prostheses (xenografts, allografts, and autografts) and their complications. \u0000This review contains 6 figures, 13 tables, 69 references.\u0000Keywords: Valvular heart disease, stenosis, regurgitation, mitral regurgitation, mitral valve prolapse (MVP), aortic stenosis, congenital bicuspid valve, senile valvular calcification, aortic regurgitation, chordae or papillary muscles","PeriodicalId":10989,"journal":{"name":"DeckerMed Family Medicine","volume":"23 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86022706","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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