Goal-Directed Diagnosis -- A Diagnostic Reasoning Framework for ExploratoryCorrective Domai
实验诊断下名词解释考试双语

医学决定水平decision level,DL:是一种阈值,高于或低于该值,可判断人体的健康状况,也可判断疾病的严重程度,决定对病人采取适当措施。
医学决定水平与参考范围不同肿瘤标志物tumor marker:是由肿瘤细胞本身合成,释放,或者是机体对肿瘤细胞反应产生或升高的一类物质实验诊断laboratory diagnosis:是指医生的医嘱通过临床实验室分析所得到的信息为预防、诊断、治疗疾病和预后评价所用的医学临床活动,包括实验室前、实验室和实验室后3个部分红细胞比容h emotocrit, Hct;packed cell volume, PCV:又称红细胞压积,血细胞在血液中所占容积的比值,可反映红细胞的增减,但受血浆容量改变和红细胞体积大小的影响红细胞沉降率erythrocyte sedimentation rate,ESR:又称血沉率,是指红细胞在一定条件下沉降的速率,受多种因素影响(血浆中各种蛋白比例改变、红细胞数量和形状的改变)正常人参考值男性0~15/1h末;女性0~20/1h末红细胞体积分布宽度RDW:是反映外周血红细胞体积异质性的参数,由血细胞分析仪测量而获得。
对贫血的诊断有重要的意义嗜多色性红细胞polychromatic erythrocyte:RBC呈淡灰蓝或紫灰色,是一种刚脱核的RBC,体积较正常RBC较大,称噬多色RBC 或多染色性RBC。
增多反映骨髓造血功能活跃,RBC系增生旺盛,见于增生性贫血,尤以溶贫多见网织红细胞reticulocyte,Ret:是晚幼红细胞脱核后尚未完全成熟的红细胞,是由正常骨髓释放至外周血液中最年轻的红细胞。
细胞内残留的核糖体,核糖核酸经特殊染色呈网状结构而得名,外周血液中网织红细胞计数可反映骨髓内红细胞的增生程度小红细胞:红细胞直径小于6μm,中央淡染区扩大,红细胞呈小细胞低色素。
见于低色素性贫血,如缺铁性贫血红细胞大小不均amisocytosis:红细胞大小悬殊,直径可相差一倍以上。
学术英语(第二版)医学教学课件Unit 10

• We need to provide more of some things even as we provide fewer of others.
Do you see logic connection between them?
Para. 3 Language focus
to find a way to cover all of our people
Logic
in
the
paragraph
• One urgent national need: a way to cover all of our people
• Part of the problem: money
• The answer: rationalizing
• Blanket allocation: never a good idea
- people of all ages with End-Stage Renal Disease (ESRD) (permanent kidney failure requiring dialysis or a kidney transplant).
• Medicaid is available only to certain low-income individuals and families who fit into an eligibility group that is recognized by federal and state law.
Para. 1 Language focus
medical c_o_v_e_r_a_g_e_(医疗保险支付范围) Medicare and M__e_d_ic_a_i_d_(联邦医疗保险和医
RECSIT1.1中英文对照全文

New response evaluation criteria in solid tumours: Revised RECIST guideline (version 1.1)新版实体瘤疗效评价标准:修订的RECIST指南(1.1版本)Abstract摘要Background背景介绍Assessment of the change in tumour burden is an important feature of the clinical evaluation of cancer therapeutics: both tumour shrinkage (objective response) and disease progression are useful endpoints in clinical trials. Since RECIST was published in 2000, many investigators, cooperative groups, industry and government authorities have adopted these criteria in the assessment of treatment outcomes. However, a number of questions and issues have arisen which have led to the development of a revised RECIST guideline (version 1.1). Evidence for changes, summarised in separate papers in this special issue, has come from assessment of a large data warehouse (>6500 patients), simulation studies and literature reviews.临床上评价肿瘤治疗效果最重要的一点就是对肿瘤负荷变化的评估:瘤体皱缩(目标疗效)和病情恶化在临床试验中都是有意义的判断终点。
护理英语

P:
N: P:
N:
P:
Let me have a check. Oh, great. Dr.Smith will be available on Friday afternoon this week.
That’s fine. Thank you, I’ll come then.
Text
What are the roles of contemporaty nurse?
What role is central to all nursing roles? How does the nurse help the client regain health when giving care? What kinds of changes have taken place in nurses’ roles with the development of medical model?
N: P: N: P: N:
For yourself or for someone else?
For myself. What’s your trouble? I had a bad stomachache.
Well, let me see. I’m afraid he is fully booked on Monday and Tuesday.
Unit 2
Roles of Nurse
``````
Rview
come to the point in a mess not set an only……but example also make good use of give up instead of
Review
Out-patient occupation registration physician corridor
Definition, diagnosis and classification of diabetes mellitus and its complications

WHO/NCD/NCS/99.2Original: EnglishDistr.: General Definition, Diagnosisand Classificationof Diabetes Mellitusand its ComplicationsReport of a WHO ConsultationPart 1: Diagnosis and Classification ofDiabetes MellitusWorld Health OrganizationDepartment of Noncommunicable Disease SurveillanceGeneva© World Health Organization 1999This document is not a formal publication of the World Health Organization (WHO), and all rights are reserved by the Organization. The document may, however, be freely reviewed, abstracted, reproduced and translated, in part or in whole, but not for sale nor for use in conjunction withcommercial purposes.The views expressed in documents by named authors are solely the responsibility of those authorsContents1. Introduction12. Definition and diagnostic criteria for diabetes mellitus andother categories of glucose intolerance22.1 Definition22.2 Diagnosis and diagnostic criteria32.2.1 Diagnosis32.2.2 Diabetes in children42.3 Diagnostic criteria42.3.1 Change in diagnostic value for fastingplasma/blood glucose concentrations52.3.2 Epidemiological studies62.3.3 Individual diagnosis73. Classification83.1 Earlier classifications83.2 Revised classification93.2.1 Application of the new classification93.3 Terminology (Table 2)114. Clinical staging of diabetes mellitus and other categoriesof glucose tolerance (Figure 2) 144.1 Diabetes mellitus144.2 Impaired glucose regulation - Impaired GlucoseTolerance and Impaired Fasting Glycaemia144.3 Normoglycaemia165. Aetiological types (see also section 7. and Table 2)175.1 Type 1175.2 Type 2185.3 Other specific types (Table 3)186. Gestational Hyperglycaemia and Diabetes196.1 Diagnosis of gestational diabetes207. Description of aetiological types217.1 Type 1 (beta-cell destruction, usually leading toabsolute insulin deficiency)217.1.1 Autoimmune Diabetes Mellitus217.1.2 Idiopathic227.2 Type 2 (predominantly insulin resistance with relativeinsulin deficiency or predominantly an insulinsecretory defect with/without insulin resistance)237.3 Other Specific Types257.3.1 Genetic defects of beta-cell function257.3.2 Genetic defects in insulin action267.3.3 Diseases of the exocrine pancreas277.3.4 Endocrinopathies277.3.5 Drug- or chemical-induced diabetes287.3.6 Infections287.3.7 Uncommon but specific forms ofimmune-mediated diabetes mellitus297.3.8 Other genetic syndromes sometimesassociated with diabetes30 8. The Metabolic Syndrome318.1 Definition328.2 Future needs33 References34 Annex 1 The Oral Glucose Tolerance Test48 Annex 2 Methods for measuring substances in blood and urine49MembersKGMM Alberti, University of Newcastle upon Tyne, UK (Co–Chairman)P Aschner, ACD and Javerlana University, Bogota, ColombiaJ–P Assal, University Hospital, Geneva, SwitzerlandPH Bennett, NIDDK, Phoenix, AZ, USAL Groop, University of Lund, Malmö, SwedenJ Jervell, Rikshospitalet, Oslo, NorwayY Kanazawa, Jichi Medical School, Omiya, JapanH Keen, Guy's Hospital and Medical School, London, UKR Klein, University of Wisconsin Medical School, Madison, WI, USA J–C Mbanya, Centre Hospitalier et Universitaire de Yaoundé,CameroonD McCarty, International Diabetes Institute, Caulfield, Australia(Rapporteur)A Motala, University of Natal, Congella, South AfricaPan X–R, China–Japan Friendship Hospital, Beijing, China PR(deceased 8 July 1997)A Ramachandran, Diabetes Research Centre, Madras, IndiaN Samad, Dow Medical College & Civil Hospital, Karachi, Pakistan N Unwin, University of Newcastle upon Tyne, UK (Rapporteur)P Vardi, Schneider Children's Centre, Petah–Tikvah, IsraelPZ Zimmet, International Diabetes Institute, Caulfield, Australia (Co–Chairman)SecretariatA Alwan, World Health Organization, Geneva, SwitzerlandH King, World Health Organization, Geneva, SwitzerlandObserversM Berrens, Bayer, GermanyR Kahn, American Diabetes Association, USAJ Nolan, Institute for Diabetes Discovery, USA S Pramming, Novo Nordisk, DenmarkRA Rizza, American Diabetes Association, USA1.IntroductionIn the late 1970s both WHO (1) and the National Diabetes Data Group (2) produced new diagnostic criteria and a new classification system for diabetes mellitus. This brought order to a chaotic situation in which nomenclature varied and diagnostic criteria showed enormous variations using different oral glucose loads. In 1985 WHO slightly modified their criteria to coincide more closely with the NDDG values (3). There are now many data available, and also much more aetiological information has appeared. It seemed timely to re–examine the issues and to update and refine both the classification and the criteria, and to include a definition of the “Metabolic Syndrome”.An American Diabetes Association (ADA) expert group was convened to discuss these issues. It published its recommendations in 1997 (4). WHO convened a Consultation on the same subject in London, United Kingdom, in December 1996. In general, the ADA and WHO groups reached similar conclusions.The provisional report of the WHO Consultation (5) solicited comments which were considered in preparing the present report. Both the provisional and the present report were prepared by Professor K.G.M.M. Alberti and Professor P.Z. Zimmet on behalf of the members of the Consultation. The meeting was made possible with financial support from Bayer, UK; Bayer, Germany; Novo Nordisk, Copenhagen, Denmark; and The Institute for Diabetes Discovery, New Haven, USA.12.Definition and diagnostic criteria fordiabetes mellitus and other categoriesof glucose intolerance2.1DefinitionThe term diabetes mellitus describes a metabolic disorder of multiple aetiology characterized by chronic hyperglycaemia with disturbances of carbohydrate, fat and protein metabolism resulting from defects in insulin secretion, insulin action, or both. The effects of diabetes mellitus include long–term damage, dysfunction and failure of various organs. Diabetes mellitus may present with characteristic symptoms such as thirst, polyuria, blurring of vision, and weight loss. In its most severe forms, ketoacidosis or a non–ketotic hyperosmolar state may develop and lead to stupor, coma and, in absence of effective treatment, death. Often symptoms are not severe, or may be absent, and consequently hyperglycaemia sufficient to cause pathological and functional changes may be present for a long time before the diagnosis is made. The long–term effects of diabetes mellitus include progressive development of the specific complications of retinopathy with potential blindness, nephropathy that may lead to renal failure, and/or neuropathy with risk of foot ulcers, amputation, Charcot joints, and features of autonomic dysfunction, including sexual dysfunction. People with diabetes are at increased risk of cardiovascular, peripheral vascular and cerebrovascular disease.2Several pathogenetic processes are involved in the development of diabetes. These include processes which destroy the beta cells of the pancreas with consequent insulin deficiency, and others that result in resistance to insulin action. The abnormalities of carbohydrate, fat and protein metabolism are due to deficient action of insulin on target tissues resulting from insensitivity or lack of insulin.2.2Diagnosis and diagnostic criteria2.2.1DiagnosisIf a diagnosis of diabetes is made, the clinician must feel confident that the diagnosis is fully established since the consequences for the individual are considerable and lifelong. The requirements for diagnostic confirmation for a person presenting with severe symptoms and gross hyperglycaemia differ from those for the asymptomatic person with blood glucose values found to be just above the diagnostic cut–off value. Severe hyperglycaemia detected under conditions of acute infective, traumatic, circulatory or other stress may be transitory and should not in itself be regarded as diagnostic of diabetes. The diagnosis of diabetes in an asymptomatic subject should never be made on the basis of a single abnormal blood glucose value. For the asymptomatic person, at least one additional plasma/blood glucose test result with a value in the diabetic range is essential, either fasting, from a random (casual) sample, or from the oral glucose tolerance test (OGTT). If such samples fail to confirm the diagnosis of diabetes mellitus, it will usually be advisable to maintain surveillance with periodic re–testing until the diagnostic situation becomes clear. In these circumstances, the clinician3should take into consideration such additional factors as ethnicity, family history, age, adiposity, and concomitant disorders, before deciding on a diagnostic or therapeutic course of action. An alternative to blood glucose estimation or the OGTT has long been sought to simplify the diagnosis of diabetes. Glycated haemoglobin, reflecting average glycaemia over a period of weeks, was thought to provide such a test. Although in certain cases it gives equal or almost equal sensitivity and specificity to glucose measurement (6), it is not available in many parts of the world and is not well enough standardized for its use to be recommended at this time.2.2.2Diabetes in childrenDiabetes in children usually presents with severe symptoms, very high blood glucose levels, marked glycosuria, and ketonuria. In most children the diagnosis is confirmed without delay by blood glucose measurements, and treatment (including insulin injection) is initiated immediately, often as a life–saving measure. An OGTT is neither necessary nor appropriate for diagnosis in such circumstances. A small proportion of children and adolescents, however, present with less severe symptoms and may require fasting blood glucose measurement and/or an OGTT for diagnosis.2.3Diagnostic criteriaThe clinical diagnosis of diabetes is often prompted by symptoms such as increased thirst and urine volume, recurrent infections, unexplained weight loss and, in severe cases, drowsiness and coma; high levels of glycosuria are usually present. A single blood glucose estimation in excess4of the diagnostic values indicated in Figure 1 (black zone) establishes the diagnosis in such cases. Figure 1 also defines levels of blood glucose below which a diagnosis of diabetes is unlikely in non–pregnant individuals. These criteria are as in the 1985 report (3). For clinical purposes, an OGTT to establish diagnostic status need only be considered if casual blood glucose values lie in the uncertain range (i.e. between the levels that establish or exclude diabetes) and fasting blood glucose levels are below those which establish the diagnosis of diabetes. If an OGTT is performed, it is sufficient to measure the blood glucose values while fasting and at 2 hours after a 75 g oral glucose load (Annexes 1 and 2). For children the oral glucose load is related to body weight: 1.75 g per kg. The diagnostic criteria in children are the same as for adults. Diagnostic interpretations of the fasting and 2–h post–load concentrations in non–pregnant subjects are shown in Table 1.2.3.1Change in diagnostic value for fastingplasma/blood glucose concentrationsThe major change recommended in the diagnostic criteria for diabetes mellitus is the lowering of the diagnostic value of the fasting plasma glucose concentration to 7.0 mmol l–1 (126 mg dl–1) and above (3), from the former level of 7.8 mmol l–1 (140 mg dl–1) and above. For whole blood the proposed new level is 6.1 mmol l–1 (110 mg dl–1) and above, from the former 6.7 mmol l–1 (120 mg dl–1).The new fasting criterion is chosen to represent a value which is at the upper end of the range that corresponds in diagnostic significance in many persons to that of the 2–h post–load concentration, which is not changed. This equivalence has5been established from several population–based studies (6–8) and it also represents an optimal cut–off point to separate the components of bimodal frequency distributions of fasting plasma glucose concentrations seen in several populations. Furthermore, several studies have shown increased risk of microvascular disease in persons with fasting plasma glucose concentrations of 7.0 mmol l–1 (126 mg dl–1) and over (6), and of macrovascular disease in persons with such fasting concentrations, even in those with 2–h values of < 7.8 mmol l-1 (140 mg dl–1) (9). Nevertheless, in less obese subjects, in some ethnic groups and in the elderly lower fasting glucose levels may be seen in persons who have 2–h post–load glucose values that are diagnostic for diabetes.2.3.2Epidemiological studiesFor population studies of glucose intolerance and diabetes, individuals have been classified by their blood glucose concentration measured after an overnight fast and/or 2 h after a 75 g oral glucose load. Since it may be difficult to be sure of the fasting state, and because of the strong correlation between fasting and 2–h values, epidemiological studies or diagnostic screening have in the past been restricted to the 2–h values only (Table 1). Whilst this remains the single best choice, if it is not possible to perform the OGTT (e.g. for logistical or economic reasons), the fasting plasma glucose alone may be used for epidemiological purposes. It has now been clearly shown, however, that some of the individuals identified by the new fasting values differ from those identified by 2–h post glucose challenge values (10,11). The latter include the elderly (12) and those with less obesity, such as many Asian populations. On the other hand, middle-aged, more obese6patients are more likely to have diagnostic fasting values (10). Overall population prevalence may (13) or may not (7,10,14) be found to differ when estimates using fasting and 2–h values are compared.2.3.3Individual diagnosisThe requirements for individual diagnosis differ from those of population studies. The diagnosis should not be based on a single glucose determination but requires confirmatory symptoms or blood/plasma determination. Diagnosis requires the identification of people at risk for development of complications in whom early preventive strategies are indicated. Ideally therefore both the 2–h and the fasting value should be used. These recommendations contrast with those of the ADA Expert Committee which gives primacy to the fasting plasma glucose (4).73.Classification3.1Earlier classificationsThe first widely accepted classification of diabetes mellitus was published by WHO in 1980 (1) and, in modified form, in 1985 (3). The 1980 and 1985 classifications of diabetes mellitus and allied categories of glucose intolerance included clinical classes and two statistical risk classes. The 1980 Expert Committee proposed two major classes of diabetes mellitus and named them, IDDM or Type 1, and NIDDM or Type 2. In the 1985 Study Group Report the terms Type 1 and Type 2 were omitted, but the classes IDDM and NIDDM were retained, and a class of Malnutrition–related Diabetes Mellitus (MRDM) was introduced. In both the 1980 and 1985 reports other classes of diabetes included Other Types and Impaired Glucose Tolerance (IGT) as well as Gestational Diabetes Mellitus (GDM). These were reflected in the subsequent International Nomenclature of Diseases (IND) in 1991, and the tenth revision of the International Classification of Diseases (ICD–10) in 1992. The 1985 classification was widely accepted and is used internationally. It represented a compromise between clinical and aetiological classification and allowed classification of individual subjects and patients in a clinically useful manner even when the specific cause or aetiology was unknown. The recommended classification includes both staging of diabetes mellitus based on clinical descriptive criteria and a complementary aetiological classification.83.2Revised classificationThe classification encompasses both clinical stages and aetiological types of diabetes mellitus and other categories of hyperglycaemia, as suggested by Kuzuya and Matsuda (15). The clinical staging reflects that diabetes, regardless of its aetiology, progresses through several clinical stages during its natural history. Moreover, individual subjects may move from stage to stage in either direction. Persons who have, or who are developing, diabetes mellitus can be categorized by stage according to the clinical characteristics, even in the absence of information concerning the underlying aetiology. The classification by aetiological type results from improved understanding of the causes of diabetes mellitus.3.2.1Application of the new classificationThe new classification contains stages which reflect the various degrees of hyperglycaemia in individual subjects with any of the disease processes which may lead to diabetes mellitus.All subjects with diabetes mellitus can be categorized according to clinical stage, and this is achievable in all circumstances. The stage of glycaemia may change over time depending on the extent of the underlying disease processes (Figure 2). The disease process may be present but may not have progressed far enough to cause hyperglycaemia. The aetiological classification reflects the fact that the defect or9process which may lead to diabetes may be identifiable at any stage in the development of diabetes – even at the stage of normoglycaemia. Thus the presence of islet cell antibodies in a normoglycaemic individual makes it likely that that person has the Type 1 autoimmune process. Unfortunately, there are few sensitive or highly specific indicators of the Type 2 process at present, although these are likely to be revealed as aetiology is more clearly defined. The same disease processes can cause impaired fasting glycaemia and/or impaired glucose tolerance without fulfilling the criteria for the diagnosis of diabetes mellitus. In some individuals with diabetes, adequate glycaemic control can be achieved with weight reduction, exercise and/or oral agents. These individuals, therefore, do not require insulin and may even revert to IGT or normoglycaemia. Other individuals require insulin for adequate glycaemic control but can survive without it. These individuals, by definition, have some residual insulin secretion. Individuals with extensive beta–cell destruction, and therefore no residual insulin secretion, require insulin for survival. The severity of the metabolic abnormality can either regress (e.g. with weight reduction), progress (e.g. with weight gain), or stay the same.103.3Terminology (Table 2)It is recommended that the terms “insulin–dependent diabetes mellitus” and “non–insulin–dependent diabetes mellitus” and their acronyms “IDDM” and “NIDDM” no longer be used. These terms have been confusing and frequently resulted in patients being classified on the basis of treatment rather than pathogenesis.C The terms Type 1 and Type 2 should be reintroduced.The aetiological type named Type 1 encompasses themajority of cases which are primarily due to pancreaticislet beta–cell destruction and are prone toketoacidosis. Type 1 includes those cases attributableto an autoimmune process, as well as those with beta–cell destruction and who are prone to ketoacidosis forwhich neither an aetiology nor a pathogenesis isknown (idiopathic). It does not include those forms ofbeta–cell destruction or failure to which specificcauses can be assigned (e.g. cystic fibrosis,mitochondrial defects, etc.). Some subjects with thistype can be identified at earlier clinical stages than“diabetes mellitus”.C The type named Type 2 includes the common majorform of diabetes which results from defect(s) in insulinsecretion, almost always with a major contributionfrom insulin resistance. It has been argued that a leanphenotype of Type 2 diabetes mellitus in adults foundin the Indian sub–continent may be very distinct fromthe more characteristic form of Type 2 found in11Caucasians. Not enough information is available,however, to characterize such subjects separately.C A recent international workshop reviewed the evidencefor, and characteristics of, diabetes mellitus seen inundernourished populations (16,17). Whilst it appearsthat malnutrition may influence the expression ofseveral types of diabetes, the evidence that diabetescan be caused by malnutrition or protein deficiency perse is not convincing. Therefore, it is recommended thatthe class “Malnutrition–related diabetes” (MRDM) bedeleted. The former subtype of MRDM, Protein–deficient Pancreatic Diabetes (PDPD or PDDM), maybe considered as a malnutrition modulated or modifiedform of diabetes mellitus for which more studies areneeded. The other former subtype of MRDM,Fibrocalculous Pancreatic Diabetes (FCPD), is nowclassified as a disease of the exocrine pancreas,fibrocalculous pancreatopathy, which may lead todiabetes mellitus.C The class “Impaired Glucose Tolerance” is nowclassified as a stage of impaired glucose regulation,since it can be observed in any hyperglycaemicdisorder, and is itself not diabetes.C A clinical stage of Impaired Fasting Glycaemia hasbeen introduced to classify individuals who havefasting glucose values above the normal range, butbelow those diagnostic of diabetes.12C Gestational Diabetes is retained but now encompassesthe groups formerly classified as Gestational ImpairedGlucose Tolerance (GIGT) and Gestational DiabetesMellitus (GDM).134.Clinical staging of diabetes mellitusand other categories of glucosetolerance(Figure 2)4.1Diabetes mellitusDiabetes mellitus, regardless of underlying cause, is sub–divided into: Insulin requiring for survival (corresponding to the former clinical class of “Insulin Dependent Diabetes Mellitus – IDDM”), e.g. C–peptide deficient; Insulin requiring for control, i.e. metabolic control, rather than for survival, e.g. some endogenous insulin secretion but insufficient to achieve normoglycaemia without added exogenous insulin; and Not insulin requiring, i.e. those who may be controlled satisfactorily by non–pharmacological methods or drugs other than insulin. Together, the latter two sub–divisions constitute the former class of NIDDM.4.2Impaired glucose regulation – ImpairedGlucose Tolerance (IGT) and Impaired FastingGlycaemia (IFG)Impaired glucose regulation (IGT and IFG) refers to a metabolic state intermediate between normal glucose homeostasis and diabetes. It should be stated unequivocally, however, that IFG and IGT are not interchangeable and represent different abnormalities of glucose regulation, one in the fasting state and one post–prandial.14IGT, rather than being a class as in the previous classification, is categorized as a stage in the natural history of disordered carbohydrate metabolism. A stage of IFG is also recognized because such subjects, like those with IGT, have increased risks of progressing to diabetes and macrovascular disease, although prospective data are sparse and early data suggest a lower risk of progression than IGT (18), although a similar CVD risk factor profile has been shown in IFG and IGT subjects (19). IFG refers to fasting glucose concentrations which are lower than those required to diagnose diabetes mellitus but higher than the “normal”reference range.The values for IFG are a fasting plasma glucose concentration of 6.1 mmol l–1 (110 mg dl–1) or greater (whole blood 5.6 mmol l–1; 100 mg dl–1), but less than 7.0 mmol l–1 (126 mg dl–1) (whole blood 6.1 mmol l–1; 110 mg dl–1). If an OGTT is performed, some individuals with IFG will have IGT or diabetes, but this cannot be determined without an OGTT. If resources allow, it is recommended that all those with IFG have an OGTT to exclude the diagnosis of diabetes. Individuals who meet criteria for IGT or IFG may be euglycaemic in their daily lives as shown by normal or near–normal glycated haemoglobin levels. IGT and IFG are not clinical entities in their own right, but rather risk categories for future diabetes and/or cardiovascular disease (20,21). They can occur as an intermediate stage in any of the disease processes listed in Table 2. IGT is often associated with the Metabolic Syndrome (Insulin Resistance Syndrome) (22). Thus, IGT may not be directly involved in the pathogenesis of cardiovascular disease, but rather may serve as an indicator or marker of enhanced risk by virtue of its correlation with the other elements of the Metabolic15Syndrome that are cardiovascular risk factors. Self–evidently, those individuals with IGT manifest glucose intolerance only when challenged with an oral glucose load.4.3NormoglycaemiaA fasting venous plasma glucose concentration of less than6.1 mmol l–1 (110 mg dl S1) has been chosen as “normal”(Table 1). Although this choice is arbitrary, such values are observed in people with proven normal glucose tolerance, although some may have IGT if an OGTT is performed. Values above this are associated with a progressively greater risk of developing micro– and macrovascular complications (8,9,21,23).The pathological or aetiological processes which often lead to diabetes mellitus begin, and may be recognizable, in some subjects who have normal glucose tolerance. Recognition of the pathological process at an early stage may be useful if progression to more advanced stages can be prevented. Conversely, effective treatments, or occasionally the natural history of some forms of diabetes mellitus, may result in reversion of hyperglycaemia to a state of normoglycaemia. The proposed classification includes a stage of normoglycaemia in which persons who have evidence of the pathological processes which may lead to diabetes mellitus, or in whom a reversal of the hyperglycaemia has occurred, are classified.165.Aetiological types(see also section 7 and Table 2)The aetiological types designate defects, disorders or processes which often result in diabetes mellitus.5.1Type 1Type 1 indicates the processes of beta–cell destruction that may ultimately lead to diabetes mellitus in which “insulin is required for survival” to prevent the development of ketoacidosis, coma and death. An individual with a Type 1 process may be metabolically normal before the disease is clinically manifest, but the process of beta–cell destruction can be detected. Type 1 is usually characterized by the presence of anti–GAD, islet cell or insulin antibodies which identify the autoimmune processes that lead to beta–cell destruction. In some subjects with this clinical form of diabetes, particularly non–Caucasians, no evidence of an autoimmune disorder is demonstrable and these are classified as “Type 1 idiopathic”. Aetiological classification may be possible in some circumstances and not in others. Thus, the aetiological Type 1 process can be identified and sub–categorized if appropriate antibody determinations are performed. It is recognized that such measurements may be available only in certain centres at the present time. If these measurements are performed, then the classification of individual patients should reflect this.175.2Type 2Type 2 is the most common form of diabetes and is characterized by disorders of insulin action and insulin secretion, either of which may be the predominant feature. Both are usually present at the time that this form of diabetes is clinically manifest. By definition, the specific reasons for the development of these abnormalities are not yet known.5.3Other specific types (Table 3)Other specific types are currently less common causes of diabetes mellitus, but are those in which the underlying defect or disease process can be identified in a relatively specific manner. They include, for example, fibrocalculous pancreatopathy, a form of diabetes which was formerly classified as one type of malnutrition–related diabetes mellitus.18。
2020版GINA哮喘指南(中文版)

23
Box 1-3.
Steps f or conf irming the diagnosis of asthma in a patient already taking controller treatment
26
Box 1-4.
How to step down controller treatment to help conf irm the diagnosis of asthma
123
Box 4-5.
Discharge management af ter hospital or emergency department care f or asthma
127
5
ASTHMA, COPD AND ASTHMA+COPD
Box 5-1.
Current def initions of asthma and COPD, and clinical description of asthma-COPD overlap
33
Box 2-2.
GINA assessment of asthma control in adults, adolescents and children 6–11 years
35
Box 2-3.
Specif ic questions f or assessment of asthma in children 6–11 years
第 1 节。成人,青少年和儿童 6 岁及以上 19 第 1 章。哮喘的定义,描述和诊断 19 哮喘的定义 20 哮喘的描述 20 进行初步诊断 21 在已经接受控制治疗的患者中确认哮喘的诊断 26 鉴别诊断 27 在其他情况下如何进行哮喘的诊断 28 第 2 章哮喘评估 31 概述 32 评估哮喘症状控制 33 评估不良后果的未来风险 37 肺功能在评估哮喘控制中的作用 37 评估哮喘严重程度 39 第 3 章。治疗哮喘以控制症状并使危险最小化 A 部分:哮喘管理的一般原则 42 哮喘治疗的长期目标 42 病人与医疗服务提供者的伙伴关系 43 基于个性化控制的哮喘管理 44 B 部分。控制症状和降低风险的药物和策略 47 哮喘药物 48 哮喘治疗步骤 57 审查反应并调整治疗 64 治疗其他可改变的危险因素 67 其他疗法 68 非药物策略 70 推荐给专家意见的指征 78 C 部分:引导性哮喘自我管理教育和技能培训 79
2010ICSI+稳定性冠心病诊治指南

Thirteenth EditionApril 2009I NSTITUTE FOR C LINICAL S YSTEMS I MPROVEMENTThe information contained in this ICSI Health Care Guideline is intended primarily for health profes-sionals and the following expert audiences:• physicians, nurses, and other health care professional and provider organizations;• health plans, health systems, health care organizations, hospitals and integrated health care delivery systems;• health care teaching institutions;• health care information technology departments;• medical specialty and professional societies; • researchers;• federal, state and local government health care policy makers and specialists; and •employee benefit managers.This ICSI Health Care Guideline should not be construed as medical advice or medical opinion related to any specific facts or circumstances. If you are not one of the expert audiences listed above you are urged to consult a health care professional regarding your own situation and any specific medical questions you may have. In addition, you should seek assistance from a health care professional in interpreting this ICSI Health Care Guideline and applying it in your individual case.This ICSI Health Care Guideline is designed to assist clinicians by providing an analytical framework for the evaluation and treatment of patients, and is not intended either to replace a clinician's judgment or to establish a protocol for all patients with a particular condition. An ICSI Health Care Guideline rarely will establish the only approach to a problem.Copies of this ICSI Health Care Guideline may be distributed by any organization to the organization's employees but, except as provided below, may not be distributed outside of the organization without the prior written consent of the Institute for Clinical Systems Improvement, Inc. If the organization is a legally constituted medical group, the ICSI Health Care Guideline may be used by the medical group in any of the following ways:• copies may be provided to anyone involved in the medical group's process for developing and implementing clinical guidelines;•the ICSI Health Care Guideline may be adopted or adapted for use within the medical group only, provided that ICSI receives appropriate attribution on all written or electronic documents; and•copies may be provided to patients and the clinicians who manage their care, if the ICSI Health Care Guideline is incorporated into the medical group's clinical guideline program.All other copyright rights in this ICSI Health Care Guideline are reserved by the Institute for Clinical Systems Improvement. The Institute for Clinical Systems Improvement assumes no liability for any adaptations or revisions or modifications made to this ICSI Health Care Guideline.I NSTITUTE FOR C LINICALMain AlgorithmS YSTEMS I MPROVEMENTPharmacologic AlgorithmAlgorithms and Annotations .......................................................................................1-26Algorithm (Main) (1)Algorithm (Pharmacologic)................................................................................................2ForewordScope and Target Population .........................................................................................4Clinical Highlights and Recommendations ..................................................................4Priority Aims ..............................................................................................................4-5Key Implementation Recommendations .......................................................................5Related ICSI Scientific Documents ...........................................................................5-6Disclosure of Potential Conflict of Interest ...................................................................6Introduction to ICSI Document Development ..............................................................6Description of Evidence Grading ..................................................................................7Annotations ...................................................................................................................8-20Annotation (Main) ...................................................................................................8-14Annotation (Pharmacologic) ..................................................................................14-20Appendices ..................................................................................................................21-26Appendix A – Comorbid Conditions............................................................................21Appendix B – Medication Tables.................................................................................22Appendix C – Grading of Angina Pectoris ..................................................................23Appendix D – Omega-3 Fatty Acids ......................................................................24-26Supporting Evidence ....................................................................................................27-33Brief Description of Evidence Grading ............................................................................28References ...................................................................................................................29-33Support for Implementation .....................................................................................34-41Priority Aims and Suggested Measures .......................................................................35-36Measurement Specifications ..................................................................................37-38Key Implementation Recommendations ..........................................................................39Knowledge Resources ......................................................................................................39Resources Available .....................................................................................................40-41Table of ContentsWork Group LeaderGreg Lehman, MD Internal Medicine, Park Nicollet Clinic Work Group MembersCardiologyJoe H. Nguyen, MD CentraCareFamily Medicine Spencer Bershow, MD Fairview Health Services General InternistPhil Kofron, MD, MPH Park Nicollet Clinic Health Education Susan M. Hanson, RD Park Nicollet InstituteNursingShauna Schad, RN, CNS Mayo ClinicPharmacyPeter Marshall, PharmD HealthPartners Medical GroupFacilitatorsPenny Fredrickson ICSIMyounghee Hanson ICSIForewordScope and Target PopulationAdults who have a diagnosis of stable coronary artery disease. The criteria, as noted on the Main algorithm,includes patient presenting with:• previously diagnosed coronary artery disease without angina, or symptom complex that has remained stable for at least 60 days;• no change in frequency, duration, precipitating causes or ease of relief of angina for at least 60 days;and• no evidence of recent myocardial damage.Clinical Highlights and Recommendations• Prescribe aspirin in patients with stable coronary artery disease if there are no medical contraindications.(Annotations #2, 21a; Aim #2)• Evaluate and treat the modifiable risk factors, which include smoking, sedentary activity level, stress, hyperlipidemia, obesity, hypertension and diabetes. (Annotation #5; Aim #3)• Patients with chronic stable coronary artery disease should be on statin therapy regardless of their lipid levels unless contraindicated. (Annotation #21a; Aim #3)• Perform prognostic testing in patients whose risk determination remains unclear. This may precede or follow an initial course of pharmacologic therapy. (Annotation #7; Aim #7)• Refer the patient for cardiovascular consultation when clinical assessment indicates the patient is at high risk for adverse events, the non-invasive imaging study or electrocardiography indicates the patient isat high risk for an adverse event, or medical treatment is ineffective. (Annotations #15, 16; Aim #4)• For relief of angina, prescribe beta-blockers as first-line medication. If beta-blockers are contraindicated, nitrates are the preferred alternative. Calcium channel blockers may be an alternative medication if thepatient is unable to take beta-blockers or nitrates. (Annotations #21a, 21e; Aim #1) Priority Aims1. Increase the percentage of appropriate patients with an appropriate diagnosis of stable coronary arterydisease (SCAD), who are prescribed aspirin and antianginal medications. (Annotation #21a)2. Improve education/understanding around the management of stable coronary artery disease.3. Increase the percentage of patients with stable coronary artery disease who receive an intervention formodifiable risk factors.4. Improve the assessment of patients with a diagnosis of stable coronary artery disease who present withangina symptoms.5. Increase the use of angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers(ARBS) in patients with coronary artery disease, including those patients with a diagnosis of diabetes,chronic kidney disease, and hypertension.6. Increase the percentage of patients with a diagnosis of stable coronary artery disease who receive educa-tion around nutritional supplement therapy.7. Increase prognostic testing for patients whose risk determination remains unclear.Key Implementation RecommendationsThe following system changes were identified by the guideline work group as key strategies for health care systems to incorporate in support of the implementation of this guideline.1. Develop systems for providing patient education around:• Proper use of nitroglycerin• Consistent use of aspirin (unless contraindicated) or consistent use of clopidogrel as directed• When to call 911Education should also provide for patient to "teach back" in order to demonstrate their understanding of what they should do in an acute cardiac event.2. Develop/provide patients education materials around use of aspirin (unless contraindicated), interven-tions around modifiable risk factors.3. Provide patient education around the use and benefits of angiotensin-converting enzmes (ACE inhibi-tors) and/or angiotensin II receptor blockers (ARBs).Related ICSI Scientific DocumentsGuidelines• Diagnosis and Treatment of Chest Pain and Acute Coronary Syndrome (ACS)• Heart Failure in Adults• Hypertension Diagnosis and Treatment• Lipid Management in Adults• Major Depression in Adults in Primary Care• Diagnosis and Management of Type 2 Diabetes Mellitus• Preventive Services for Adults• Prevention and Management of Obesity in Adults and Mature Adolescents• Primary Prevention of Chronic Disease Risk FactorsTechnology Assessment Reports• Biochemical Markers of Cardiovascular Disease Risk (#66, 2003)• B-type Natriuretic Peptide (BNP) for the Diagnosis and Management of Congestive Heart Failure (#91, 2005)• Cardiac Rehabilitation (#12, 2002)• Drug-Eluting Stents for the Prevention of Restenosis in Native Coronary Arteries (#78, 2003)• Electron-Beam and Helical Computed Tomography for Coronary Artery Disease (#34, 2004)• Intracoronary Brachytherapy to Treat Restenosis after Stent Placement (In-stent Restenosis) (#34, 2002)• Omega-3 Fatty Acids for Coronary Artery Disease (#94, 2006)Disclosure of Potential Conflict of InterestICSI has adopted a policy of transparency, disclosing potential conflict and competing interests of all indi-viduals who participate in the development, revision and approval of ICSI documents (guidelines, order sets and protocols). This applies to all work groups (guidelines, order sets and protocols) and committees (Committee on Evidence-Based Practice, Cardiovascular Steering Committee, Women's Health Steering Committee, Preventive & Health Maintenance Steering Committee and Respiratory Steering Committee).Participants must disclose any potential conflict and competing interests they or their dependents (spouse, dependent children, or others claimed as dependents) may have with any organization with commercial, proprietary, or political interests relevant to the topics covered by ICSI documents. Such disclosures will be shared with all individuals who prepare, review and approve ICSI documents.No work group members have potential conflicts of interest to disclose.Introduction to ICSI Document DevelopmentThis document was developed and/or revised by a multidisciplinary work group utilizing a defined process for literature search and review, document development and revision, as well as obtaining input from and responding to ICSI members.For a description of ICSI's development and revision process, please see the Development and Revision Process for Guidelines, Order Sets and Protocols at .Evidence Grading SystemA. Primary Reports of New Data Collection:Class A: Randomized, controlled trialClass B: Cohort studyClass C: Non-randomized trial with concurrent or historical controlsCase-control studyStudy of sensitivity and specificity of a diagnostic testPopulation-based descriptive studyClass D: Cross-sectional studyCase seriesCase reportB. Reports that Synthesize or Reflect Upon Collections of Primary Reports:Class M: Meta-analysisSystematic reviewDecision analysisCost-effectiveness analysisClass R: Consensus statementConsensus reportNarrative reviewClass X: Medical opinionCitations are listed in the guideline utilizing the format of (Author, YYYY [report class]). A full explanation of ICSI's Evidence Grading System can be found at .Algorithm AnnotationsMain Algorithm Annotations1. Patient with Stable Coronary Artery DiseaseThis guideline applies to patients with coronary artery disease either with or without angina. Examplesinclude patients with prior myocardial infarctions, prior revascularization (i.e., percutaneous transluminalcoronary angioplasty [PTCA], coronary artery bypass graft [CABG]), angiographically proven coronaryatherosclerosis, or reliable non-invasive evidence of myocardial ischemia.A patient presenting with angina must meet all the following criteria (Hurst, 1990 [R]; Rutherford, 1992[R]; Shub, 1990 [R]):• Symptom complex has remained stable for at least 60 days• No significant change in frequency, duration, precipitating causes or ease of relief of angina for at least 60 days• No evidence of recent myocardial damageThe patient may already have undergone some diagnostic workup as a result of a prior presentation of chestpressure, heaviness and/or pain with or without radiation of the pain and/or shortness of breath. The clinicianshould have heightened awareness that many patients have atypical symptoms that reflect cardiac ischemia,especially women and the elderly. Initial care of such patients falls under the auspices of the ICSI Diagnosisand Treatment of Chest Pain and Acute Coronary Syndrome (ACS) guideline.2. Perform Appropriate History, Physical Examination, LaboratoryStudies and Patient EducationThorough history taking and physical examination, including medication and compliance reviews, areimportant to confirm diagnosis, to assist in risk stratification, and to develop a treatment plan (Rutherford,1992 [R]; Shub, 1990 [R]). Important points to elicit on history taking are:• recognition that women may have atypical symptoms of cardiac ischemia. These may include fatigue, shortness of breath (SOB) without chest pain, nausea and vomiting, back pain, jaw pain, dizzinessand weakness (Bell, 2000 [R]; Harvard Medical School, 2005 [R]; Kordella, 2005 [R]);• history of previous heart disease;• possible non-atheromatous causes of angina pectoris (e.g., aortic stenosis);• comorbid conditions affecting progression of coronary artery disease;• symptoms of systemic atherosclerosis (e.g., claudication, transischemic attack [TIAs] and bruits);and• severity and pattern of symptoms of angina pectoris.The physical examination should include a thorough cardiovascular examination, as well as evaluation forevidence of hyperlipidemia, hypertension, peripheral vascular disease, heart failure, anemia, thyroid disease,and renal disease.Initial laboratory studies should include an electrocardiogram and a fasting lipid profile (total cholesterol,HDL-cholesterol, calculated LDL-cholesterol and triglycerides). Further tests, based on history and physicalexamination findings, may include chest x-ray, measurement of hemoglobin, and tests for diabetes, thyroid function, and renal function.An important aspect to treatment of stable coronary artery disease is education to help the patient understand the disease processes, prognosis, treatment options, and signs of worsening cardiac ischemia so that prompt medical assistance is sought when necessary and appropriate. Education may be accomplished in a number of ways among the various medical groups. It may be ongoing, occur in a formal class, and/or be done at the provider visit. Instruction on the proper use of aspirin and sublingual nitroglycerin, as needed, should also be reviewed at this time.3. Non-Atherogenic Causes (e.g., Aortic Stenosis)?Aortic stenosis is an important non-atherogenic cause of angina. This and any other non-atherogenic causes are considered to be outside the scope of this clinical guideline (Shub, 1990 [R]).5. Address Modifiable Risk Factors and Comorbid ConditionsComorbid conditions that could affect myocardial ischemia may include hypertension, anemia, thyroid disease, hypoxemia and others.Modifiable risk factors for coronary heart disease need to be evaluated and may include smoking, inadequate physical activity, stress, hyperlipidemia, obesity, hypertension and diabetes mellitus. Intervention involving any risk factor pertinent to the patient is encouraged and may include education, goal setting, and follow-up as necessary (Rutherford, 1992 [R]; Shub, 1990 [R]).Please see Appendix A, "Comorbid Conditions," for treatment recommendations in the presence of comorbid conditions.Emerging Risk FactorsAn association between homocysteine levels and cardiovascular disease has been demonstrated. The NORVIT trial and HOPE 2 trial found that folate and vitamins B6 and B12 did not reduce the risk of recur-rent cardiovascular events in patients with vascular disease. These supplements cannot be recommended as routine treatment in patients with stable coronary artery disease (Bønaa, 2006 [A]; HOPE 2 Investigators, 2006 [A]).In select patients, clinicians may want to consider obtaining a lipoprotein (a) and highly sensitive C-reactive protein (hsCRP) (Ridker, 2005 [A]). Highly sensitive C-reactive protein and related markers of inflamma-tion may provide useful prognostic information and help guide further therapy for patients with coronary artery disease.InfluenzaPatients with cardiovascular disease should have an influenza vaccination as recommended by the American College of Cardiology/American Heart Association (ACC/AHA) Chronic Stable Coronary Artery Disease guideline (Smith, 2006 [R]).SmokingCigarette smoking may cause an acute cardiac ischemic event and may interfere with the efficacy of medi-cations to relieve angina.Please refer to the ICSI Preventive Services for Adults guideline for recommendations regarding smoking cessation.Sedentary Activity LevelAn important aspect of the provider's role is to counsel patients regarding appropriate work, leisure activities, eating habits and vacation plans. Patients should be encouraged to exercise regularly to obtain cardiovas-cular benefit and to enhance their quality of life. The American College of Cardiology (ACC) endorses a minimum schedule of 30-60 minutes of aerobic activity (walking, jogging, etc.) three to four times per week, supplemented by an increase in daily lifestyle activities (walking breaks at work, gardening, etc.) Medically supervised programs are recommended for moderate- to high-risk patients. Exercise can be an important adjunct to modification of risk factors such as hypertension, hyperlipidemia and obesity. In addition, it can enhance patients' perception of their quality of life. Strenuous activities should be modified if they produce severe or prolonged angina; caution is needed to avoid consistent reproduction of ischemic symptoms or situations that may precipitate ischemic complications. Education is critical in achieving these goals. A study (Hambrecht, 2005 [A]) showed less progression of coronary artery disease and significantly fewer ischemic events in patients who regularly exercised.StressPsychophysiologic stress is a notable feature of the relationship between myocardial ischemia and the patient's daily environment. Depressive symptoms are common in stable coronary artery disease patients, with prevalence estimates ranging from 15% to 30% (Kop, 2001 [R]). The American Heart Association recommends that depression be routinely screened for and appropriately treated in patients with coronary heart disease (Lichtman, 2008 [R]).HyperlipidemiaA fasting lipid profile should be evaluated for appropriate patients with stable coronary artery disease. Secondary prevention is important in these patients, who should be treated aggressively for hyperlipidemia. Many patients will require both pharmacologic and non-pharmacologic interventions to reach target goals. Target goals for hyperlipidemic patients with coronary artery disease include:LDL – less than 100 mg/dLHDL – 40 mg/dL or greaterTriglycerides – less than 150 mg/dLPlease refer to the ICSI Lipid Management in Adults guideline for recommendations on lowering lipid levels.ObesityThe American Heart Association considers obesity to be a major risk factor for coronary artery disease. Obesity is defined as a body mass index greater than 30. The loss of 5%-10% of an individual's weight can have health benefits such as decreasing blood pressure, cholesterol, decreasing the severity of obstructive sleep apnea, and improving glucose tolerance (Eckel, 1998 [X]).HypertensionGeneral health measures include the treatment of hypertension, which is not only a risk factor for develop-ment and progression of atherosclerosis, but also causes cardiac hypertrophy, augments myocardial oxygen requirements, and thereby intensifies myocardial ischemia in patients with obstructive coronary disease. Please refer to the ICSI Hypertension Diagnosis and Treatment guideline for recommendations regarding blood pressure management. The recommended target blood pressure is 130/80 mmHg or less.DiabetesDiabetes is associated with a marked increase in coronary artery disease. Patients with diabetes without known coronary artery disease have as high risk of a myocardial infarction as patients without diabetes with coronary artery disease. Therefore, patients with diabetes should have aggressive lipid and blood pressure management (similar to patients with coronary artery disease), and should be treated per the recommenda-tions of the ICSI Diagnosis and Management of Type 2 Diabetes Mellitus in Adults guideline, ICSI Lipid Management in Adults guideline and ICSI Hypertension Diagnosis and Treatment guidelines.Please refer to the ICSI Management of Type 2 Diabetes Mellitus guideline for recommendations regarding management of diabetes.Every attempt should be made to achieve meticulous glucose control in patients with diabetes, because there is a clear relationship between lower hemoglobin Alc's and lower risk of myocardial infarction (Haffner, 1998 [B]). In the UKPDS (United Kingdom Prospective Diabetes Study Group, 1998 [A]), obese patients with type 2 diabetes who were treated with metformin showed a statistically significant reduction in rates of myocardial infarction, suggesting metformin as a possible therapy of choice for these patients. A meta-analysis (Selvin, 2004 [M]) showed a 20% increase in cardiovascular events and mortality for every 1%c over 5%.increase in HbA1The Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial showed an increase rate of mortality in the intensive treatment arm compared to the standard arm (hazard ratio of 1.22), and there was a similar increase in cardiovascular deaths (ACCORD, 2008 [A]). Many of these patients were treated with insulin and multiple oral agents, with a target of A1c < 6. There were more hypoglycemic reactions in the inten-sively treated group, and more weight gain compared to the standard treatment group. Compared to other trials of intensive control, patients in the ACCORD trial may have had diabetes for a longer period of time and started with a higher A1c before entering the intensive treatment arm. Implications for SCAD patients can be summarized in a joint paper published by the American Diabetes Association, the American College of Cardiology, and the American Heart Association (Skyler, 2009 [R]). In general older, more frail SCAD patients with more comorbid disease (like chronic kidney disease) may be at greater risk for hypoglycemia and other complications of intensive diabetes therapy; perhaps patients such as these should be allowed higher A1c goals, such as maintaining A1c < 8.0. Other SCAD patients with a more recent diagnosis of diabetes, and those with less risk for hypoglycemia and other complications of intensive treatment will still warrant aggressive therapy to a target of < 7.0. For all patients, lifestyle modification, including exercise, smoking cessation, maintaining ideal body weight, and proven risk factor reduction (Boden, 2007 [A]) will continue to be the focus of primary and secondary cardiovascular disease prevention. The A1c goal ought to be individualized based on each patient's particular cardiovascular risk factors.Hormone Therapy (HT)The HERS II trial showed no cardioprotective benefit from hormone therapy, and in fact showed an increase in risk of other complications (breast cancer, venous thromboembolism, etc.) (Hulley, 1998 [A]). Risk-benefit analyses unequivocally support NOT starting hormone therapy for primary prevention. Should a patient already on hormone therapy present with acute coronary syndrome or be at risk for venous thromboembolism(e.g., prolonged immobilization), hormone therapy should be discontinued immediately. Clinical judgementis required in making the decision whether to continue hormone therapy in other circumstances.6. Assessment Yields High Risk of Adverse Event?Some patients are considered to be at high risk for infarction or death on the basis of history, physical exami-nation and initial laboratory findings. Patients presenting with accelerating symptoms of angina (NYHA (New York Heart Association) Class III or IV, see Appendix C, "Grading of Angina Pectoris"), symptoms ofperipheral vascular disease, or symptoms of left ventricular dysfunction should be referred to a cardiologist unless precluded by other medical conditions.7. Need for Prognostic Testing?Prognostic testing is appropriate for patients in whom risk determination remains unclear after initial evalu-ations have been completed, or in whom cardiac catheterization is deemed inappropriate by the cardiologist.Prognostic testing may precede or follow an initial course of pharmacological therapy (Frye 1989 [R];Shub, 1990 [R]).8. Patient/Electrocardiogram Allows Exercise Electrocardiography?Sensitivity of exercise electrocardiography (Masters 2-Step Exercise Test, Graded Exercise Test, Bicycle Test, Ergometry) may be reduced for patients unable to reach the level of exercise required for near maximal effort, such as:• patients taking beta-blockers;• patients in whom fatigue, dyspnea or claudication symptoms develop; and• patients with vascular, orthopedic or neurological conditions who cannot perform leg exercises.Reduced specificity may be seen in patients with abnormalities on baseline electrocardiography, such as those taking digitalis medications, and in patients with left ventricular hypertrophy or left bundle branch block (Rutherford, 1992 [R]).9. Perform Exercise ElectrocardiographyMost patients with normal resting electrocardiographys who can exercise and are not taking digoxin can undergo standard treadmill exercise testing.10. Perform Non-Invasive Imaging StudyA non-invasive imaging study such as myocardial perfusion scintigraphy or stress echocardiography shouldbest meet the patient's needs while providing the most clinical usefulness and cost effectiveness within the provider's institution. An imaging study should be selected through discussion with the cardiologist or imaging expert (Frye, 1989 [R]).11. Results Yield High Risk of Adverse Event?Exercise electrocardiography and prognostic imaging studies may yield results that indicate high, interme-diate or indeterminate or low risk of adverse clinical events. High-risk patients should have a cardiology consultation unless they are not considered to be potential candidates for revascularization. Patients who are at intermediate or indeterminate risk may benefit from cardiology consultation and/or further non-invasive imaging if an exercise electrocardiogram has been performed. Low-risk patients can generally be managed medically, with a good prognosis. Low-risk patients may benefit from angiography if the diagnosis remains unclear; however, angiography is unlikely to alter outcome in these patients (Rutherford, 1992 [R]).13. Is Medical Treatment Effective?Effectiveness of pharmacologic treatment is measured by whether the anginal pain is controlled within the definition of stable coronary artery disease as stated in Annotation #1, "Patient with Stable Coronary Artery Disease."。
THE INTERNATIONAL JOURNAL OF MEDICAL ROBOTICS AND COMPUTER ASSISTED SURGERY Int J Med Robot

Introduction
Computer-assisted surgery (CAS) is a methodology that translates into accurate and reliable image-to-surgical space guidance. Neurosurgery is a very complex procedure and the surgeon has to integrate multi-modal data to produce an optimal surgical plan. Often the lesion of interest is surrounded by vital structures, such as the motor cortex, temporal cortex, vision and audio sensors, etc., and has irregular configurations. Slight damage to such eloquent brain structures can severely impair the patient (1,2). CASMIL, an imageguided neurosurgery toolkit, is being developed to produce optimum plans resulting in minimally invasive surgeries. This system has many innovative features needed by neurosurgeons that are not available in other academic and commercial systems. CASMIL is an integration of various vital modules, such as rigid and non-rigid co-registration (image–image, image–atlas and
组织诊断Organization diagnosis

组织发展篇O D 深藏精度之:组织诊断Organization d i a g n o s i s组织发展过程The Process of Organization Deve lopment1、进入与签约Entering and Contracting2、组织诊断Diagnosing Organizations◆What is diagnosis ? 诊断是什么?◆The need for diagnostic models 对诊断模型的需求◆Open systems model 开放系统模型◆Organization-level diagnosis 组织层级的诊断3、工作群体与职位诊断Diagnosing Groups and Jobs4、收集和分析诊断信息Collecting and Analyzing Diagnostic Information5、反馈诊断信息Feeding Back Diagnostic Information6、设计干预措施Designing Interventions7、领导和管理变革Leading and Managing Change8、评估和制度化“组织发展变革”Evaluating and Institutionalizing Organization Development Interventions诊断是什么?When done well, diagnosis clearly points the organization and the OD practitioner toward a se t of appropriate intervention activities that will improve organization ef fectivenes s.Diagnosis is the process of understanding a system’s current functioning. It involves collecting pertinent information about current operations, analyzing those data, and drawing conclusions for potential change and improvement. Effective diagnosis provides the systematic knowledge of the organization needed to des ignappropriate interventions. Thus, OD interventions derive from diagnosis and include specific actions intended to impro ve organizational functionin g.Diagnostic models derive from conceptions about how o rganizati ons function, and they tell OD practitioners what to look for in diagno sing organizations, departments, groups, or jobs. They serve as a road map for discovering current functioning. A general, compreh ensive diagnostic model is presented based on open systems t heory.WHAT IS DIAGNO SIS?Diagnosis is the process of understanding how the organization is currently functioning, and it provides the information necessary to design change interventions. It generally follows from successful entry and contracting, which set the stage for successful diagnosis. Thos e processes help OD practitioners and client members jointly deter mine organizational issues to focus on, how to collect and analyze data to understand them, and how to work together to develop action st eps from the diagnosis. In another sense, diagnosis is happening all the time. Managers, organization members, and OD practitioners ar ealways trying to understand the drivers of organization effectiveness, and how and why change is proceeding in a particular way.诊断是一种对组织当前如何运作的理解过程,为设计组织变革/发展干预措施提供必须的信息成功的【进入和签约】,奠定诊断成功的基础该过程帮助客户和OD 共同决定应集中力量解决的组织问题,如何收集和分析数据,如何协作以确定组织诊断的具体行为步骤在另一种意义上,诊断一直发生管理者、组织成员和OD 总是尝试理解组织有效性的驱动因素、变革是如何/为什么以特定方式进行Unfortunately, the term diagnosis can be misleading when applied to organizations. It suggests a model of organization change analogous to the medical model of diagnosis: An organization (pat ient) experiencing problems seeks help from an OD practitioner (doctor); the practitioner examines the organization, finds the causes of t he problems, and prescribes a solution. Diagnosis in orga nization development, however, is much more collaborative than such a medical perspective implies and does not accept the imp licit assumption that something is wrong with the organiz ation.遗憾的是,诊断在组织应用中常被误解:存在问题的组织(病人)到OD(医生)寻求帮助;OD 检查组织、寻找问题成因、提出解决方案组织发展中的【诊断】比医学中的诊断更强调合作精神,并且反对“组织可能出了问题”的潜在假设First, the values and ethical beliefs that underlie OD suggest tha tboth organization members and change agents should be involved in discovering the determinants of current organization ef fectiveness. Similarly, both should be involved actively in developing appropri ate interventions and implementing them. For example, a manager mi ght seek an OD practitioner’s help to reduce absenteeism in his or herdepartment. The manager and an OD consultant jointly might d ecideto diagnose the cause of the problem by examining comp any absenteeism records and by interviewing selected employees abou t possible reasons for absenteeism. Alternatively, they might exami ne employee loyalty and discover the organizational elements that encourage people to stay. Analysis of those data could uncover determinants of absenteeism or loyalty in the department, thushelping the manager and the OD practitioner jointly to develop an appropriate intervention to address the issue.指导OD 的职业价值观和道德信念指出,组织成员和变革推动者应参与到发现当前组织更有效的决定因素同样,组织成员和变革推动者积极参与到构思合理的干预措施,以及参与实施这些干预措施Second, the medical mode l of diagnosis also implies that something is wrong with the patient and that one needs to uncover the cause of the illness. In those cases where organizations do have specific problems, diagnosis can be problem oriented, seeking reasons for the probl ems. On the other hand, as suggested by the absenteeism example ab ove, the OD practitioner and the client may choose one of the newer views of organization change and frame the issue positively. Additionall y,the client and the OD practitioner may be looking for ways to enh ance the organizati on’s existing functioning. Many managersinvolve d with OD are not experiencing specific organizational problems. Here, diagnosis is development oriented. It assesses the current functi oningof the organization to d i scover areas for futur e development. For example, a manager might be interested in using OD to improve a department that already seems to be functioning well. Diagnosis might include an overall assessment of both the task performanc e capabilities of the department and the impact of the department on its individual members. This process seeks to uncover specific areas for future development of the departm ent’s ef fectivenes s.诊断的医学模型暗示“病人出了问题并且需要寻找病因”。
Gheyas疾病诊断

Project Title: A Decision Support ToolFor Disease DiagnosisAbstractThe goal of this project was to develop a complementary decision support system PathNet for an existing system DemNet. The DemNet helps in the diagnosis of dementia, whereas PathNet is expected to facilitate diagnosis of various pathologies (such as Alzheimer's disease, vascular dementia, frontotemporal dementia, dementia with lewy bodies) causing dementia in patients. The intended users of this system are the clinical nurses who are involved in initial diagnosis of the disease. Dementia can be caused by these pathologies alone or in combination. The system provides interfaces (JCombo boxes) for users to specify symptoms and test results of the patients and based on this information, displays updated likelihood of different pathologies by bar diagrams. To facilitate faster diagnosis without compromising accuracy of the diagnosis, the system indicates the next most important questions (for all pathologies as a whole and for each pathology) to ask for the test to be conducted based on knowledge about the patient. The system PathNet operates on a Bayesian Belief Network (BBN) developed by Lloyd Oteniya and co-workers at the University of Stirling. The PathNet system follows MVC (Model-View-Controller) design architecture. The system was developed using an incremental process. To estimate the next most important question, the system estimates Mutual Information Index for different variables. The software packages used to implement the project were Eclipse 3.0 and Netica 1.12. Java programming language was used to implement the project. The BBN was implemented by Netica-J (Java version of Netica-API). White box testing and Usability testing were carried out to test the PathNet system. The result of White box testing reveals that the system can perform its intended functions properly. Users in Usability tests provided some useful feedback about the program. PathNet system is easy to use, once the user gets familiar with it. The users liked the way the outputs are displayed. But they complained about some aspects of the colour scheme. The users suggested providing extensive 'Help services'. They also suggested that an improved interface which can efficiently reset JCombo box will be helpful. Based on the feedback, some improvements were made to the PathNet system (such as extensive help services were included, colour scheme was changed). However, some of their suggestions (such as a facility to reset the JCombo boxes, printing facility etc) could not be implemented due to time constraints. One of the strengths of the developed PathNet system is that it can make fairly good inferences even when information is incomplete. Future work will focus on extending the system so that the system can store and manage old case files, which will help update the probabilities in BBN.项目名称:一个决策支持工具疾病诊断摘要这个项目的目标是开发一种补充决策支持系统的现有系统DemNet PathNet。
510(k)SUBSTANTIALEQUIVALENCEDETERMINATION

510(k) SUBSTANTIAL EQUIVALENCE DETERMINATIONDECISION SUMMARYA. 510(k) Number:k083314B. Purpose for Submission:Modification to deviceC. Measurand:Allergen Specific IgE (Red Maple, White Hickory, Red Cedar, Sweet Gum, Common Sagebrush, Wing Scale)D. Type of Test:Quantitative, chemiluminiscent immunoassayE.Applicant:Siemens Healthcare Diagnostics, Inc.F.Proprietary and Established Names:IMMULITE® 2000 3gAllergy™ Specific IgE Assay kitG.Regulatory Information:1. Regulation section:21 CFR § 866.5750, Radioallergosorbent (RAST) test systems2. Classification:Class II3. Product code:DHB System, Test, Radioallergosorbent (RAST), Immunological4. Panel:Immunology (82)H. Intended Use:1. Intended use(s):For in vitro diagnostic use with the IMMULITE 2000 Analyzer – for thequantitative measurement of allergen-specific IgE in human serum, as an aid inthe clinical diagnosis of IgE-mediated allergic disorders.2. Indication(s) for use:Same as Intended use.3. Special conditions for use statement(s):For prescription only.4. Special instrument requirements:IMMULITE 2000 Analyzer (k970227)I. Device Description:Each device contains the following: 3gAllergy™ specific IgE bead pack (3 packs of 200 beads coated with anti-ligand); specific IgE reagent wedge: 30 mL alkalinephosphatase (bovine calf intestine) conjugated to monoclonal murine anti-human IgE antibody in a human/nonhuman serum buffer matrix (equally dispensed in 1 wedge with B & C chambers); specific IgE adjustors: low and high (2 vials, 2 mL each) of human IgE in a nonhuman serum matrix with preservative; specific IgE adjustorantibody: 2 tubes, 2.75 mL each) ready to use ligand-labeled polyclonal goat anti-human IgE antibody with preservative; specific IgE universal kit controls: (2 vials, 2 mL each) human IgE in a nonhuman sample matrix with preservative; specific IgEcontrol antibody: (2 tubes, 2.75 mL each) ready to use ligand-labeled polyclonal goat anti-human IgE antibody with preservative. Kit components supplied separately: 3gAllergy™ specific IgE sample diluent (concentrated ready to use 1 vial, 25 mL);chemiluminiscent substrate; probe wash; probe cleaning kit; disposable reactiontubes; bar coded allergen holder wedges serially coded 1-33; 34 -66; 67-99; allergen tube caps and tube septa.J. Substantial Equivalence Information:1. Predicate device name(s):IMMULITE® 2000 3gAllergy™ Specific IgE2. Predicate K number(s):k0131343. Comparison with predicates:SimilaritiesItem New Device Predicate Device Intended use For in vitro diagnostic usewith the IMMULITE 2000Analyzer – for thequantitative measurement ofallergen-specific IgE inhuman serum, as an aid in theclinical diagnosis of IgE-mediated allergic disorders.SameTechnology Chemiluminescence SameAssay performance Assay to be specific toallergen-specific IgESameCalibrators Low and high Same Controls Specific IgE and Antibodyand Specific IgE UniversalControlsSame Sample type Serum SameResult Interpretation Quantitative values in kU/L; Interpretation of class resultsfor two scoring systems:Standard and Extended standard: refer to tablesattached below.SameThe Standard classification system utilizes the following class cutoffs:Class kU/L Reactivity for Individual/Component Allergen(s) < 0.10 Absent or ND†0*0.10 – 0.34 Very LowI 0.35 – 0.69 LowII 0.70 – 3.49 ModerateClass kU/L Reactivity for Individual/Component Allergen(s)III 3.50 – 17.49 HighIV 17.5 – 52.49V 52.5 – 99.99Very HighVI ≥ 100* Class 0 in the standard system signifies: not detectable by second-generation assays.† ND: not detectable by IMMULITE 2000 3gAllergy.The Extended standard classification system utilizes the following class cutoffs.Class kU/L Reactivity for Individual/Component Allergen(s)0 < 0.10 Absent or ND†0/1 0.10 – 0.24 VeryLowI 0.25 – 0.39LowII 0.40 – 1.29 ModerateIII 1.30 – 3.89 HighIV 3.90–14.99Very High24.99V 15.00–VI ≥ 25† ND: not detectable by IMMULITE 2000 3gAllergy.The choice of classification systems can be made by the user within the IMMULITE 2000 operational software.Reference: Hoffman, DR. Comparison of methods of performing theRadioallergosorbent test: Phadebas, Fadal-Nalebuff and Hoffman protocols. Ann Allergy. 1980 Dec; 45(6)K. Standard/Guidance Document Referenced (if applicable):Standard documents:CLSI I/LA 20-A: Evaluation Methods and Analytical Performance Characteristics of Immunological Assays for Human Immunoglobulin E (IgE)CLSI EP5-A2: Evaluation of Precision Performance of Quantitative Methods;Approved Guideline – Second EditionGuidance document:FDA Guidance – Radioallergosorbent Test (RAST) Methods for Allergen-Specific Immunoglobulin E (IgE) 510(k); Final GuidanceL. Test Principle:The assay is a solid-phase, two-step, chemiluminiscent immunoassay that exploits liquid phase kinetics in a bead format. The allergens are covalently bound to a soluble polymer/co-polymer matrix, which is labeled with a ligand. The assay specificantibody is labeled with alkaline phosphatase. The use of an amino acid co-polymer amplifies the amount of allergen that the matrix can support. The chemiluminiscent detection system is a phosphatase ester of stabilized dioxatane. Cleavage of thephosphate ester by alkaline phosphatase results in the decomposition of dioxatane and the emission of photons, which are quantified by a Luminometer.M. Performance Characteristics (if/when applicable):1. Analytical performance:a. Precision/Reproducibility:For the intra-assay study, three positive samples and one negative controlsample for each of the six allergens (Red Maple, White Hickory, Red Cedar,Sweet Gum, Common Sagebrush, Wing Scale) were analyzed 80 times (foreach allergens) in one run. For the inter-assay study, the same samples wereanalyzed 80 times in 2 different runs. The acceptable criterion for the negativesample is for the average dose must be <0.10 kU/L. All negative sampleresults were within the acceptance criterion. The acceptable criterion for thepositive samples is ≤15% for both intra-assay and inter-assay studies. Theintra-assay CV ranges were from 3.04% to 5.24%. The inter-assay CV rangeswere from 4.27% to 7.03% (see table below).Allergen: Red MapleIntra-assay Inter-assay Sample Mean(kU/L) SD(kU/L) %CV SD(kU/L)%CVPositive #1 2.17 0.073 3.36 0.117 5.39 Positive #2 3.19 0.096 3.01 0.162 5.08 Positive #3 12.06 0.452 3.75 0.634 5.26 Allergen: White HickoryIntra-assay Inter-assay Sample Mean(kU/L) SD(kU/L) %CV SD(kU/L)%CVPositive #1 1.12 0.038 3.39 0.053 4.73 Positive #2 4.54 0.238 5.24 0.312 6.87 Positive #3 6.25 0.214 3.42 0.267 4.27 Allergen:Red CedarIntra-assay Inter-assay Sample Mean(kU/L) SD(kU/L) %CV SD(kU/L)%CVPositive #1 1.34 0.056 4.18 0.071 5.30 Positive #2 7.63 0.393 5.15 0.421 5.52 Positive #3 10.09 0.521 5.16 0.560 5.55Allergen:Sweet GumIntra-assay Inter-assay Sample Mean(kU/L) SD(kU/L) %CV SD(kU/L)%CVPositive #1 2.70 0.082 3.04 0.139 5.15 Positive #2 3.00 0.115 3.83 0.154 5.13 Positive #3 7.97 0.332 4.17 0.502 6.30 Allergen: Common SagebrushIntra-assay Inter-assay Sample Mean(kU/L) SD(kU/L) %CV SD(kU/L)%CVPositive #1 1.42 0.049 3.45 0.069 4.86 Positive #2 4.14 0.191 4.61 0.291 7.03 Positive #3 10.47 0.425 4.06 0.558 5.33 Allergen: Wing ScaleIntra-assay Inter-assay Sample Mean(kU/L) SD(kU/L) %CV SD(kU/L)%CVPositive #1 1.56 0.056 3.59 0.072 4.62Positive #2 5.20 0.246 4.73 0.267 5.13Positive #3 9.81 0.324 3.30 0.424 4.32Lot to lot reproducibility:Three lots were analyzed using 3 positive samples on each of the six allergenswere analyzed 240 times. The acceptable criterion is ≤20%. The lowestvariability was 1% and highest variability was 2%. All three different lots forthe six allergens had <20% variability.b. Linearity/assay reportable range:Linearity studies:For each allergen, two samples were diluted in 2-fold serial dilutions to 5levels. The undiluted (neat) and diluted samples were tested with the specificallergen to demonstrate linearity at concentrations within the assay limits.Regression statistics for each allergen comparing observed to expected resultsare presented below.Allergen RegressionEquationN Slope 95% CI Intercept 95% CIRed Maple Y= 1.00X + 0.06 12 0.999 0.961–1.037 0.059 –0.124-0.242 White Hickory Y= 1.00X + 0.06 12 1.004 0.981–1.028 0.062 –0.122-0.246 Red Cedar Y= 1.00X – 0.01 12 1.003 0.987–1.019 –0.007 –0.081-0.067 Sweet Gum Y= 1.00X + 0.31 12 0.997 0.965–1.029 0.306 0.051-0.561 CommonSagebrushY= 1.00X + 0.62 12 0.999 0.970–1.028 0.615 –0.400-1.270 Wing scale Y= 1.00X – 0.10 12 0.998 0.981–1.015 –0.098 –0.252-0.056Assay working ranges: 0.1 – 100 kU/L.c. Traceability, Stability, Expected values (controls, calibrators, or methods): The calibrators and controls are traceable to the WHO 2nd IRP 75/502 reference standard. Stability studies:Expiration date claim for the six allergens: 2 years.Three positive samples and one negative sample were tested on three lots per allergen. Acceptance criteria for the accelerated stability study were asfollows: Positive sample: no more than 30% loss; Negative sample: remained negative (<0.10 kU/L). Results were as follows:ALLERGEN ID LOT # TESTED AVG %RECOVERY AT 57 o CT27 – Red Maple 110, 111, 112 76% T41 – White Hickory 110, 111, 112 80% T211 – Sweet Gum 110, 111, 112 85% T219 – Red Cedar 110, 111, 112 79% W43–Common Sagebrush 110, 111, 112 91% W75 – Wing scale114, 115, 11680%d. Detection limit:Analytical sensitivity: 0.1 kU/L e. Analytical specificity: Inhibition studies:Specificity of each allergen was verified through competitive inhibition testing using a single serum sample or pool of sera. A negative sample was used to measure the background response.To initiate the inhibition experiment, 70µL of undiluted and 4 levels of 5-fold serially diluted inhibitor extract were mixed with 250 µL of sample or pool. This mixture was incubated at room temperature (15-28°C) for 1 hour allowing the immunological reaction to occur. Each sample mixturecontaining the inhibitor extract and the appropriate controls was assayed with 1 lot of each allergen. The percent (%) inhibition was calculated according to the following formula: X 100The inhibition study demonstrated that the allergens tested are inhibited by the relevant inhibitor extract in a concentration dependent fashion. Also, the target % inhibition of 50% was met. These results indicate specificity of the red maple, white hickory, red cedar, sweet gum, common sagebrush and wingscale specific allergens. Summary inhibition table is presented below.Red MapleWhite HickoryRed CedarInhibitor Concentration (mg/mL) % Inhibition Inhibitor Concentration (mg/mL) % Inhibition Inhibitor Concentration (mg/mL)% Inhibition 5 100.00 5 100.00 5 97.59 1 99.04 1 100.00 1 93.78 0.2 96.83 0.2 97.87 0.2 83.63 0.04 79.15 0.04 89.03 0.04 70.98 0.008 0.00 0.008 27.33 0.008 69.28Sweet GumCommon SagebrushWing scaleInhibitor Concentration (mg/mL) % Inhibition Inhibitor Concentration (mg/mL) % Inhibition Inhibitor Concentration (mg/mL)% Inhibition 5 98.53 5 100.00 5 87.49 1 96.07 1 100.00 1 72.05 0.2 92.61 0.2 100.00 0.2 38.26 0.04 68.03 0.04 89.71 0.04 20.46 0.008 10.15 0.008 69.61 0.008 5.30Cross-reactivity: The manufacturer states there is no detectable crossreactivitywith human serum immunoglobulins IgG, IgA, IgM or IgD at normal physiological levels. f. Assay cut-off: Not applicable 2. Comparison studies:a. Method comparison with predicate device: Refer to Clinical studies 3. Clinical studies:a. Clinical Sensitivity and specificityClinical performance of the allergens was demonstrated by testing samples from non-atopic individuals and atopic patients with case histories of suspected clinical reactions to the specific allergen or allergy group in the IMMULITE ® 2000 3gAllergy Specific IgE assay and comparing results to accompanying clinical information. Testing was performed on 201 samples for Red Maple, White Hickory, Red Cedar; Sweet Gum; and 148 samples on Common Sagebrush and Wing Scale. Sensitivity and specificity, based on diagnosis of atopic status is shown in the tables below.Clinical DiagnosisAllergen: Red MapleAtopic Non-atopic Totalpositive 36 8 44 negative 12 145 157 IMMULITE 2000 Total 48 153 20195% CI Sensitivity 75% (36/48) 53-87% Specificity 95% (145/153)91-98%Clinical DiagnosisAllergen: White HickoryAtopic Non-atopic Totalpositive 32 11 43 negative 16 142 158 IMMULITE 2000 Total 48 153 20195% CISensitivity 67% (32/48) 53-80%Specificity 93% (142/153) 89-97%Clinical DiagnosisAllergen: Red CedarAtopic Non-atopic Totalpositive 36 4 40 negative 12 149 161 IMMULITE 2000 Total 48 153 20195% CISensitivity 75% 36/48) 63-87% Specificity 97% (149/153) 95-100%Clinical DiagnosisAllergen: Sweet GumAtopic Non-atopic Totalpositive 31 9 40 negative 17 144 161 IMMULITE 2000 Total 48 153 20195% CI Sensitivity 67% (31/48) 51-78% Specificity 94% (144/153)90=98%Clinical Diagnosis Allergen: Common Sagebrush Atopic Non-atopic Total positive 33 3 36 negative 15 97 112 IMMULITE 2000 Total 48 100 14895% CI Sensitivity 69% (33/48) 56-82% Specificity 97% (97/100)94-100%Clinical DiagnosisAllergen: Wing ScaleAtopic Non-atopic Totalpositive 28 2 30 negative 20 98 118 IMMULITE 2000 Total 48 100 14895% CI Sensitivity 58% (28/48) 44-72% Specificity 98% (98/100) 95-100%c. Other clinical supportive data (when a. and b. are not applicable): Not applicable. 4. Clinical cut-off :Not applicable.5. Expected values/Reference range: Not detected. N. Proposed Labeling:The labeling is sufficient and it satisfies the requirements of 21 CFR Part 809.10. O. Conclusion:The submitted information in this premarket notification is complete and supports a substantial equivalence decision.。
朱章志运用扶正祛邪法论治糖尿病经验

ʌ临证验案ɔ朱章志运用扶正祛邪法论治糖尿病经验❋曾绘域1,朱章志2ә,周㊀海3,陈㊀珺3,张文婧3(1.深圳市中西医结合医院,广东深圳㊀518104;2.广州中医药大学第一附属医院,广州㊀510405;3.广州中医药大学,广州㊀510405)㊀㊀摘要:糖尿病属于中医学 消渴病 范畴,以往医家多认为其病机为阴虚燥热,治疗以滋阴清热为法㊂朱章志教授通过长期的临床观察与实践,立足于张仲景 保胃气,扶阳气 的理论,认为糖尿病的病机为正虚邪滞,即太阴虚损㊁阳气不足㊁收敛不及,寒㊁水㊁湿之邪阻滞阳气运行通道㊂治疗上不囿陈法,以扶正祛邪为大法,通过固护太阴㊁扶助阳气㊁收敛阳气,祛除寒水湿之邪,恢复阳气运行之通畅,使阳气功能复常㊁运行有序,为糖尿病的治疗提供临床新思路㊂㊀㊀关键词:扶正祛邪;糖尿病;朱章志㊀㊀中图分类号:R587.1㊀㊀文献标识码:A㊀㊀文章编号:1006-3250(2021)01-0149-03Discussion on ZHU Zhang-zhi's Experience in Treating Diabetes Mellitus by Using The Method of Reinforcing The Healthy Qi and Eliminating The Pathogenic FactorsZENG Hui-yu 1,ZHU Zhang-zhi 2ә,ZHOU Hai 3,CHEN Jun 3,ZHANG Wen-jing 3(1.Shenzhen Hospital of Integrated traditional Chinese and Western Medicine,Guangdong,Shenzhen 518104,China;2.The First Affiliated Hospital of Guangzhou University of Chinese Medicine,Guangzhou 510405,China;3.Guangzhou University of Chinese Medicine,Guangzhou 510405,China)㊀㊀Abstract :Diabetes mellitus belongs to the category of "xiao ke"in traditional Chinese medicine.Doctors used to think that its pathogenesis was Yin deficiency and dryness heat ,and the treatment was nourishing Yin and clearing heat.Through long-term clinical observation and practice ,and based on ZHANG Zhong-jing's theory of protecting stomach Qi and supporting Yng Q ,professor ZHU Zhang-zhi believes that the pathogenesis of diabetes is deficiency of healthy Qi and stagnation of pathogen.Because of the deficiency of greater Yin and Yang Qi ,and the lack of convergence ,the cold ,water and dampness block the operational channel of Yang Qi.The treatment of diabetes mellitus should be based on reinforcing the healthy Qi and eliminating the pathogenic factors.By strengthening Taiyin ,supporting Yang Qi ,astringent Yang Qi ,dispelling the evil of cold ,water and dampness ,we can restore the smooth operation of Yang Qi ,restore the function of Yang Qi to normal and operate orderly ,which provides a new clinical method for the treatment of diabetes mellitus.㊀㊀Key words :Reinforcing the healthy Qi and eliminating the pathogenic factors ;Diabetes mellitus ;ZHU Zhang-zhi❋基金项目:国家自然科学基金资助项目(81873190)-降糖三黄片在糖脂毒性所致胰岛β细胞损伤的自噬调控作用作者简介:曾绘域(1990-),女,广东云浮人,住院医师,硕士研究生,从事六经辨治内分泌疾病的临床与研究㊂ә通讯作者:朱章志(1963-),男,湖南衡阳人,主任医师,博士研究生导师,从事六经辨治内分泌疾病的临床与研究,Tel :************,E-mail :zhuangi@ ㊂㊀㊀随着人口老龄化和生活方式的改变,我国糖尿病的患病率呈上升趋势,2013年我国18岁以上人群糖尿病患病率为10.4%[1]㊂中医药在延缓糖尿病的进展及防治其并发症方面具有一定优势[2-4]㊂糖尿病属于中医学 消渴病 范畴,以往医家多认为其病机为阴虚燥热,治疗以滋阴清热为法,但疗效尚不能令人满意㊂朱章志教授通过长期的临床观察与实践,认为正虚邪滞乃糖尿病病机之核心,采用扶正祛邪法治之屡获奇效㊂1㊀正虚邪滞之糖尿病病机‘素问㊃经脉别论篇“曰: 饮入于胃,游溢精气,上输于脾,脾气散精 水精四布,五经并行㊂食物入胃,经脾胃运化化生精气,然后输布全身㊂糖尿病患者常嗜食肥甘,起居无常,烦劳紧张,致太阴虚损,正气内虚,阳气戕伐,津液代谢异常,而生寒水湿之邪㊂寒㊁水㊁湿之邪气作为阴邪,又可阻滞阳气运行之通道㊂阳气运行通道不畅,不能敷布温煦四肢,可见手足逆冷;阳气运行受阻,又可出现郁而化热之象㊂因此朱章志认为,疗糖尿病的关键在于恢复阳气运行之通畅,根据糖尿病正虚邪滞的病机,治疗以扶正祛邪为法,顾护太阴㊁扶助阳气㊁收敛阳气,祛除寒水湿之邪,使阳气功能复常则行有序㊂2㊀运用扶正祛邪法治疗糖尿病2.1㊀扶正2.1.1㊀固护中气,扶助阳气㊀张仲景遣方用药常体现 保胃气 之思想[5],如桂枝汤中配伍生姜㊁大枣㊁炙甘草,发汗祛邪不忘顾护中气;又如白虎汤中加梗米㊁炙甘草以和中益胃,又可防止石膏㊁知母大寒伤中㊂ 有胃气则生,无胃气则死 ,故扶正之要以保胃气为先㊂朱章志认为,阳气在人体的生命活动中占主导9412021年1月第27卷第1期January 2021Vol.27.No.1㊀㊀㊀㊀㊀㊀中国中医基础医学杂志Journal of Basic Chinese Medicine地位㊂‘素问㊃生气通天论篇“曰: 阳气者若天与日,失其所则折寿而不彰 是故阳因而上,卫外者也㊂ ‘黄帝内经“把阳气比作太阳,阳气运行失常可致短寿㊂阳气具有抵御外邪㊁护卫生命㊁维持机体生命活动的作用,津液的气化㊁血液的运行均需阳气的温煦与推动㊂因此,在人体的阴阳平衡中阳气起着主导作用㊂朱章志认为,正气虚衰㊁太阴虚损㊁阳气不足是糖尿病发生发展之根本原因,因此扶正首当 固护中气,扶助阳气 ,故常以附子理中汤为底方,固护中宫㊂太阴脾土居中央,犹如足球比赛之中场,能联系前锋与后卫进可攻退可守,进可充养肺卫之气抵御外邪,退可顾护少阴以防寒邪内陷㊂‘四圣心源㊃卷二太阴湿土“提到: 湿者,太阴土气之所化也故胃家之燥,不敌脾家之湿,病则土燥者少而土湿者多也㊂[6] 阴脾土易挟寒湿,附子理中汤功善固护中气㊁温补脾阳而散寒湿,为治疗太阴阳虚寒湿之要方㊂方中附子辛温大热,补坎中真阳,又能散寒湿,荡去群阴;干姜去脏腑沉寒痼冷,温暖脾土,复兴火种;人参被誉为 百草之王 能大补元气,为扶正固本之极品;白术味苦性温,功善健脾燥湿,乃扶植太阴之要药;炙甘草善益气补中,调和药性,诸药合用以收培补中阳㊁散寒除湿之效㊂若其人神疲懒言,气虚较甚,在附子理中汤的基础上可重用红参㊁北芪以大补元气,健脾益气;若其人四肢不温㊁肢体困重㊁寒湿较重者,可加重附子㊁干姜之量,并加细辛㊁吴茱萸以散久寒;若其人口干口苦㊁舌苔黄腻㊁大便黏滞不爽兼夹湿热之象,可仿当归拈痛汤之意,加茵陈㊁当归㊁黄芩以利湿清热㊂2.1.2㊀收敛阳气,阳密乃固㊀朱章志认为, 阴 可理解为 阳气 的收敛㊁收藏状态,糖尿病 阴虚燥热 之象乃阳气不足㊁收敛不及㊁升发太过所致[7]㊂‘素问㊃生气通天论篇“提到: 阳气者,烦劳则张 ㊂现代人起居无节,以妄为常,阳气因而不能潜藏,常常浮越于外容易出现假热之象,医者不察,妄投清热泻火之品,实乃雪上加霜㊂ 凡阴阳之要,阳密乃固 ,收敛阳气即是扶正,犹如太极之能收能放,收敛是为了聚集能量,阳气固密,正气才能强盛,方能更好的制敌㊂朱章志常用砂仁㊁肉桂㊁白芍㊁山萸肉㊁泽泻等药物收敛阳气㊂砂仁辛温,既能宣太阴之寒湿,又能纳气归肾,使阳气收敛于少阴,少火生气㊂‘本草经疏“提到: 缩砂蜜,辛能散,又能润 辛以润肾,故使气下行 气下则气得归元㊂[8] 肉桂引火归原,导浮越之阳气归于命门,益火消阴㊂若患者出现咽痛㊁牙龈肿痛㊁痤疮等阳气不敛㊁虚火上冲之象,常用砂仁㊁肉桂以收敛阳气,纳气归肾,引火归原㊂白芍味酸能敛,敛降甲木胆火,使相火归位㊂‘本草求真“曰: 气之盛者,必赖酸为之收,故白芍号为敛肝之液,收肝之气,而令气不妄行也㊂[9] 朱章志常使用白芍以补肝之体㊁助肝之用,收敛肝气,肝平则郁气自除,火热自消㊂山萸肉秘精气㊁敛阳气,使龙雷之火归于水中㊂朱章志常用山萸肉收敛正气,遇汗出多者,常重用以固涩敛汗㊂泽泻能泻能降,能入肾泻浊,开气化之源,泻浊以利扶正,又能降气而引火下行㊂朱章志常用泽泻打通西方潜藏之要塞[10],在温阳之品中加入泽泻,利于阳气潜藏,使孤阳有归㊂2.1.3㊀填补阴精,以滋化源㊀‘素问㊃金匮真言论篇“提到: 夫精者,身之本也㊂ 精 是人体生命活动的物质基础,能化气生髓,濡养脏腑㊂人体之精禀受于父母,又由后天水谷之精不断充养,归藏于肾中㊂ 孤阴不生,独阳不长 ,无阳则阴无以生,无阴则阳无以化㊂肾乃水火之脏,阴精充足才能涵养坎中真火,使真阳固密于内,化生正气㊂朱章志常在秋冬之季嘱糖尿病患者进补阿胶等血肉有情之品填补肾精㊂肾主封藏,秋冬进补使肾精充养,以滋阳气化生之源㊂阿胶用黄酒烊化,既能祛除阿胶之腥,又能借黄酒通行之性解阿胶滋腻碍胃之弊,每日少量服用,以有形之精难以速生,填补肾精以缓补为要㊂除此之外,遣方用药时亦会注意顾护阴精,在使用温阳药的同时常常配伍山萸肉㊁白芍等养阴药,以防温燥伤阴之弊㊂2.2㊀祛邪2.2.1㊀外散寒水以运太阳㊀ 太阳为开 ,太阳乃三阳之表,巨阳也,其性开泄以应天,为祛邪之重要通道㊂在运气里,太阳在天为寒,在地为水,合而为太阳寒水㊂张仲景太阳病篇研究的是水循环过程,治太阳就是治水[11]㊂寒㊁水之邪闭郁在表,气血运行不畅,可见肌肤麻木不仁㊂邪气滞留太阳,阻碍阳气运行,当因势利导㊁开太阳之表以发汗,外散寒㊁水之邪㊂糖尿病患者正气亏虚为本,祛邪不能伤正,朱章志临床常用桂枝麻黄各半汤小发其汗,使玄府开张,邪有出路㊂桂枝麻黄各半汤乃发汗轻剂,为桂枝汤与麻黄汤相合而得,其中麻黄㊁桂枝㊁生姜㊁北杏发散宣肺以开皮毛,芍药㊁大枣㊁炙甘草酸甘化阴以益营,诸药相合,刚柔相济,祛邪而不伤正㊂邪去正安,阳气运行通畅,水液代谢复常则阳气自充,而无寒水之扰㊂若寒邪较重可用三拗汤,此为麻黄汤去桂枝而成,功善开宣肺气,疏散风寒,因去辛温之桂枝发汗力不及麻黄汤,祛邪而不伤正㊂2.2.2㊀下利水湿以健少阴㊀少阴乃水火交会之脏,元气之根,人身立命之本㊂‘医理真传“提到: 坎中真阳,一名龙雷火,发而为病,一名元阳外越,一名孤阳上浮,一名虚火上冲㊂此际之龙,乃初生之龙,不能飞腾而兴云布雨,惟潜于渊中,以水为家,以水为性,遂安其在下之位㊂水盛一分龙亦盛一分,水高一尺龙亦高一尺,是龙之因水盛而游 [12]㊂阴盛051中国中医基础医学杂志Journal of Basic Chinese Medicine㊀㊀㊀㊀㊀㊀2021年1月第27卷第1期January2021Vol.27.No.1则阳衰,水湿之邪泛滥,则龙雷之火因而飞越在外㊂叶天士深谙张仲景之理,提到 通阳不在温,而在利小便 [10,13],通过利小便的方法,使水湿之邪从下而解,阳气运行通道无水湿之邪阻碍,则阳气无需温养而自通,水盛得除则真龙亦安其位㊂朱章志常用五苓散㊁真武汤下利水湿,以复阳气之通达,少阴之健运㊂五苓散具有通阳化气利水之效,治疗膀胱气化不利形成的蓄水证㊂方中猪苓㊁茯苓㊁泽泻导水湿之邪下行;白术健脾燥湿,杜绝生湿之源;桂枝助膀胱气化,通阳化气行水又通气于表,使全身在表之湿邪皆得解,五药合用,膀胱气化复常,水道通调使小便得利,水湿得出㊂真武汤为治疗少阴阳虚㊁水气泛滥之主方,方中附子振奋少阴阳气,使水有所主;白术㊁茯苓健脾制水;生姜助附子敷布阳气,宣散水气;芍药利小便,制附㊁姜之燥,五味相合共奏温阳利水之功㊂2.2.3㊀开郁逐寒以畅厥阴㊀肝为将军之官,肝气主动主升发,能统帅兵马,捍卫君主㊂厥阴肝经,体阴用阳,内寄相火,相火敷布阳气,祛阴除寒,是祛邪的先锋主力军㊂朱章志常用吴茱萸汤祛除厥阴肝经之寒邪,恢复肝经阳气之运行㊂方中吴茱萸辛苦而温,芳香而燥,‘本草汇言“曰: 开郁化滞,逐冷降气之药 [14],能温胃暖肝,降浊阴止呕逆,为治疗肝寒之要药㊂配以生姜温胃散寒,佐以人参㊁大枣健脾益气补虚,全方散寒与降逆并施,共奏暖肝温胃㊁降逆止呕之效㊂‘素问㊃至真要大论篇“说: 帝曰:厥阴何也?岐伯曰:两阴交尽也㊂ 物极必反,重阴必阳㊂厥阴为阴尽阳生之脏,足厥阴肝经与足少阳胆经互为表里,若出现肝气不疏㊁枢机不利㊁气郁化火,朱章志常用小柴胡汤和畅枢机,开郁以复气机调达㊂方中柴胡疏泄肝胆之气;黄芩清泄胆火,一疏一清,气郁通达,火郁得发;生姜㊁半夏和胃降逆;人参㊁大枣㊁炙甘草固护中宫,全方寒温并用㊁补泻兼施,以复厥阴疏泄之职,使气机和畅㊁阳气运行有序㊂3㊀典型病案患者杨某,女,65岁,2017年3月10日初诊:2型糖尿病病史6年余,症见疲乏,双下肢轻度浮肿,下肢冰凉,背部易汗出,口苦口干,偶有腰膝酸软,纳眠可,二便调,舌淡暗,苔黄腻,脉沉细㊂辅助检查示糖化血红蛋白10.8%,空腹血糖14.59mmol/L,总胆固醇6.38mmol/L,甘油三酯3.66mmol/L,低密度脂蛋白胆固醇4.34mmol/L㊂西医诊断2型糖尿病㊁高脂血症,治疗给予门冬胰岛素30(早餐前22u晚餐前20u)控制血糖,阿托伐他汀钙片(20mg, qn)调脂㊂中医诊断消渴病,少阴阳虚寒湿证㊂患者少阴阳气衰微不足以养神,固见疲乏;腰为肾之府,少阴阳虚则见腰膝酸软,阳虚寒盛则见下肢冰凉;背部正中乃督脉运行之所,阳气虚衰无以固摄则见背部汗出;少阴阳虚不能主水,寒水泛滥则见双下肢浮肿;水湿内停有郁而化热之象,则见口苦口干㊁舌苔黄腻㊁舌淡暗,脉沉细为少阴阳虚寒湿之征,治以温阳散寒㊁利水除湿为法㊂方以扶正祛邪方合当归拈痛汤加减:炮附片10g(先煎1h),红参10g (另炖),干姜15g,白术30g,炙甘草15g,桂枝12 g,麻黄8g,生姜30g,猪苓10g,泽泻30g,茯苓30 g,白芍30g,酒萸肉45g,当归15g,茵陈10g,5剂水煎服,2d1剂,水煎至250ml,饭后分2次服用,次日复煎㊂方中以附子理中汤为底方温补中焦,散寒除湿;加桂枝㊁麻黄使寒湿之邪从皮毛而解;加五苓散通阳化气,使湿邪从下而出;生姜散寒除湿;白芍㊁酒萸肉收敛阳气,以助正气祛邪;当归活血利水;茵陈清热利湿㊂2017年3月24日二诊:患者双下肢浮肿减轻,疲乏较前好转,无口干口苦,无腰膝酸软,仍觉下肢冰凉,背部仍有汗出,动则尤甚,大便每日二行,质偏烂,舌淡暗,苔白腻,脉细㊂患者大便质烂,乃邪有出路,导水湿之邪从大便而解㊂患者无口干口苦,舌苔由黄腻转为白腻,知湿郁化热之象已除,遂去茵陈㊂仍觉下肢冰凉乃内有久寒,加制吴茱萸12g以散沉寒痼冷;上方加酒萸肉至60g以加强收敛阳气㊁固摄敛汗之效,加黄芪60g以健脾益气敛汗;加砂仁6g(后下)㊁肉桂3g(焗服)以加强收敛阳气㊁扶助正气之效,7剂水煎服,服法同前㊂2017年4月7日三诊:患者背部汗出减少,下肢转温,余症皆除,大便每日二行质软,舌淡红,苔薄白,脉细较前有力,继续服二诊方药5剂㊂后给予附子理中丸(每次8粒,每日3次)服用1个月巩固疗效㊂2017年11月17日复诊:患者上述症状皆除,纳眠可,二便调㊂复查糖化血红蛋白6.8%,空腹血糖6.5mmol/L,总胆固醇5.14mmol/L,甘油三酯1.65 mmol/L,低密度脂蛋白胆固醇2.43mmol/L㊂4㊀结语以往医家多以滋阴清热为法治疗糖尿病,通过长期的临床实践,朱章志不囿陈法,根据糖尿病患者当前之病因病机特点,运用扶正祛邪法治疗糖尿病,通过顾护太阴㊁扶助阳气㊁收敛阳气,祛除寒水湿之邪气,恢复阳气运行之通畅,为糖尿病的治疗提供新思路㊂参考文献:[1]㊀WANG L GAO-P-ZHANG-M,et al.Prevalence and EthnicPattern of Diabetes and Prediabetes in China in2013[J].JAMA,2017,317(24):2515-2523.[2]㊀谭宏韬,刘树林,朱章志,等. 首辨阴阳,再辨六经 论治惠州地区2型糖尿病的临床观察[J].中华中医药杂志,2018,33(9):4240-4244.(下转第181页)offspring of sleep-deprived mice[J].Psychoneuroendocrinology,2009,35(5):775-784.[9]㊀覃甘梅,覃骊兰.心肾不交型失眠动物模型研究进展[J].中华中医药杂志,2018,33(1):229-231.[10]㊀吕志平,刘承才.肝郁致瘀机理探讨[J].中医杂志,2000,41(6):367-368.[11]㊀游秋云,王平,田代志,等.老年肝郁失眠证候大鼠模型的建立和评价[J].中国实验方剂学杂志,2013,19(2):222-225. [12]㊀唐仕欢,杨洪军,黄璐琦. 以方测证 方法应用的反思[J].中国中西医结合杂志,2007,27(3):259-262.[13]㊀卢岩,刘振华,于晓华,等.疏肝调神针法针刺对睡眠剥夺模型大鼠神经递质的影响[J].山东中医杂志,2017,36(4):322-325. [14]㊀YANG CR,SEAMANS JK,GORELOVA N.Developing aneuronal model for the pathophysiology of schizophrenia based onthe nature of electrophysiological actions of dopamine in theprefrontal cortex[J].Neuropsychopharmacology,1999,21(2):161-194.[15]㊀何林熹,诸毅晖,杨翠花,等.失眠肝郁化火证大鼠模型的建立及其评价[J].中华中医药杂志,2018,33(9):3890-3894. [16]㊀李越峰,徐富菊,张泽国,等.四逆散对大鼠睡眠时相影响的实验研究[J].中国临床药理学杂志,2014,30(10):936-938. [17]㊀张晓婷,刘文超,刘俊昌,等.电击法建立SD大鼠焦虑型心理应激-失眠模型的研究[J].现代中西医结合杂志,2018,27(30):3316-3319.[18]㊀钱伯初,史红,郑晓亮.新的失眠动物模型研究概述[J].中国新药杂志,2008,17(1):1-4.[19]㊀朱洁,申国明,汪远金,等.肝郁证失眠大鼠模型的建立与评价[J].中医杂志,2011,52(8):689-692.[20]㊀刘倩,李蜀平,廖磊,等.调和肝脾方治疗失眠的实验研究[J].北京中医药,2018,37(8):768-770.[21]㊀全世建,焦蒙蒙,黑赏艳,等.交泰丸对睡眠剥夺大鼠下丘脑Orexin A及γ-氨基丁酸的影响[J].广州中医药大学学报,2015,32(1):103-105.[22]㊀KOBAN M,SWINSON KL.Chronic REM-sleep deprivation ofrats elevates metabolic rate and increases UCP1gene expressionin brown adipose tissue[J].Am J Physiol Endocrinol Metab,2005,289(1):68-74.[23]㊀赵俊云,杨晓敏,胡秀华,等.失眠动物模型HPA轴和表观遗传修饰的变化及交泰丸的干预作用[J].中医药学报,2018,46(4):19-21.[24]㊀GORGULU Y,CALIYURT O.Rapid antidepressant effects ofsleep deprivation therapy correlates with serum BDNF changes inmajor depression[J].Brain Res Bull,2009,80(3):158-162.[25]㊀BENCA RM,PETERSON MJ.Insomnia and depression[J].Sleep Med,2008,9(1):S3-S9.[26]㊀郜红利,涂星,卢映,等.心肾不交所致失眠大鼠模型[J].中成药,2014,36(6):1138-1141.[27]㊀杨钰涵,孙雨,王珺,等.中医病证相符的大鼠心肾不交失眠模型的建立及其血清代谢组学研究[J].中国中药杂志,2020,45(2):383-390.[28]㊀石皓月,鲁艺,李钰昕,等.中药治疗对氯苯丙氨酸失眠模型大鼠影响的基础研究进展[J].中国医药导报,2018,15(11):33-36.[29]㊀全世建,何树茂,钱莉莉.交泰丸交通心肾治疗失眠作用机理研究[J].辽宁中医药大学学报,2011,13(8):12-14. [30]㊀GULEC M,OZKOL H,SELVI Y,et al.Oxidative stress inpatients with primary insomnia[J].Pro NeuropsychopharmacolBiol Psychiatry,2012,37(2):247-251.[31]㊀ZHANG H,CAO D,CUI W,et al.Molecular bases ofthioredoxin and thioredoxin reductase-mediated prooxidant actionsof(-)-epigallocatechin-3-gallate[J].Free Radic Biol Med,2010,49(12):2010-2018.[32]㊀谢光璟,刘源才,胡辉,等.基于Trx系统介导的抗氧化应激探讨天王补心方对失眠模型大鼠的干预作用[J].时珍国医国药,2019,30(4):805-808.[33]㊀黄攀攀,王平,李贵海,等.老年阴虚失眠动物模型的建立与评价[J].中华中医药学刊,2010,28(8):1719-1723.[34]㊀XIONG L,HUANG XJ,SONG PX.The experiment ofstudymodel of Deficiency of yin Insomnia by Yangyin anshenkoufuye[J].Chin J Pract Chin Mod Med,2005,18(18):1187-1188.[35]㊀韦祎,唐汉庆,李克明,等.脾阳虚证失眠大鼠模型的建立和附子理中汤的干预效应[J].中国实验方剂学杂志,2013,19(16):289-292.[36]㊀王志鹏.桂枝甘草龙骨牡蛎汤对阳虚证失眠大鼠脑内5-HT㊁NE含量的影响[D].南京:东南大学,2015.[37]㊀MURRAY NM,BUCHANAN GF,RICHERSON GB.InsomniaCaused by Serotonin Depletion is Due to Hypothermia[J].Sleep,2015,38(12):1985-1993.[38]㊀宋亚刚,李艳,崔琳琳,等.中医药病证结合动物模型的现代应用研究及思考[J].中草药,2019,50(16):3971-3978. [39]㊀李晓娟,白晓晖,陈家旭,等.中医动物模型研制方法及展望[J].中华中医药杂志,2014,29(7):2263-2266.[40]㊀刘臻,谢晨,赵娜,等.失眠动物模型的制作与评价[J].中医学报,2013,28(12):1846-1848.收稿日期:2020-05-18(上接第151页)[3]㊀司芹芹,牛晓红,杨海卿,等.温阳益气养阴活血方治疗2型糖尿病肾病的临床疗效[J].中华中医药学刊,2018,36(3):703-705.[4]㊀郭仪,石岩.中药复方治疗糖尿病大血管病变临床疗效及对血糖㊁血脂影响的系统评价[J].中华中医药学刊,2017,35(6):1369-1375.[5]㊀方春平,刘步平,朱章志.‘伤寒论“中 胃气 思想在病脉辨证中的运用[J].浙江中医药大学学报,2014,38(8):948-950.[6]㊀黄元御.四圣心源[M].北京:中国中医药出版社,2009:24.[7]㊀朱章志,林明欣,樊毓运.立足 阳主阴从 浅析糖尿病的中医治疗[J].江苏中医药,2011,43(4):7-8.[8]㊀缪希雍.本草经疏[M].北京:中国医药科技出版社,2011:56.[9]㊀黄宫绣.本草求真[M].北京:中国中医药出版社,2008:132.[10]㊀林明欣,裴倩,朱章志.浅析 通阳不在温,而在利小便 [J].中医杂志,2011,52(19):1705-1706.[11]㊀刘力红.思考中医[M].桂林:广西师范大学出版社,2006:457.[12]㊀郑寿全.医理真传[M].北京:中国中医药出版社,2008:3.[13]㊀刘涛,张毅,李娟,等.结合‘伤寒论“探讨 通阳不在温而在利小便 [J].中国中医药信息杂志,2017,24(9):106-107.[14]㊀倪朱谟.本草汇言[M].北京:中医古籍出版社,2010:87.收稿日期:2020-04-27。
English For Medical Purpose

∙Images ∙quizzes ∙Lists∙∙∙∙∙∙diagnosis,the process of determining the nature ofa disease or disorder and distinguishing it from other possible conditions. The termcomes from the Greek gnosis, meaning knowledge.The diagnostic process is the method by which health professionals select one disease over another, identifying one as the most likely cause of a person’s symptoms.Symptoms that appear early in the course of a disease are often more vague and undifferentiated than those that arise as the disease progresses, making this the most difficult time to make an accurate diagnosis. Reaching an accurate conclusion depends on the timing and the sequence of the symptoms, past medical history and risk factors for certain diseases, and a recent exposure to disease. The physician, in making a diagnosis, also relies on various other clues such as physical signs, nonverbal signals of distress, and the results of selected laboratory andradiological and other imaging tests. From the large number of facts obtained, alist of possible diagnoses can be determined, which are referred to as thedifferential diagnosis. The physician organizes the list with the most likely diagnosis given first. Additional information is identified, and appropriate tests are selected that will narrow ... (200 of 8,117 words)Unit 2 text A∙Images∙Videos∙quizzes∙Lists∙∙∙∙∙∙therapeutics,treatment and care of a patient for the purpose of both preventing and combating disease or alleviating pain or injury. The term comes from the Greek therapeutikos, which means “inclined to serve.”In a broad sense therapeutics means serving and caring for the patient in acomprehensive manner, preventing disease as well as managing specific problems.Exercise, diet, and mental factors are therefore integral to the prevention, as well as the management, of disease processes. More specific measures that are employed to treat specific symptoms include the use of drugs to relieve pain or treat infection, surgery to remove diseased tissue or replace poorly functioning or nonfunctioning organs with fully operating ones, and counseling or psychotherapy to relieve emotional distress. Confidence in the physician and in the method selected enhances effectiveness.Unit 2 text BDaring to Practice Low-Cost Medicine in a High-Tech EraSean Palfrey, M.D.N Engl J Med 2011; 364:e21March 17, 2011DOI: 10.1056/NEJMp1101392Share:ArticleCiting Articles (5)A child with chest pain or tics, a toddler who is limping, a 12-year-old girl with abdominalpain or headaches, an infant whose fever does not respond to antibiotics — these areage-old challenges that pediatricians face. I have been teaching pediatrics to residents and medical students for more than three decades, but over the past few years, as I've watched trainees at work, sitting at their computers, and ordering and monitoring tests, I've grownworried that the practice of medicine has tipped out of balance.Recent advances in scientific knowledge and technology have resulted in the development of a vast array of new tests, new pharmacologic agents, and new diagnostic andtherapeutic procedures. These are so accessible to us in the United States that few of uscan resist using them at every opportunity. By being impatient, by mistrusting ourhard-earned clinical skills and knowledge, and by giving in to the pressures andopportunities to test too much and treat too aggressively, we are bankrupting our healthcare system. Ironically, by practicing this way, we are perpetuating serious economic andracial disparities and have built a health care system that rates in the bottom tier among all developed countries in many categories of children's health outcomes.Most doctors are intensely risk-averse. We don't tolerate uncertainty. Not wanting anything bad to happen, we reflexively overtest and overtreat in order to protect our patients — and ourselves. We feel judged by everyone — ourselves, our colleagues, our patients, thehealth care system, and the lawyers. The meaning of ―first do no harm‖ has changed for us.We feel that ―doing everything‖ is the best practice and the way to prevent harm, and webelieve that it will shelter us from blame. We order tests and treatments because they areavailable to us, well before their importance has been established, their safety has beendetermined, and their cost–benefit ratio has been calculated.The evaluation of a child with fever and cough is a good example. There are many possible causes, and we have a huge battery of available tests that might give us potentiallyrelevant information. But why should we no longer trust our physical exam, our knowledge of the possible causes and their usual courses, and our clinical judgment? How much willwe gain by seeing an x-ray, now, and how likely is it that the result will necessitate achange in our management? How dangerous would it be if we chose to perform certaintests later or not at all? Might our residents not learn more by thinking, waiting, andwatching? Who is actually benefiting when we order a test — the patient, the laboratory,the drug company, the health plan administrators, or their investors? And who is losinghealth care as we spend these dollars? We need to ask these questions of ourselves and our residents at every step of the clinical process.I believe that we must rediscover the value of clinical judgment and relearn the importance of the personal, intellectual, scientific, and administrative thought that is central to the best practice of medicine. We need comparative-effectiveness research, as well as cost-benefit and long-term–benefit analyses, to inform us how to integrate traditional clinical skills with the use of new tests and therapies. Our time and attention have been diverted to the task of sorting out data instead of sorting out what is important to our patients, their families, and the community at large. This new style of test-avid, cover-all-possibilities practice is bankrupting our health care system and depriving many families of access to health care and a medical home. Not having a medical home can be as devastating as not having a physical home. If children have no primary care, we have no way to prevent their asthma attacks, poisonings, obesity, or suicides, and if they are unimmunized, they may spread vaccine-preventable illnesses to their young siblings and aged grandparents. Society as a whole is the loser.We as clinicians must change our practice patterns, but first the medical community, through standard-of-practice guidelines, must give us permission (or better yet, encourage us) to practice in a less costly way, so we don't feel we are expected and incentivized to order expensive tests or treatments. Similarly, clinician-teachers must develop the confidence (or be given the imperative) to teach students, residents, and fellows how to practice in the most knowledge-based, least invasive, most frugal fashion possible and to seek input from physicians with more clinical experience when they feel the urge to order a test or initiate a treatment.Education of the public is also critically important. We need to admit to our fellow citizens that the United States, despite its wealth, technology, and research expertise, is 21st in the world in terms of many indicators of health, and we must convince them thatpopulation-wide changes designed to improve health outcomes would be in everyone's best interest. We need to teach our patients that more medicine is not better medicine, that it is poor health care for doctors to order too many tests or too many interventions, and that costly efforts do not equal better health care. As we address their personal needs, we need to explain to our patients that we have to use new medical technology with care and wisdom. Indiscriminate health care spending is not fiscally sustainable at a national level and actually hampers the achievement of many universal health benefits.Every participant in our health care system must focus on ways to optimize health while decreasing cost, at every step of the process. We need to change the financial incentives currently embedded in health care reimbursement systems that reward the use of tests, procedures, consultations, and high-cost therapies. And finally, the legal system needs to be more restrained about pursuing lawsuits when a difficult diagnosis is missed or atreatment fails, to diminish the pressure on health care providers to practice expensive,defensive medicine at every turn.These are major changes, but today we are far from providing good care for all our citizens and far from achieving health care equal to that in many other countries. We need toincorporate more realistic clinical, scientific, and financial information into practice in order to bring our health care practices, and our health care system, back into balance.Unit 3 text A∙∙∙∙∙∙∙∙∙∙system of A visit to a traditional Chinese∙∙∙∙∙∙nursing,< Sean >profession that assumes responsibility for the continuous care of the sick, the injured, the disabled, and the dying. Nursing is also responsible for encouraging the health of individuals, families, and communities in medical and community settings. Nurses are actively involved in health care research, management, policy deliberations, and patient advocacy. Nurses with postbaccalaureate preparation assume independent responsibility for providing primary health care and specialty services to individuals, families, and communities.Professional nurses work both independently and in collaboration with other health care professionals such as physicians. Professional nurses supervise the work of nurses who have limited licenses, such as licensed practical nurses (LPNs) in the United States and enrolled nurses (ENs) in Australia. Professional nurses also oversee the work of nursing assistants in various settings.Nursing is the largest, the most diverse, and one of the most respected of all the health care professions. There are more than 2.9 million registered nurses in the United States alone, and many more millions worldwide. While true demographic representation remains an elusive goal, nursing does have a higher proportional representation of racial and ethnic minorities than other health care professions. In some countries, however, men still remain significantly underrepresented. The ... (200 of 4,122 wordsText a ChangingFaces ofNursing:A PersonalStoryby Traci TayloIt all started for her, as it had for nurses for generations, with a pristine whitenurse’s cap, starched, with a new black band freshly attached. Her neatly pressedwhite uniform had a new graduation pin telling the world that she was now anurse. Her idealism and vision were palpable; she had started a new part of herlife and had the diploma to prove it.As an awkward, uncertain teenager, I was in awe of my mother, this womanwho had worked so hard to do something amazing. This was perhaps thetime in my life when I started to seriously consider nursing as a profession;maybe I could do something really exciting if Icould wear a white uniform, pass a chemistryclass, and work wherever I wanted to (thisfrom the perspective of a fifteenyear old). This wasn’t a career forthe faint-hearted; this was special.A few years later, I wore that whiteuniform (minus the cap) and knewthat this was more than a science classor mere job choice — this was life!The definition of nursing has beendramatically revised and shaped in the past25 years, being influenced by nursing theorists,new diseases, and new technology. Mom startedher nursing career at a different time, which seemsarchaic by some standards nowadays. Gloves were usedprimarily for sterile procedures and wound dressings.Syringes were glass (and reusable!), and nursing theorywas only then being revised and utilized. Patients were atthe hospital until they were almost well, and there was time for back massages at night. My mother still believes in this holistic type of nursing—she has been a home health nurse for over twenty years, specializing in wound care. She still believes in giving time to her patients. Her uniforms are still starched, and though the cap is gone,she has the excitement and optimism that she had when she graduated, balanced with more realism. Because of the work of others “behind the scenes” in nursing, she is able to continue to do what she believes in. Nursing theorists’ ideas and research provided much of the scientific basis for nursing as we know it today. For instance, in the 1970s and 1980s, Martha Rogers wrote several works, all of which explaining that nursingis an essential discipline, separate from others—namely, medicine—and that it is a science, with a unique body of knowledge (Garon, 2002). Goneis the thought that we are physicians’ handmaidens or only change bedpans throughout the day. Treating nursing as a discipline in and of itself elevates the profession and enables us to research and provide care for patients from a perspective different than that of any other discipline. Currently, it is widely accepted that nursing is an independent profession, though debate isstill common regarding that status. A similar discussion occurred inthe 1980s, when the courts did not routinely define nursing as an autonomous profession and often used medical doctors as “experts” in nursing care (Segal, 1985). (Continued on page 38 2)My mother graduated in a time whencomputers were not really for the averageperson—she still has trouble turning onher PC—and were not generally used atthe bedside. In fact, a study published in1985 showed that a Medline search forarticles took an average of 5-18 minutesby an experienced librarian (Haynes,McKibbon, Walker, & Mousseau et.al,1985). Now, I expect to find a Medlinearticle in 5-18 seconds, depending on howfast I can type—no librarian required Using the Medline search recently, I found journal articles from 1985 that reportedthe new drugs of the day. These includedglyburide and glipizide, medicationsthat no diabetic patient is without today,and other medications such as nicotineresin complex (also known as Nicorette,Merrell Dow) and labetolol that are stillused routinely (Hussar, 1985). I mustconfess a certain fondness for these articles- I used to read my mother’s nursingjournals, and vividly remember the formatof Nursing83-88. Of course, at that ageI was mo re interested in “ActionStat!”and similar columns that were easierfor a 16 year-old to read, as they weremore exciting than information aboutmedications.Not only did my mother become anurse after my parents’ divorce, myfather enrolled in nursing school afterhe remarried. When I started collegea few years later, I listed my major as“nursing,” mostly because I couldn’t thinkof anything better than nursing. The onlyalternatives that I could see were businessrelated: how exciting could insurance andnumber crunching really be? So nursingbecame my destiny.Parker Palmer, the great modern-dayeducator, speaks of the power of ourmentors and that a great mentor has thecapacity to cause an awakening of truthwithin us; that he or she can give “fullvoice to the gift of thought” (1998). Asa person who freely gives his heart to thepeople he loves, my father became mymentor by simply expressing his love fornursing—this nebulous, complicatedworld that I was only beginning toopen my eyes to in the early 1990s. Hereceived his nursing diploma in 1990,then immediately began pursuing a bachelor’s degree at the same universityI attended. We eventually graduated together in 1992, and I remember being fascinated before and after our graduation with his stories of nursing in a real hospital setting. Nursing was new to both of us and he told great stories of funny patients, nasty wounds, and physicians with delusions of grandeur. His hospital stories of patients and “real life” helped prepared me for the real thing—how to treat people, wash my hands properly, and handle sometimes difficult physicians. Our first few years of practice were during a transition period in nursing’s history; this was the time when the potential power of computers and other technology was only beginning to be recognized, and legislation affecting health economics was initiated. Dad bought a computer in 1990, at a time when they were handybut considered by many to be just an easier way to write a paper. As I read38 literature from that time period, I realize that there is so much we take for granted, like computerized bedside charting, the internet, and easy access to information. Little did we know at that time the effect that technology would have on our future practice. Could any nursing studenteven consider completing an assignment without internet access? Our textbooks are out of date before they are printed—we update portfolios online and we track patient histories via digital records.There are so many things that I do routinely in the course of a day that simply were not an option for my parents, or even for me in my early career, IV pumps for routine use in the hospital, knowledge of infection control techniques, wound care protocols(that I still ask my mother about), andprivacy acts to enforce. There was othertechnology as well that transformednursing. Shortly before my dad and Istarted our practice, the Infuse-A-Portwas introduced; this device changed thequality of care patients could receive,decreased pain, and improved their qualityof life (Speciale, 1985). And isn’t thatwhat nursing is about? Intravenous fluidpumps, which were once only availablein the most high-tech hospitals, replacedthe roller clamp for intravenous fluid andmedication regulation, helping decreasea nurse’s workload and increasing clientsafety. Technology such as this, combinedwith economic changes such as diagnosisrelated group [DRG] requirements by the government, paved the way for patientsto leave the hospital sooner than everbefore, increasing the required level ofcare at home (Coleman & Smith, 1984).DRGs, the diagnosis-based paymentsystem initiated by Medicare, caused adecreased length of stay in the hospital,resulting in a proliferation of home healthservices. This changed the face and focusof many nursing careers, including myfather’s. He started in home health inthe mid-1990s, learning to interpret thenew rules while learning to be a nurse ina new environment. His stories of thejoys and pitfalls of home care encouragedme to eventually choose this route aswell, and I became involved in caring for people at home. I eventually chose hospice as my passion—a place in nursingwhere becoming part of a family is almostnecessary, and life changes for all thoseinvolved.In ten years, perhaps you, too, may bewriting an article on “how it used to be.”You will laugh at the procedures you did,at how long it took to get information,and at the medications that were beingproduced that will be obsolete at the timeof your writing. And I hope you will beable to look back on the really importantthings other nurses taught you; like whatit means to “be with” a patient and thedifference between being a real nurse anda person “who performs tasks.”Nursing has become not just a job or evena career, but part of who I am, mostlyas a result of the investment of othernurses in my life. As a nursing studentyet again, I am reminded that the nursingthat my parents and their contemporariespracticed laid the foundation for the typeof nursing I practice today. Nursing isn’twhat it used to be. Or, perhaps, it is morelike what my mother envisioned whenshe started nursing: patients are importantand health care professionals can work as ateam to effectively advocate for them. GReferencesColeman, J.R., & Smith, D.S. (1984). DRGs and thegrowth of home health care. Nursing Economics, 2,391-408.Garon, M. (2002). Science of unitary human beings:Martha E. Rogers. In J. George (Ed.), Nursing theories:The base for professional nursing practice (pp. 269-289). Upper Saddle River, NJ: Prentice Hall. Haynes, R.B., McKibbon, A., Walker, C.J., Mousseau,J., Baker, L., et.al. (1985). Computer searching of themedical literature. Annals of internal medicine, 103(5),812-816.Hussar, D.A. (June, 1985). New drugs. Nursing85,15(6), 33-39.Palmer, P. (1998). The courage to teach: Exploring theinner landscape of a teacher’s life. San Francisco, CA:Jossey-Bass.Segal, E.T. (June, 1985). Is nursing a profession?Nursing85, 15(6), 41-43.Speciale, J.L. (October, 1985). Infuse-a-port: New pathfor I.V. chemotherapy. Nursing85, 15(10), 40-43.Traci Taylor Traci Taylor, RN,MSN, CHPN, hasbeen practicingnursing for 17 years,primarily in geriatricand hospice care.She is currently aninstructor of nursing at West TexasA&M University, Canyon, Texas,where she received both her BSNand MSN (education). Her nursingand teaching interest is in end-of-lifecare and she has been a Certified Hospice and Palliative Nurse since 2006., RN, BSN, CHPN, MSN-c, is (bio t/k。
Clinicai Diagnostic1

Ultrasonic imaging
CT imaging
MRI
PET
Medical record
Medical record is a systematized way of storing the required data, information and other relevant documents
A fundamental course of clinical medicine 临床医学的基本课程
Fundamental elements of Diagnostics
Diagnosis
Identification Analysis
Diagnosis (诊断)
☆ Derived from Greek words
Clinical Diagnostics
Department of Gastroenterology Affiliated Hospital of Nantong University
What is Clinical Diagnostics?
Fundamental theory 基础理论/知识
Techniques of diagnosing disease 诊断疾病的技术
Sign (体征) Abnormality observed by the physician Physical examination (体格检查)
Evidence-Based Medicine 产品介绍说明书

Purpose and procedure.......................................................T he purpose of Evidence-Based Medicine is to alert clinicians to important advances in internal medicine,general and family practice,surgery,psychiatry,paediatrics,and obstetrics and gynaecology by selecting from the biomedical literature those original and review articles whose results are most likely to be both true and useful.These articles are summar-ised in value-added abstracts and commented on by clinical experts.The author of the original article is given an opportu-nity to review the abstract and commentary before publication. The procedures we follow to achieve this purpose areN Detecting,using prestated criteria,the best original and review articles on the cause,course,diagnosis,prevention, treatment,quality of care,or economics of disorders in the foregoing fieldsN Introducing these articles with declarative titles and summarising them accurately in structured abstracts that describe their objectives,methods,results,and conclusions N Adding brief,highly expert commentaries to place each of these summaries in its proper clinical and healthcare context N Disseminating these summaries in a timely fashion.CRITERIA FOR REVIEW AND SELECTION FOR ABSTRACTINGGeneralAll English-language original and review articles in an issue of a candidate journal are considered for abstracting if they concern topics important to the clinical practice of internal medicine,general and family practice,surgery,psychiatry, paediatrics,or obstetrics and gynaecology.Access to foreign-language journals is provided through the systematic reviews we abstract,especially those in the Cochrane Library,which sum-marises articles from over800journals in several languages. Prevention or treatment;quality improvementN Random allocation of participants to interventionsN Outcome measures of known or probable clinical importance for>80%of the participants who entered the investigation.DiagnosisN Inclusion of a spectrum of participants,some(but not all)of whom have the disorder or derangement of interest N Each participant must receive the new test and thediagnostic standard testN Either an objective diagnostic standard or a contemporary clinical diagnostic standard with demonstrably reproduci-ble criteria for any subjectively interpreted component N Interpretation of the test without knowledge of the diagnostic standard resultN Interpretation of the diagnostic standard without knowl-edge of the test result.PrognosisN An inception cohort of persons,all initially free of theoutcome of interestN Follow up of>80%of patients until the occurrence of either a major study end point or the end of the study.CausationN Observations concerning the relation between exposuresand putative clinical outcomesN Prospective data collection with clearly identified compar-ison group(s)for those at risk for the outcome of interest (in descending order of preference from randomised controlled trials,quasi-randomised controlled trials,non-randomised controlled trials,cohort studies with case by case matching or statistical adjustment to create compar-able groups,to nested case control studies)N Masking of observers of outcomes to exposures(this criterion is assumed to be met if the outcome is objective).Economics of health care programmes or interventions N The economic question must compare alternative coursesof action in real or hypothetical patientsN The alternative diagnostic or therapeutic services or quality improvement strategies must be compared on the basis of both the outcomes they produce(effectiveness)and the resources they consume(costs)N Evidence of effectiveness must come from a study(or studies)that meets criteria for diagnosis,treatment,quality assurance,or review articlesN Results should be presented in terms of the incremental or additional costs and outcomes incurred and a sensitivity analysis should be done.Clinical prediction guidesN The guide must be generated in1set of patients(training set)and validated in an independent set of real not hypothetical patients(test set),and must pertain to treatment,diagnosis,prognosis,or causation. Differential diagnosisN A cohort of patients who present with a similar,initiallyundiagnosed but reproducibly defined clinical problem N Clinical setting is explicitly describedN Ascertainment of diagnosis for>80%of patients using a reproducible diagnostic workup strategy and follow up until patients are diagnosed or follow up of>1month for acute disorders or>1year for chronic or relapsing disorders. Systematic reviewsN The clinical topic being reviewed must be clearly stated;there must be a description of how the evidence on this topic was tracked down,from what sources,and with what inclusion and exclusion criteriaN>1article included in the review must meet the above-noted criteria for treatment,diagnosis,prognosis,causation,quality improvement,or the economics of healthcare programmes. Evidence-Based Medicine has a related journal,ACP Journal Club. It is generated using procedures identical to those used for Evidence-Based Medicine and is published by the American College of Physicians.Approximately one third of the abstracts in ACP Journal Club are published in Evidence-Based Medicine,and the abstracts not published are listed,by their declarative titles,in the section titled Additional Articles Abstracted in ACP Journal Club.33EBM on December 25, 2023 by guest. Protected by copyright./ Evid Based Med: first published as 10.1136/ebm.12.2.33 on 30 March 2007. Downloaded from。
检验医学决定水平

实验室医学决定水平医学决定水平(Medicine decide level,MDL)是指不同于参考值的另一些限值,通过观察测定值是否高于或低于这些限值,可在疾病诊断中起排除或确认的作用,或对某些疾病进行分级或分类,或对预后作出估计,以提示医师在临床上应采取何种处理方式,如进一步进行某一方面的检查,或决定采取某种治疗措施等等。
例如ALT,它的升高通常都为肝细胞损伤所致,其中又可分为两类,一类是ALT的极度升高,一般由病毒性肝炎、药物性肝炎或肝性休克所引起的大的肝损伤所造成,它的ALT的测定范围一般在100~4000IU/L之间。
另一类则反映中度的肝细胞损伤,通常由酒精性肝炎、传染性单核细胞增多症和多肌炎所引起,它的ALT测定范围一般为30~300IU/L。
ALT的参考范围为5~40IU/L,它们含意仅指有95.5%的健康人其ALT测定值是在这一区间之内,但其医学决定水平则有三个,第一个决定水平是300IU/L,它可区别上述肝细胞损伤的二个临床类型,300IU/L以上的值表示极度的肝细胞损伤。
第二个决定水平是60IU/L,此值比参考值上限高50%左右,因为一般当ALT测定值在40~60IU/L之间时,并不能确定ALT的升高是否属于病理性改变,许多不很健康的肥胖者,其ALT值就通常浮动在这范围之内,只有当ALT值大于60IU/L时,才可明确诊断为肝细胞损伤,所以它是一个确认值。
ALT的第三个医学决定水平是20IU/L—比参考值限还低,这是一个排除值,低于此值则可排除许多与ALT升高有关的疾病。
医学决定水平与参考值的根本区别在于:它不仅对健康人的数值进行研究,以决定健康人的数值区间,同时还对有关疾病的不同病情的数据进行研究,以定出不同的决定性限值。
可提示及引导医师采取不同的临床措施。
所医学决定水平看来更合理、更客观、更有助于临床的应用。
当然,真正建立起每一项试验的医学决定水平是一个十分复杂的问题,存在着许多的实际困难。
美国CLIA88临床检验室内质量控制文件

美国CLIA’88临床检验各专业室内质量控制文件(一)美国CLIA’88质量控制要求美国临床实验室改进修正法案最终规则(CLIA final rule)于2003年1月24日通过,2003年4月24日实施。
其中K-非豁免试验的质量体系,分析系统中493.1256标准:控制程序(control procedures)对各专业质量控制提出具体要求。
1、控制程序根据美国CLIA’88最终规则Sec.493.1256标准:控制程序(a)对于每一检测系统,实验室负责制定控制程序,监测整个分析过程的准确度和精密度。
(b)实验室必须建立检测控制物的数量、类型和频率,如果适合,实验室应按Sec.493.1256(b)(3)规定验证或建立性能规范。
(c)控制程序必须(1)立即检测出由于检测系统故障、不利的环境条件及操作者性能而产生的误差。
(2)长期监测由于检测系统性能和环境条件改变和操作者性能变化而可能影响到的准确度和精密度性能。
(d)除了CMS批准的程序,如国家操作手册附录C中规定(CMS Pub.7)的外,提供了等效质量检测,实验室必须(1)执行本节规定的质量控制程序,除非在493.1261到493.1278部分其他专业和亚专业有其他的规定。
(2)对于每一检测系统,当他们满足或超出本节(d)(3)部分要求时,执行的质量控制程序使用厂家规定或实验室建立的个数和频率。
(3)每天检测患者标本时至少每天检测一次控制品,或执行如下的步骤(i)每一定量检测程序,包括两个不同浓度水平的控制品;(ii)对每一定性的检测程序,包括一个阴性和一个阳性控制品;(iii)对于产生分级或滴度结果的检测程序,分别包括阴性控制品和具有分级或滴度反应性的控制品;(iV)对于具有提取阶段的每一检测系统,包括两个控制品,其中一种能够检出提取阶段的误差;(v)对于每一种分子扩增程序,包括两个控制品,如果反应抑制性是假阴性结果的显著性来源,一个控制品能够检出抑制性作用。
应用品管圈提高强直性脊柱炎患者英夫利西单抗使用规范率

应用品管圈提高强直性脊柱炎患者英夫利西单抗使用规范率[摘要]目的运用品管圈提高强直性脊柱炎(AS)患者英夫利西单抗使用规范率。
方法成立品管圈活动小组,确立活动主题,分析AS患者输注英夫利西单抗规范率低的原因,拟定对策并组织实施,比较活动前后AS患者输注英夫利西单抗规范率。
结果 AS患者英夫利西单抗使用规范率从活动前的[1]7.25%提升至90.75%,比较活动前后,差异有统计学意义(P<0.05)。
雷达图显示:圈员解决问题能力、品管圈运用手法较前显著提升。
结论品管圈活动可以有效提高AS患者英夫利西单抗使用规范率,提升护理团队发展,提高圈员能力和素质。
[关键词]品管圈;强直性脊柱炎;英夫利西单抗;规范率Application of quality control circle to improve the standard rate of infliximab use in patients with ankylosing spondylitisSHI Na/WANG Zhiyan/MA Xining/YAO Hui/FU Rong[Abstract]Objective Use quality control circle to improve the standard rate of infliximab in AS patients.Methods Establish a quality control circle activity group, determine the theme of the activity, analyze the reasons for the low standard rate of infliximab infusionin AS patients, formulate countermeasures and organize implementation, and compare the standard rate of infliximab infusion in AS patients before and after the actibities.Results The standard rate ofinfliximab use in AS patients increased from 67.25% before theactivity to 90.75%. There was statistically significant (P<0.05).The radar chart shows that the solving ability of circle members and theuse of quality control circle methods have been significantly improved.Conclusion Quality control circle activity can effectively increase the standard rate of infliximab use in AS patients, enhance the development of the nursing team, improve the ability and quality of the circle members.[Key words]Quality Control circle;AS;Infliximab;Standard强直性脊柱炎(Ankylosing spondylitis,AS)是以脊柱为主要病变部位的一种慢性结缔组织疾病,病变多累及骶髂关节、脊柱和髋关节,常表现为关节疼痛及运动功能障碍[1]。
- 1、下载文档前请自行甄别文档内容的完整性,平台不提供额外的编辑、内容补充、找答案等附加服务。
- 2、"仅部分预览"的文档,不可在线预览部分如存在完整性等问题,可反馈申请退款(可完整预览的文档不适用该条件!)。
- 3、如文档侵犯您的权益,请联系客服反馈,我们会尽快为您处理(人工客服工作时间:9:00-18:30)。
Goal-Directed Diagnosis–Diagnostic Reasoning in Exploratory-Corrective DomainsRon RymonDepartment of Computer and Information ScienceUniversity of PennsylvaniaRoom419C,3401Walnut Street,Philadelphia,PA19104E-mail:rymon@(Proceedings IJCAI-93)AbstractIn many diagnosis-and-repair domains,diagnosticreasoning cannot be abstracted from repair actions,nor from actions necessary to obtain diagnostic in-formation.In general,in exploratory-correctivedomains an agent has to interleave exploratory ac-tivity with activity aimed at achieving its goals.In TraumAID2.0,a consultation system for multi-ple trauma management,we implement a reasoningframework for such domains which integrates di-agnostic reasoning with planning and action.Thispaper presents Goal-Directed Diagnosis(GDD),aformalization of TraumAID2.0’s diagnostic rea-soning.Taking the view that a diagnosis is onlyworthwhile to the extent that it can affect repair de-cisions,GDD uses goals to focus on such.Goalsare also useful as a means of communicating withits accompanying planner.1Background and MotivationIn many domains,it is common to distinguish reasoning andactivity concerned with what problems need be addressedfrom that reasoning concerned with how to address those prob-lems.As such,Artificial Intelligence(AI)subsumes as sepa-rate sub-disciplines diagnosis research,seeking the source(orsources)of a system’s faulty behavior,and planning research,concerned with the construction of action plans to achievecertain goals.Based on that dichotomy,most formalizationsof diagnosis aim at a diagnosis object as a solution.In some domains,however,this may be inadequate.Intrauma management,for one,therapy is the ultimate objectiveand diagnosis is the“price”that one has to pay in order toachieve that objective.In such domains,we argue,diagnosisshould only persist so long as it can affect those decisionsfor which it was carried out in thefirst place,namely repairdecisions.We call this the Goal-Directed Diagnosis(GDD)principle.The GDD principle suggests that diagnostic and therapeu-tic decisions be considered together.Furthermore,in many diagnosis-and-repair domains multiple diagnostic and thera-peutic needs require,and compete for,the agent’s activity.In1Three trauma surgeons were asked to blindly compare the actual care in97trauma cases to the management that would have been proposed by TraumAID2.0.The judges indicated a significant preference for TraumAID2.0plans over actual plans by a ratio of64 to17with16ties(0.001by binomial test).For more details see [Rymon,93].2Related Work2.1Formalizations of diagnosisRecent years have seen significant advances in formal ap-proaches to diagnosis.A large number of approaches and frameworks have been suggested:probabilistic classifiers and discriminators,logical consistency-based and abductive paradigms,graph-based formulations in which causal and co-incidental relations are modeled,etc.What is common,how-ever,to all these formalizations is that they take a diagnosis object–broadly defined as a characterization of the current state of affairs–as a solution and therefore as their goal.Our Goal-Directed Diagnostic paradigm takes a different view of diagnosis and its objectives:recommendations are impor-tant!.To understand this view,considerfirst that diagnosis is rarely an independent task,but rather serves the purpose of another process,e.g.repair.With incomplete information, general theories of diagnosis will often give rise to a large number of hypothetical diagnoses.As it often happens,many of these are irrelevant.Their computation,and the need on the part of the matrix process to sort through them,are thus a waste.An important observation made by Poole and Provan[90] is that the optimality of a diagnosis must depend on post-diagnosis goals.To that end,they advocate the use of utilities [91b];in[91a]they further note that there is often no need fora complete explanation and that the granularity of a solution again depends on its uses(and also on available tests).In some domains,explicitly specified utilities can be used to reflect issues of importance to the matrix process in diag-nostic process decisions.However,while utility-theory sees increased use in Artificial Intelligence in general and medi-cal decision making in particular,it also requires a level of completeness and precision in characterizing a domain that is sometimes hard to obtain and may not be available.The GDD principle can be viewed as a qualitative analogue of a utility-maximization principle.The GDD framework sup-ports the implementation of this principle in ECM agents by explicitly representing and reasoning about goals.In particu-lar,alternative actions are being ruled in or out according to direct and indirect(i.e.through action)goal interactions,e.g. suppression,subsumption,compatibility,preferences,etc.In exploratory-corrective domains,it is often hard to sepa-rate diagnosis from repair.The GDD paradigm is thus part of a total approach for reasoning which combines diagnostic rea-soning,planning and action.Friedrich et al.[91]and Sun and Weld[92]share much of this view.Considering diagnosis as part of an overall diagnosis-and-repair process,Friedrich et al. note that repair does not always require a complete diagnostic explanation.Unlike other formalizations,their theory has no explicit notion of a diagnosis object.Instead,a sequence of tests and repair actions is sought,that if applied to the current state,will imply(as in a logical proof)a restoration of the diag-nosed system to a proper working condition.Presented not as a theory of diagnosis but as a theory of repair planning,their work applies a possible-models planning approach[Winslett, 88]to a diagnostic domain.Friedrich and Nejdl[92]de-scribe a set of algorithms for diagnosis-and-repair plans.Sun and Weld use UWL,a STRIPS-like language,in an approach which integrates GDE-style diagnosis and STRIPS-style plan-ning.The link between diagnosis and repair planning in real applications is also emphasized by Pepper and Kahn[87]. Also related,although to a lesser extent,is work by Rushby and Crow[91]who formalize reconfiguration,a form of re-pair,using an extension of Reiter’s[87]theory of diagnosis. In GDD,we use goals to focus on repair-worthy issues.In the goal-level,we use GDD rules to resolve direct interactions between goals;indirect interaction between goals is resolved by the accompanying planner.In exploratory-corrective domains,actions are often neces-sary to obtain diagnostic information.While this is also true of many other domains,sequential diagnostic frameworks of-ten take a simplistic view of information acquisition.Often what is considered is the potential,or expected,discriminatory power of a given piece of information.The potential ramifi-cations of diagnostic activity,even on the very condition it is aimed at diagnosing,are often not considered;most models assume costless questions,or at best attach a simple cost to each piece of information.However,rather than worrying about these issues,research in diagnosis can simply rely on planning research which,studying these issues extensively, should come handy.Goals,the architectural duty of the GDD reasoner,serve as a natural interface with an accompanying planner.2.2AMORDAMORD[deKleer et al.,77]is a general purpose prob-lem solver which is accompanied with truth-maintenance and planning facilities.The main thesis behind AMORD’s rea-soning component is that combinatorial forward-chaining can be avoided via meta-reasoning,i.e.if the problem solver reasons explicitly about its reasoning strategy.In particu-lar,AMORD’s reasoner posts inference goals,distinct from those posted to its planner,which are used to control reason-ing.GDD shares this intuition.The key to the differences between AMORD’s reasoner and GDD’s are the distinct ob-jectives of their matrix systems:AMORD’s objective is to control reasoning,whereas in the ECM architecture our pur-pose is to control actions.Thus,the goals posted by GDD serve none of its own purposes but are rather aimed at the plan-ner.Although some of GDD’s goals are aimed at knowledge, knowledge goals are only encoded when action is required. In the ECM architecture,GDD is used to explicitly encode local strategies,and goal-level interaction between strategies. Most of the mediation and coordination between a number of concurrently pursued strategies is done by the planner im-plicitly,i.e.on thefly,as the diagnosis-and-repair session proceeds,based on general principles[Rymon,93].3Goal-Directed Diagnostic FrameworkGoal-Directed Diagnosis(GDD)begins with the point of view that diagnosis is only worthwhile if it has the potential to affect future decisions.Thus,while we accept the common definition of a diagnosis as a case characterization,we believe that different purposes can lead to different characterizations of the same situation.For example,different purposes may lead to different refinement efforts.GDD allows explicit encoding of purposes,which it uses to guide its problem solving.More specifically,throughout a problem solving session,the GDD reasoner will maintain both a belief–a description of the current characterization,and an attitude–encoding a sense of purpose by pointing to goals worth pursuing.In a recurrent cycle,the GDD reasoner takes as input a diagnostic problem,characterized by(1)observations;and (2)mappings(rules)from from observations to conclusions (belief),and from observations and conclusions to goals(at-titude).A solution to such problem is a new attitude-belief assignment.Goals,propositions regarded as relevant by the current attitude,are the addressed by the accompanying plan-ner and served by the actor(the physician in our case).New observations result in a modified diagnostic problem,and a new cycle is initiated.In this section,we describe a rule-based language for speci-fying diagnostic problems in GDD a corresponding inference scheme.3.1Underlying framework:Multi-valued logicsMulti-Valued Logics(MVL)[Ginsberg,88]is a formal frame-work for inference in which each proposition is assigned not only a truth value,corresponding to the strength of belief in that proposition being true or false,but also a knowledge as-sessment,measuring roughly the amount of knowledge used to derive such belief.Bilattices,in which one partial order ()corresponds to the truthfulness measure and the other ()to the knowledge one,are used in MVL as domains for truth-value assignment.Bilattice values are then combined along the truthfulness dimension using the regular and operators(join and meet of the lattice).The operator (join in the lattice)can be used to combine knowledge sources.Figure2depicts the smallest non-trivial bilattice, with four points:T rue,F alse,U nknown,and(representing the presence of contradictory evidence).FUTTruthfulnessKnowledgeFigure2:Basic Truth-Knowledge BilatticeWe havefirst formalized GDD using a three-valued logic: true,false and unknown[Rymon et al.,91].The MVL refor-mulation buys us expressiveflexibility(e.g.by extending the domain bilattices with default values).Tofit our needs,we have specialized MVL to a rule-based representation;Gins-berg’s original formulation uses a fullfirst-order logic,and thus requires an underlying theorem prover.While the mate-rial presented here is self-contained,the reader is referred to [Ginsberg,88]for a more complete coverage of MVL.3.2Attitude and beliefDuring the diagnostic process,the GDD reasoner will main-tain and update an attitude and a belief for propositional state-ments.To remain general,propositions may be any fact about the patient or the world that the reasoner may know to hold,may know not to hold,may assume,may want to know whether hold,may want to achieve,may be confused about,etc.The reasoner’s attitude towards and/or belief in a given proposition will change over time as a result of new in-formation becoming available,new inferences drawn,activity carried out,etc.In GDD,each proposition is assigned a value drawn from the cross product of two(possibly distinct)bilattices:one representing belief,the other attitude(or desire).The notion of belief is interpreted regularly,whereas the attitude component represents problem-solving control information and measures the relevance of acquiring information about,or achieving the condition described by,the particular proposition.The belief bilattice still has the truthfulness and knowledge partial orders;the attitude bilattice has relevance()and knowledge dimensions.Definition3.1Attitude and BeliefGiven a set of primitivepropositionsH def1,an attitude maps H to an attitude bilattice;a belief maps H to a belief bilattice.An attitude-belief combines the two mapping H to.Conversely,an attitude-belief can also be viewed as a pair of attitude and belief functions. Although not necessarily so,for the purpose of this pa-per we shall assume that both B and B are4-point bilat-tices.The belief bilattice,following Ginsberg’s suggestion, is defined by the truth-knowledge partial orders.In the at-titude bilattice,the truth partial order is replaced with a rel-evance measure.Notably,one’s knowledge with respect to the truthfulness of a proposition need not equal,in general, one’s knowledge with respect to the relevance of that same proposition.Technically,our attitude bilattice is made of R elevant,I rrelevant,U nknown,and values.Extensions to more complex bilattices are discussed in[Ginsberg,88; Rymon,93]3.3GoalsGoalhood is a semantic interpretation of an attitude-belief assignment.Generally speaking,a proposition is a goal if its attitude assignment is highly relevant(in our bilattice if=R).Of course,not every relevant proposition is an operational goal.If=T,for example,then we believe holds and may want to consider it“achieved”.(in morecomplex bilattices,one has to define which combinations of relevance and achievement levels need be addressed,in what order of preference,etc.)The GDD inference,we should note,is purely syntactic and is thus indifferent to these semantic subtleties;within the ECM architecture,it is the planner’s role to decide which goals to pursue.However,we wish to note here a potential distinction that is based on whether a proposition denotes a diagnostic(knowledge)goal or a therapeutic(state achieving) one,namely that while a diagnostic goal may often be regarded satisfied whenever the proposition is proved either true or false,we may want to actually achieve(i.e.=T)a therapeutic one.3.4RepresentationWe use rules to represent knowledge.Two types of rules are used:one for inferring belief,the other for inferring atti-tude(goals).Antecedents in both types of rules are stated in belief terms.A rule’s consequent(header)must be either a proposition or its negation.Definition3.2Rules1.Evidential rules are used to infer belief.For example,the following rule concludes whether a patient’s shock is due to abdominal bleeding:ShockSingle to chestunless(PericardialHemothorax)unless(Tensionof abdominalwound abdomenBullet abdomenPericardialTamponade"Conclude that the problem exists".3.Setting a Therapeutic goal:()pressure sac"It is necessary to address the problem".4.Satisfying a Therapeutic Goal:()Relieve pericardial2A condition in which bloodfills the pericardial sac,interfering with the heart’s operation.3.5Solving a diagnostic problemSolving a diagnostic problem requires computing the inferen-tial closure of the observations,given the rules.Our closure definition is based on Ginsberg’s,and can be viewed as its simplification to the rule-based case.Definition3.5Inferential ClosureAn attitude-belief is an inferential closure for a problem instance P iff1.It coincides with OBS,i.e h0(h)=OBS(h);2.For any proposition H–M0,let1be all theevidential rules with in their header,;Where represents the belief term obtained from the conjunction of antecedents of the rule R.3.Similarly,for any proposition H,let1be allthe goal-setting rules with in their header,;Essentially,all rules for a proposition and against it are weighted as individual knowledge sources,and thus com-bined using the operator.The correspondence between this formulation and Ginsberg’s is that there all proofs for a given statement have to be weighted whereas here the only proofs are the specific rules.Even with this limited scope,we should note that in general there is no guarantee that such inferential closure is unique,computable,or even exists.However,the following straightforward algorithm has worked for us so far: Algorithm3.6Computing an Inferential Closure1.Start off with the observations,by setting()def,for all h H()def0otherwise2.Forward-chain on the rules,enforcing conditions2and3above,until reaching afixed point.The formal definition of a solution in the GDD framework emphasizes its distinction from other diagnostic frameworks. Definition3.7A DiagnosisLet be the inferential closure for a problem in-stance P,then is a diagnosis for P.Most formalizations of diagnosis take a diagnosis as their solution.In GDD,however,we associate more importance with the goals(and consequently the actions)adopted during the diagnosis process.In the ECM architecture,solving the current diagnostic problem has an operational purpose:it defines the goals to be pursued next by the planner.Definition3.8A Solution to a Diagnostic ProblemA solution to a diagnostic problem P is the complete infer-ential closure.4The Diagnosis-and-Repair ProcessSo far,we have described how a single diagnostic problem is defined,and how it is solved to produce a new set of goals and conclusions.In this section,we describe how GDD is used, in conjunction with the ECM’s planner,to produce desirable management plans.4.1The ECM algorithm:integrating diagnosticreasoning and planningAlgorithm4.1calls the diagnostic reasoner whenever new ev-idence defines a new diagnostic problem.The solution,par-ticularly the relevant goals,guides the complementary planner in the choice of activity which,in turn,may start a new cycle. Algorithm4.1ECM Diagnosis-and-Repair Algorithm1.Initialize to coincide with OBS;pute an inferential closure for;3.Construct a plan P for the combination of goals indicatedby that closure;4.Unless P is empty doExecute P until new evidence arrives;Update to reflect this evidence;Go to step2.Note that the termination criterion is not necessarily related to the concreteness of the working diagnosis.The process terminates when the plan is empty,i.e.when all goals have been addressed,or no means are available for addressing remaining goals,etc.4.2Mediating between local strategiesThe decomposition of reasoning in the ECM architecture sug-gests a way to encode strategies,appropriate responses to anticipated situations,in it.We do that by using GDD to explicitly encode local strategies,and using planning to im-plicitly merge(on-line)a patient-specific combination of such. In particular,In the trauma management domain,strategies can be localized around diagnosis and/or treatment of a single problem,or of a common combination of problems.The rules abstracted in Example3.3,for instance,can be viewed as part of a strategy for diagnosis and treatment of a pericardial tamponade:pursuing the knowledge goal PericardialPneumothorax)known(TensionPericardialWound(Left)Hemothorax(Left)At this point,control is transferred to the planner which recommends a chest X-ray as a diagnostic means.In thepresence of other problems,the planner will have to order the X-ray with respect to actions aimed at other needs.Different means may be selected if more efficient given the combination of goals.Suppose the physician orders an X-ray and reports signs of hemothorax and fractured ribs.Each of thesefindings will then be updated in the system’s belief,and may trigger further investigation.The hemothoraxfinding will trigger the following evidential rule:(2)X shows Hemothorax(Left)SimpleHemothorax(Left)) from U to T.That change may be interpreted as a satisfac-tion of the diagnostic goal set by(1).Note too that we must distinguish a hemothoraxfinding from the condition of having a hemothorax,since the condition can be diagnosed in other ways,e.g.through the presence of decreased breath sounds. The diagnosed hemothorax triggers the following goal-setting rule:(3)SimpleRx Hemothorax(Left)The attitude toward this therapeutic goal is updated from U to R.It is referred to the planner which recommends address-ing it through the insertion of a chest tube.Then,evidence that a chest tube has been inserted leads to another diagnostic goal of verifying its proper placement and that it is function-ing.In addition to these two cycles of reasoning and activity (a subsequent X-ray is required to check proper placement), the following rule is evaluated to check that the original ther-apeutic goal is actually satisfied:(4)Chest misplaced(Left)Chest istube drainingSimple。