四川大学全英语授课专业课程大纲Syllabus of English-Teaching Program at SCU

内科学 Internal Medicine

Course Code: Course Name: Internal MedicineTotal Class Hours : 192 Credit: 12

Textbook/Teaching material: Cecil Essentials of Medicine. Health Sciences Asia, Elsevier Science

Course Objective: This course is designed for senior undergraduate students in the School of clinical medicine. The basic theory and practice skills of internal medicine are covered. The intention is that the material will provide a foundation for theoretical and applied introduction in internal medicine.

Course Description:：This course will introduce both theoretic and applied internal medicine. We will introduce the etiological factors, pathomechanism, pathology, clinical manifestation, diagnosis, and differentials, complications and therapeutic principle of various systemic diseases of internal medicine. In the practice sessions, we will introduce the basic clinical skills and operations correspondingly.

Prerequisite：The prerequisite of this course includes, but is not limited to, the knowledge of, anatomy, pathophysiology, pathology, pharmacology and diagnostics. Those who are not familiar with these knowledge are encouraged to read related text books before hand.

Ways to engage students to the class：Pre-class assginments such as preparing lessons or solving certain problem will be given; In-class discussion will be conducted as often as possible; After-class assignments will be passed out from time to time. These assignments will include both problem solving and medical record writing. Besides, students are required to do some fundamental clinical skills exercises now and then. The assignments will be graded by the teaching assistant, and will be reviewed in the discussion sections.

Reference books:[1] Sleisenger & Fordtran’s Gastrointestinal and Liver Disease 6th Edition[2]Davidson’s Principles and Practice of Medicine 18th Edition[3]内科学第 8版 人民卫生出版社GradingThere will be one exam-a final exam. The final is close-book and close-note. The grading for the course will be as follows: Assignments: regular grade 30%. Final exam: 70%.

Office Hour:Wednesday: 14:30 to 17:00; And by Appointment.

呼吸系统疾病Disease of respiratory system

Bronchial asthmaPurpose and Requirement 1. Know about the relationship between asthma and its precipitating factors.2. Grasp clinical manifestation, diagnosis, and differentials, complications of asthma.3. Grasp clinical manifestation and emergency protocols of critical asthma according to its

inflammatory pathogenesis. Understand the prophylaxis and treatment of chronic asthma. Comphrensive prophylaxis and treatment can block the several links which precipitating asthma. Be familiar with pharmacology and dosage of the two kinds of drug administered in asthma.

Content1. Introduction Definition. Attack seasonally. Age of onset. Comparation of sex. 2. Etiology and pathogenesis

A. The inflammatory pathogenesis. The relationship between pathology change and ventilation dysfunction.

B. The concept and pathogenesis of airway hyperesponsiveness.C. The role of inflammatory mediator in asthma.D. Precipitating factors

1) Infection: the relationship of respiratory infection and asthma attack.2) Allergic pathogen: common allergic pathogen including: dust, pollen, fungus spore,

shrimp, crab, fish, paint3) Climate: the relationship of climate and asthma4) Physical and chemical stimulant: air pollutants, stimulating perfume etc5) Physiology factor: emotional fluctuant and behavior reflex6) Other factors: gravis exercise, some drug such as aspirin, practolol

3. PathologyBrief introduce pathologic change of asthma.

4. Clinical manifestationA. Presentation of allergic asthma.B. Presentation of infection asthmaC. Presentation of critical asthma, emphasize the precipitating factors

5. Laboratory findingsPeripheral blood eosinophil test, lung function test, chest X-ray. bronchial challenge test and

bronchodilator test, sputum smear, sputum culture and antibiotics sensitivity test, and allergy skin tests.6. Diagnosis and differentials diagnosis:

Inquire history in detail and precipitating factors. If any allergy is suspected, allergy skin tests and Blood I E may be made. It should different with the disease listed.

A. Carcinogenic asthma: describe the points of differentialsB. Asthmatic bronchitisC. Bronchogeneic carcinomaD. Hypersensitivity pneumonitis

7. ComplicationEmphasis on pneumothorax and infection.

8. Prophylaxis and treatment.A. Control infection: the classification and pharmacology and preparation of asthma medication.

1). Anti-inflammary drugs2). Bronchodilutors

B. Management of each kinds of asthma1) Manage of mild attack2) Management of moderate attack3) Management of critical asthma4) The prophylaxis and treatment of chronic asthma.

A. Preventing from recurrent attack: body exercise, removing induced factor, preventing treatment

9. PrognosisAttack may remit or be cured if management is kept at intermittent asthma. Asthma may

recurrent and exacerbate if the induced factors remain. Complicated with sever emphysema and cor pulmonale suggest a bad prognosis.

Chronic cor pumonale

Purpose and Requirement1. Understand the clinical presentation, features, and diagnostic approach of remission stage and

acute attack stage of chronic cor pumonale; Master management protocol of respiratory function insufficiency and heart failure.

2. Understand the pathogenesis of pulmonary hypertension in chronic cor pumonale.3. Master the systemic disease is based on pulmonary function insufficiency, which is

characterized by complicate and liability. Know the prophylaxis protocols of the disease.Content1. Introduction: definition, survey (including incidence, age, course), the progress and significant

achievement of prophylaxis and treatment at home in recent years.2. Etiology A. Pulmonary and bronchial disease: the most common cause is chronic bronchitis and obstructive emphysema, the less are asthma, bronchiectasis, pulmonary tuberculosis, pneumoconiosis, interstitial pulmonary disease.

B. Chest dyskinesis: such as spinal and thoracic deformity caused by diverse disorder.C. Pulmonary vascular disease: such as hyperesponsive granulomatosis, primary pulmonary

hypertension and etc.3. Pathogenesis and pathology

A. Chronic cor pulmonale is a systemic disease, which is based on pulmonary function insufficiency and characterized by complicities (muti-systemic lesion including pulmonary, cardiovascular, cerebral, gastric, hepatic, renal and system), and liability (acid-based balance disturbance and electrolyte disorder).

B. The cause of pulmonary hypertension1) Pulmonary arteriole spasm and contraction (functional factors), oxygen deficiency

associated with acidosis serves as the main cause.2) Pulmonary arteriole remodeling, dropout or impairment of pulmonary capillary bed,

pulmonary arteriolosclerosis, bulla formation (anatomic factor).3) Other factors are blood volume exceeding and hyperviscosity.

C. The cause of right ventricular hypertrophy, enlargement and failure1) The major cause is pulmonary hypertension, which is reversible in acute exacerbatio

stage, and can go into remission along with improvement of heart failure after respiratory function is improved.

2) Oxygen deficiency in cardiac muscle.3) Hydro-sodium retention.4) Hyperviscosity.

D. The effect on other organs: It depends on the severity of respiratory acidosis, acid- base derangement (metabolic

alkalosis and acidosis), electrolyte disturbance (hyponatremia, hypokalemia, and hypochloremic), upper gastrointerestinal hemorrage, arrhythmia, shock, DIC, functional renal failure.

4. Clinical manifestation and complicationsCor pulmonary presented as remission stage and acute attack stage alternately, so clinical

presentation of it is complicated and liable.A. The remission stage: heart function can compensated generally in early stage, so does

part of lung function. The disease in compensated stage manifested in symptoms of primary disease and oxygen deficit (fatigue on exertion, tachypnea, respiratory distress with simple activities, tachycardia, palpition, different degrees of cyanosis) Bicarbonate retention is slight. Physical sign reveals emphysema, pulmonary hypertension and right ventricular hypertrophy. In end stage, right ventricular function insufficiency can be detected even without acute attack.

B. Acute attack stage: respiratory infection generally predisposes to the acute attack. Dysfunction of pulmonary ventilation and gas exchange. On the base of presentation of remission stage, the disease may present as moderate and sever respiratory failure, oxygen deficit and pulmonary encephalopathy caused by compensated respiratory acidosis. The clinical presentation and its character of right heart failure. The various presentations and its feature of acid-base disturbance and electrolyte disorder. The clinical characters of main complications.

5. Laboratory findings:

Blood gram, chest X-ray, electrocardiography, echocardiography, arterial blood-gas, blood biochemistry test.6. Diagnosis and diffiential diagnosis

A. Diagnosis: it is not difficult to make exact diagnosis in end stage regarding history, clinical presentation, electcardiography and X-ray. However, in early stage laboratory findings are needed to make comphrensive diagnosis. It is necessary to consider about all the examination available to select an optimal and noninvasive one.

B. Differential diagnosis: rheumatic heart disease, coronary heart disease, myocardial disease.

7. TreatmentA. The remission stage

1) Enhance the ability to anti-disease, prevent or manage respiratory infection in time. It is critical to take methods to prevent or manage cold and acute exacerbation, such as physical exercise anti-cold exercise respiratory exercise, take drug prophaxlic and vaccination.

2) Management of primary disease. Prevention from recurrent.B. The Acute attack: It is important to improve respiratory function, control infection,

remove the obstruction of airway, to ameliorate oxygen deficit and carbonate retension. Meanwhile recorrect acid-base derangement and electrolyte disturbance. Avoid from alkacamia when diautic is used.1) Management of respiratory insufficiency

a) Control infection: select the appropriate antibiotics, prevent from cross-infection and exacerbation. Antibiotics susceptibility to the pathogen.

b) Remove airway obstruction: improve the ventilation. Remove secretion and relief from bronchospasm. The indication and precautions of steroid corticosteroid.

c) The indications and protocols and precautions of oxygen therapy.d) The indications and protocols of respiratory stimulant. list harm and good of

the drug. Indication of tacheostomy.e) The presentation of pulmonary encephalopathy: disclose it in early stage and

manage it immediately.2). Management of heart function insufficiency.

a) It should be emphasized that heart function may improve after infection get controlled and respiratory function improved.

b) The indication, preparation, precautions, and dosage of cardiac stimulant. The differences and similarities in protocols between this disease and general heart failure.

c) The indications, precautions and selection of uretic.d) Synopsis of the application of vaso-dilators.

3). Prophylaxis and treatment of acid-base derangement and electrolyte disturbance. How to prevent or manage metabolic aklamias, metabolic acidosis, hypoxemia, hyponatremia, and hypokalemia.

4). Prophylaxis and treatment of all kinds of complications.8. Prognosis

The prognosis depends on the curative effect in intermittent phase.

Chronic bronchitis and Obstructive emphysemaPurpose and Requirement1. Master the clinical manifestation, diagnosis, and principal protocols of prophylaxis and

treatment of chronic bronchitis and Obstructive emphysema.2. Be familiar with the rule of onset and progression of chronic bronchitis and Obstructive

emphysema. The impact of body and outer factor on onset of disease. The course and pathologic change that chronic bronchics develops into obstructive emphysema. Know chronic bronchitis and Obstructive emphysema are common and frequently-occurring disease. Incidence is high, and complication is serious. It is necessary to take effective prophylaxis and treatment to the harmful disease.

Content1. Definition

Chronic bronchitis refers to chronic unspecialized inflammation that occurs around bronchi, which is characterized by recurrent cough, sputum expectation, or companied by wheezing and chronic course. Chronic bronchitis can develop into obstructive emphysema and even cor pumonale if it proceeds progressively. Active prophaxlis and treatment should be emphysized due to its great hazard 2. Pathogenesis

The cause and pathogenesis of the disease remains unknown. It may arise from the comprehensive action of many internal and external factors of body. It should be noted that smoking and respiratory infection on onset of disease.3. Pathology

The pathologic feature of chronic bronchitis. The process and the pathologic change that chronic bronchitis developed into obstructive emphysema.4. Pathophysiology

Describe the respiratory function change when chronic bronchitis proceeds into obstructive emphysema, which involve ventilation dysfunction, residual volume increasing, enlargement of alveoli, intralveoli pressure increasing, compressed and dropout of pulmonary capillary bed. The lung function change may lead to ventilation/perfusion ratio derangement, pulmonary artery pressure increasing, right ventricular hypertrophy due to overburden, then develop into chronic cor pumonale which may elicit respiratory failure and heart failure. 5. Clinical manifestation

A. Symptom: the emphasis lies in the four signs including cough, sputum expectation, wheezing, inflammation, dyspnea may present and progressively worsen when emphysema complicates.

B. Physical sign: physical finding may be nonspecific in early stage, but may reveal signs of emphysema in prolonged recurrent attack.

6. Clinical classificationA. Chronic bronchitis has two types: one is simple type, the other is wheezing type. It can

also be classified into three types: acute attack phase, chronic procrastinate phase, and clinical remission phase regarding degree of illness.

B. The concept of COPD. It may be divided into two types: pink puffer (PP), and blue bloaters (BB) according to presentation features. Point out their features of clinic, chest X-ray and pathophysiology.

7. ComplicationsBrief introduction of general complications including chronic cor pumonale, spontaneous

pneumothorax, acute respiratory infection and etc.8. Laboratory findings

A. Chest X-ray: it may reveal increasing and disturbance of lung marking and sign of emphysema.

B. Respiratory function test: it may reveal obstructive ventilation deficit, increasing of residential volume in emphysema.

C. Laboratory studies: sputum culture and blood gram are helpful to make diagnosis and assessment of therapeutic effect.

9.. Diagnosis and differentials diagnosisA. Diagnosis: It can be made followed by excluding other chronic cardiac and pulmonary

disease regarding to national formulated diagnosis standard. B. Differentials: tuberculosis, asthma, bronchiectasis, and baronial cancer.

10. Treatment Various management protocols can be taken according to different phase.

A. Management of acute attack1) It is dominated by infection controlled. Choose popular antibiotics or sensitive

antibiotic regarding degree of infection2) Cough medicine and secretion clearance.3) Relieve wheezing and teat with spasmolytic agents

B. Management of remission period: It is dominated by improvement of anti-disease ability. Respiratory muscle exercise and oxygen therapy at home.

C. Management of complications11. Prognosis

Prognosis is excellent if causing factor of chronic bronchitis such as smoke accession, protection from dust can be eradicated; However prognosis is bad if therapy is not persisted in, causing factors continuously present and procrastinate, or recurrent respiratory infection precipitates the disease to progress.

PneumoniaPurpose and Requirement1. Understand the etiological factors and the pathogenesis of pneumococcal pneumonia.2. Be familiar with the pathology of pneumococcal pneumonia.3. Understand the clinical manifestations, diagnosis, differential diagnosis and therapy of

pneumococcal pneumonia.4. Be familiar with the clinical manifestation and therapy of staphylococcus pneumonia,

Klebsiella pneumonia, and mycoplasma pneumonia.

ContentⅠ.Summarization:The classifications of pneumonia and the importance of the etiological factors; bacterial pneumonia are common and pneumococcal pneumonia is the representative one. Introduce the definition of and community-acquired pneumonia (CAP) and hospital-acquired pneumonia (HAP). Introduce the clinical features of staphylococcus pneumonia, Klebsiella pneumonia, and mycoplasma pneumonia through differential diagnosis.Ⅱ.Pneumococcal pneumonia1. Etiology and pathogenesis: the biological characters, types and pathogenicity of

pneumococcus; resistance of the body; the inducements.2. Pathology and pathophysiology: pneumococcus won’t damage the structure of alveolar, but can

induce consolidation because of infiltration of serosity and cells in alveoli. When they disappear, the structure of alveoli will be normal completely. But these changes can induce imbalance of ventilation-perfusion (V/Q) and hypoxia.

3. Clinical manifestationsA. Typical symptomsB. Toxic symptoms: include gastrointestinal symptoms and symptoms of peripheral

circulatory failure. C. Signs (focal point: consolidation stage)

4. Laboratory examinations and chest radiography 5. Complications: pleurisy, organizing pneumonia, et al.6. Diagnosis: according to the typical symptoms, signs, the increased WBC, bacterium culture of

sputum or blood, and X-ray manifestations.7. Differential diagnosis

A. Other bacterial pneumoniaB. Caseous pneumonia, lung abscess, pulmonary tuberculosis, lung cancer, and pneumonia

caused by other pathogens.8. Treatment

A. Penicillin and sulfanilamide; if patients are sensitive to penicillin, use erythromycin or cillimycin or cephalosporin.

B. Severity ones can be treated with cephalosporin.Ⅲ.Self-study1. Staphylococcus pneumonia2. Klebsiella pneumonia3. Mycoplasma pneumonia

Pulmonary TuberculosisPurpose and Requirement1. Understand the course of occurrence and development of pulmonary tuberculosis; relations

with allergic reactions and immunity; diagnosis and differential diagnosis; the appropriate administration of antituberculous medications.

2. Be familiar with the relations between chest radiography and pathological changes of pulmonary tuberculosis, methods of detecting mycobacterium tuberculosis in sputum; the principles and methods of treatment; the tuberculin skin test (TST); BCG (bacilli Calmette-Guerin) vaccination.

Content1. Introduction: epidemiology of tuberculosis over the world.2. Etiology and pathogenesis:

A. Mycobacteriu tuberculosis: types, biological characters, as well as mycobacteria other than tuberculosis (MOTT).

B. Transmission and dissemination: many from airway.C. Reactivity in human body: acquired and active immunity, and allergic reactions.

3. Pathology: fundamental pathological changes (bleeding, proliferation and deterioration) and their endings.

4. Progression of pulmonary tuberculosis and the common clinical types: initial infection, onset of illness, Koch’s phenomena; primary tuberculosis and secondary tuberculosis; the pathological and clinical characters of different types of tuberculosis.

5. Clinical manifestation: general symptoms and signs of total body and airway; note some patients have no symptoms or only have some nonspecific symptoms.

6. Laboratory examinationsA. The tuberculin skin test (TST): method; dose; positive and negative responses and their

significance.B. Sputum samples analysisC. Chest radiography: X-ray examination, computed tomography (CT); the characters of

diseases on X-ray examination.7. Diagnosis and differential diagnosis: according the clinical manifestations, characters of

disease, and excreting mycobacterium tuberculosis or not, to confirm the activity.Differential diagnosis: differentiation with bronchitis, bronchiectasis, pneumonia, lung abscess and lung cancer et al.

8. TreatmentA. Principles for chemotherapy: early, combination, specific doses, regularization and

duration.DOT: directly observed therapy.

B. Antituberculous medications: Isoniazid (INH, H), rifampin (RFP, R), pyrazinamide (PZA, Z), ethambutol (EMB, E), streptomycin (Sm, S)First-line drugs and second-line drugs.

C. Standard chemotherapyD. Surgery: indications and contraindicationsE. Other therapies: the management of hemoptysis with large amount

9. Prevention: The importance of tuberculosis preventionSystems for tuberculosis prevention and treatment: propaganda, patients’ register and management, therapy (outpatient clinic or hospitalization), BCG vaccination.

Pleural EffusionPurpose and Requirement1. Understand the differential points of transudate and exudate.2. Know about the common diseases inducing pleural effusion and the clinical significance of the

targets of effusion examination.3. Understand the clinical manifestations, diagnosis and differential diagnosis of pleural

tuberculosis.4. Understand Prevention and treatment of pleural tuberculosis.ContentSummarize the mechanisms of pleural fluid production, and the differential points of transudate and exudate.1. Etiology and pathogenesis: mycobacterium tuberculosis infection; the allergenic state of body.2. Pathology: dry and exudative pleurisy3. Clinical manifestation: symptoms and signs have relations with the reactivity of body and the

amount of fluid.4. Assistant examinations: chest radiography, ultrasonography, fluid analysis, pleural biopsy, and

TST et al.5. Diagnosis and differential diagnosis: we can make diagnosis from history, clinical

manifestations, chest radiography, ultrasonography and fluid analysis et al. Different diagnosis of transudate, exudate, hemorrhagic effusion (hemothorax), and chylous effusion (chylothorax). Emphasis the differentiation of pleural tuberculosis and carcinoma effusion.

6. TreatmentA. Pleural tuberculosis

1) General treatment2) Antituberculous therapy3) Thoracentesis: principle and notes4) Usage of corticosteroids5) Improve the symptoms

B. Management of pyothorax or empyema (self-study)

Respiratory FailurePurpose and Requirement1. Understand the etiology, pathogenesis and pathophysiologic changes of respiratory failure.2. Understand Arterial Blood Gases (ABG) changes, acid-base disturbance and electrolyte

disturbance in respiratory failure.3. Understand clinical manifestations and principle of treatment of chronic respiratory failure.Content1. Summarization

Respiratory failure is a clinical syndrome caused by hypoxia and/or carbon dioxide (CO2) retention. It is divided into two types-typeⅠ(hypoxia) and typeⅡ(hypoxia accompany hypercapnia), according the ABG changes. Body can’t compensation in acute respiratory

failure. Chronic respiratory failure is common, and divided into compensation and decompensation. And it’s the focus of this chapter.

2. Etiology and classificationA. Bronchial-pulmonary diseases.B. Neuromuscular disorders.C. Chest wall abnormalities.D. Other diseases, e.g. ARDS et al.Respiratory failure often accompany with hypoxia and CO2 retention.

3. PathogenesisA. Alveolar hypoventilation.B. The ratio of ventilation-perfusion (V/Q) imbalance.C. Decreased function of diffusion.

4. PathophysiologyA. The effect of hypoxia to central nerve system, cardiovascular system, respiratory system,

cell metabolism and electrolyte.B. The effect of CO2 retention to these systems and acid-base hemostasis.

5. Clinical manifestationsA. Dyspnea.B. Cyanosis.C. Mental and neural symptoms. D. Changes of cardiovascular system, gastrointestinal system, and urinary system.

6. DiagnosisTargets of ABG: arterial oxygen tension (PO2), arterial carbon dioxide tension (PaCO2), PH

values and [HCO3-]. Their normal levels and significance. Differential diagnosis of acid-base

disturbance and electrolyte disturbance.7. Treatment

A. Oxygen therapyB. Improvement of ventilationC. Inflammation control: right usage of antibiotics.D. Improve acid-base disturbance and electrolyte disturbance: management of respiratory

acidosis, metabolic acidosis and alkalosis.E. Dehydrant, diuretic and cardiac tonic.F. CorticosteroidsG. Complications and treatment

8. Preventions: treatment of primary diseases; avoid mistakes in oxygen therapy, and usage of sedatives and diuretic.

（修订人：刘坤 呼吸内科）

心血管系统疾病Disease of cardiovascular system

Valvular heart diseasePurpose and requirement1 Grasp the pathophysiologic charactors clinical manifestations and diagnostic methods of common sorts of valvular heart disease.2 Be familial to the relationship between rheumatic fever and rheumatic heart disease,in addition,the knowledge of common differential diagnosis complications therapeutical principles and implications to surgery are also important.3 Know about some knowledge about the epidemiology and some advances in such disease.Content 1 IntroductionThe incidence of rheumatic fever has declined, and as the result the rheumatic heart disease is not the most important cause of valvular disease in developed countries; but valvular disease caused by rheumatic heart disease is still very common in the china and other developing countries.2 Mitral stenosis and mitral regurgitation

A. Pathophysiology: the effects of abnormal homodynamic caused by mitral lesions to left atrium pulmonary circulation and right heart.

B. Clinical features:1) Major symptoms and signs of mitral stenosis and mitral regurgitation2) Investigations: ECG, chest radiography, echocardiography and cardiac catheterizationC. Diagnosis and differential diagnosis1) Diagnosis is based on the major symptoms, signs and combined with the results of

investigations.2) Differential diagnosis: its necessary to distinguish other disease that can cause the similar

apical diastolic murmur (eg, Austin Flint murmur) with mitral stenosis3 aortic stenosis and aortic regurgitationA. Pathophysiology: wether stenosis or regurgitation will increase the burden of left ventricle, as the result left ventricle undergoes hypertrophy and eventually become dilated. These changes accompany series changes of homodynamic in left heart.B. Clinical features:1) Major symptoms and signs of mitral stenosis and mitral regurgitation2) Investigations: ECG, chest radiography, echocardiography and cardiac catheterizationC. Diagnosis and differential diagnosis:1) Diagnosis is based on the major symptoms, signs and combined with the results of investigations.2) Differential diagnosis:a) Differention between aortic regurgitation and pulmonary regurgitation secondary to pulmonary artery dilation;

b) Distinguish different causes of aortic regurgitation (e.g.: rheumatic, degenerative, congenital et al.);c) Aortic stenosis should be differented from obstructive hypertrophic cardiomyopathy or congenital aortic stenosis4-Mutivavular diseases5 Complications with valvular disease

A. Cardiac insufficiencyB. Acute pulmonary edemaC. Arrhythmia: especially atrial fibrillationD. Infective endocarditisE. Respiratory tracts infectionF. Systemic emboli

6 ManagementA. Therapeutical principles to patients without complications: maintain and improve cardiac

function, prevent the occurrence of complications B. Management of complications: treat cardiac insufficiency; releive acute pulmonary

edema; treatments of atrial fibrillation (restore sinus rhythm; control heart rate; anticoagulation)

C. Surgery: indications and contraindications7. Prevention of rheumatic fever and prognosis

Cardiomyopathy and myocarditisPurpose and requirement1 Understand the principles of diagnosis and treatment for cardiomyopathy2 Be familial to etiology, diagnosis and treatment for myocarditisContent1. cardiomyopathy

A. General introductionDefenition, clinical classification, pathologic classification and epidemiologyB. Dilated cardiomyopathy1) Definition2) Characters of pathophysiology3) Clinical features: symptoms and signs4) Investigetions: ECG, X-ray, UCG, catheterization and endomyocadial biopsy5) Essentials of diagnosis and treatment6) Prognosis

2. Hypertrophy cardiomyopathyA. DefinitionB. Characters of pathophysiologyC. Clinical features: symptoms and signsD. Investigetions: ECG, X-ray, UCG, catheterization and endomyocadial biopsy

E. Essentials of diagnosis and treatmentF. Prognosis

3. Miscellaneous cardiomyopathyAlcoholic cardiomyopathy; peripartum cardiomyopathy; restrictive cardiomyopathy;other special types of cardiomyopathy such as KESHAN disease4. Viral myocarditis

A.Etiology: commonly initiated by coxsackievirus BB. Pathology: focal patchy or diffuse inflammatory infiltrate with adjacent myocyte injuryC.Symptoms: asmptomatic/chest discomfort/classic symptoms of congestive heart

failure/syncopeD. Signs: vary widelyE. Investigations: ECG, X-ray, measurement of serum antibody and isolation of virus et al.F. Essentials of diagnosis and treatment:1) Diagnosis based on comprehensive analysis for clinical features, ECG, X-ray and lab

tests;2) Treatment: bed rest; management of heart failure, arrythmia and other symptoms if

existed; other uncertain treatments (steroid, immunosuppressive therapy)G. Prognosis

Heart failurePurpose and requirement1 understand causes and pathophysiological characters of heart failure2 understand clinical manefestations, diagnosis and differential diagnosis of heart failure3 understand principles of treatment for heart failure, especially the use method of digtalis,diuretics,ACEI and β-blocker. Learn the management of acute left heart failureContentⅠ.Chronic cardiac insufficiency1 causes

A. Fundamental causes: myocardial damagement; cardiac overloadB. Precipitating factors: lack of compliance (diet, drug); uncontrolled hypertension;

myocardial infarction and ischemia; cardiac arrythmia; fluid overload; infection; pregnancy et al.

2 pathophysiologyA. Compensatory homodynamic changes: distribution of blood, increase of blood volume

(retention of sodium);B. Ventricular hypertrophy and dilation;C. Most important: cardiac remolding and activation of neurohumoral system (RAAS,

sympathytic nerve system)3 clinical manifestations

A. Left heart failure: most symptoms related to pulmonary congestion, including dyspnea, cough, rals and gallop, et al.

B. Right heart failure: most symptoms related to system congeston, including upper abdominal discomfort, hepatomergaly, jugular vein distention, thoraxic effusion, et al.

4 complications: thrombosis and embolsm, cirrhosis secondary to heart failure, disbalance of electrolyte5 investigations: ECG, X-ray, UCG and noninvasive or invasive measurement of cardiac function6 diagnoses

A. Diagnosis: based on clinical features and measurement of cardiac functionB. Differential diagnosis: distinguish pulmonary disease from left heart failure, exclude

chronic pericardial temponade, cirrhosis and nephritis before making diagnosis of right heart failure.

7 Prevention and treatmentA. Prevention: avoid potential precipitating factors and manage combined disease positively.

Pay attention to daily activities and diet.B. Digitalis: indication and prohibition, methoda and dosage, toxic effect and managementC. Diuretics: principles for use of diuretics, side effects and managementD. ACEI: principles for use of ACEI, dosage, side effectsE. β-blocker:Indicatins and prohibitionF. Vasodilators and other drugs

8 management of refractory heart failureⅡ.Acute left heart failure1 cause: mitral stenosis, AMI, volume overload2 pathogenesis: cardiac output declines rapiddly, with the increase of pulmonary pressure, as the result acute pulmonary edema develops.3 Clinical features: breathless and distressed, cough up pink frothy sputum, hypotension and carcinogenic shock, many rales in bilateral lungs4 diagnoses: diagnosis based on analysis of clinical manefestations, and excluding attack of bronchial asthma.5 management

A. Sit the patient upB. Administer oxygenC. MorphineD. FrusemideE. Vasodilators: sodium nitroprusside

6.Digitalis: pay attention to indication7.Other drugs and methods

Common ArrhythmiasGeneral IntroductionPurpose and Requirement1. Grasp the etiology, clinical manifestations, diagnoses and treating principles of common

arrhythmias. 2. Be familiar with electrocardiographic features and diagnosis of common arrhythmias.

3. Understand nosogenesis of arrhythmias.Content1. Concept

A. The physiology of the heart, including myocardial automaticity, excitability, conductibility and reentry. Elucidation of the close relationship between arrhythmogenesis and the transformation of myocardial electrophysiology.

B. The etiology, pathology, mechanism and pathophysiology of cardiac arrhythmias and conduction disturbances. Both disordered automaticity and impulse conduction disturbances can cause arrhythmias. Cardiac output is influenced by altered heart rates, atrioventricular dyssynchrony or loss of contractile function.

C. The clinical manifestations, diagnoses and approach to analyzing electrocardiograms. Auscultative features. Analysis of P waves, QRS complexes, the relationship between P waves and QRS complexes, P—P intervals.

2. Sinus ArrhythmiasA. Etiology. Physiological causes include exercises, drugs, etc. Pathological causes consist

of myocardial and noncardiac ones.B. Clinical manifestation. The onset and ending of sinus arrhythmias of is a gradual

process, and is susceptible to vegetative nervous activities.C. Electrocardiogram. Electrocardiographic features of sinus rhythm.D. Treatment. Aim at causes mainly, also at symptoms.

3. Sick Sinus Syndrome IntroductionA. EtiologyB. Clinical featuresC. ElectrocardiogramD. The clinical indications for pacemaker therapy.

4. Supraventricular ArrhythmiasA. Premature beats

1) Etiology. Tension, cigarette, alcohol, tea, coffee, excited vagal nerve, structural heart diseases, drugs, cardiac mechanic stimulation, cardiac surgery.

2) Clinical features. Correlated to the number of premature beats and sensitivity of patients. Auscultative features.

3) Electrocardiogram. Premature ectopic P waves, P—R intervals, compensatory pauses.

4) Treatment. Elimination of causes. Indications and sorts of medical treatment.5) Clinical significance. Rest with influence on cardiac function.

B. Paroxysmal Supraventricular Tachycardia1) Etiology. Most of causes are unclear. A few PSVT are accompanied with structural

heart diseases or other diseases.2) Clinical manifestations. Acute onset and ending. Auscultation. Jugular venous

pulse.3) Diagnosis. Based on clinical manifestations and electrocardiograms.4) Electrocardiographic features and differential diagnosis. Classified as atrial, nodal

and supraventricular paroxysmal tachycardia.

5) Treatment. Drugs, stimulation of vagal nerve, electrical cardioversion, overspeed suppression, interventional therapy, ie, radiofrequency catheter ablation.

6) Clinical significance. Rest with influence on cardiac function. C. Atrial Fibrillation and Atrial Flutter

Classified as paroxysmal (acute) and persistent (chronic).1) Etiology. Most are accompanied with structural heart diseases.2) Clinical features. Result in cardiac dysfunction, pulse deficit and distinctive

auscultative features. 3) Diagnosis. Based on clinical manifestations and electrocardiograms.4) Electrocardiogram. No P waves, presence of f waves or F waves. 5) Treatment. Drugs, electrical cardioversion.

5. Ventricular ArrhythmiasA. The premature beats are the commonest arrhythmia.

1) Etiology. As is displayed in Supraventricular Arrhythmias.2) Clinical manifestations. Auscultative findings.3) Diagnosis. Based on clinical manifestations and electrocardiograms.4) Electrocardiogram. Premature QRS complexes and compensatory pauses.5) Treatment. The indications of medical treatment comprise: ventricular premature

beats that occurs over 5 times per minute, polymorphic ventricular premature beats or that presenting in the susceptible period. Presence of transient ventricular tachycardia. Accompanied with coronary heart disease and severe symptoms produced by ventricular premature beats.

6) Prognosis. Correlated with the causes of diseases.7) Precaution. Based on the elimination of the causes of diseases.8) Clinical significance. Rest with the influence on cardiac function.

B. Paroxysmal Ventricular Tachycardia1) Etiology2) Clinical manifestations and signs.3) Diagnosis. Based on clinical manifestations and electrocardiograms.4) Electrocardiographic features and differential diagnosis. Recapture and fusion beats

are the clues to differentiation between ventricular tachycardia and supraventricular tachycardia with aberrant ventricular conduction.

5) Treatment. Drugs, electrical cardioversion, precaution of recurrence, seeking for factors that producing stress (ventricular aneurysm, ischemic sites).

C. There is a strong linkage between sudden cardiac death and ventricular fibrillation.1) Etiology. Usually observed in cardiac infarction, electric shock, drowning, asphyxia

and anesthesia.2) Signs. Adams-Strokes’ syndrome. 3) Diagnosis. Based on clinical manifestations and electrocardiograms.4) Electrocardiogram. No QRS complexes, nor T waves. 5) Treatment. Emergent resuscitation, electrical cardioversion, precaution of recurrence

with the help of drugs, control of risk factors. Atrioventricular BlockD. Etiology. Drugs, rheumatic fever, acute cardiac infarction, acute infection, anesthesia,

coronary heart disease, rheumatic heart disease, congenital heart diseases.E. Electrocardiographic features of first-degree, second-degree and third-degree

atrioventricular block. F. Clinical manifestations. Adams-Strokes’ outbreak.G. Diagnosis.H. Treatment. Drugs, pacemakers.

6. Intraventricular BlockA. Etiology. Rheumatic heart disease, coronary heart disease, cor pulmonale and congenital

heart diseases.B. Electrocardiographic features. Left and right bundle branch blocks, left anterior and

posterior fascicular blocks.C. Treatment. Aim at etiology. Double bundle branch blocks can produce complete

atrioventricular block, and pacemaker therapy should be considered when necessary. 7. Preexcitation Syndrome

A. Mechanism. B. Electrocardiographic features of different kinds of preexcitation syndromes.C. Clinical features.D. Treatment. Drugs, precaution of atrial arrhythmias and surgery.E. Clinical significance.

Teaching Methods1. Teach by demonstration of all sorts of arrhythmias, with the help of that has been learned

during clinical novitiate before class. 2. Give lessons with slides projection and wall maps. 3. Case discussion on the etiology, pathogenesis, clinical manifestations, diagnoses, differential

diagnoses and treatments of common arrhythmias during clinical novitiate after class.

HypertensionGeneral IntroductionPurpose and Requirement1. Be familiar with the pathogenesis of hypertension.2. Grasp the classification and staging of hypertension, and the diagnostic and treating principles

of hypertensive crisis and hypertensive encephalopathy.3. Understand the developing of the disease.Teaching duration: 2 instructional classesContent1.Concept.Definition and criteria of hypertension [according to WHO and ISH]. Difference between primary hypertension and secondary hypertension. Incidence(China), related factors eg. age, gender, genetic factor, career, body weight, regional discrepancy.2. Pathogenesis

Brief introduction to the major theories: neurogenic theory, renal theory, endocrine theory,. Demonstrate the interaction between neural factors and humoral factors that lead to hypertension by changing arterial tone and blood volume.3. Pathology. Fundamental pathologic change is that arterial spasm develops into arteriosclerosis, which presses its importance on subsequent pathologic changes of heart, brain, kidneys and retinaes.4. Clinical manifestationClinical types: benign and accelerated hypertension.Clinical identity of benign hypertension: explain common symptoms, characteristics of blood pressure, end organs’(retina, heart, brain and kidney) change and laboratory tests’ results through related pathophysiological changes. Explain hypertensive cardiopathy and hypertensive encephalopathy. Clinical identity of accelerated hypertension: rapidly progressive, abound with end organs’ complications.Brief introduction to hypertensive crisis, hypertensive encephalopathy and senile hypertension.Introduce classification and staging according to blood pressure degree, risk factors of cardiovascular disease and involved end organs.5. Diagnosis and differential diagnosisEmphasize the importance of early diagnosis. Initial diagnosis should be made discreetly. Classification and staging of hypertension should be decided by clinical manifestation. Primary and secondary hypertension should be clarified. Briefly explain clinical manifestation and diagnosis of common secondary hypertensions, which may include renal hypertension(glomerulonephritis, chronic pyelonephritis, renal artery stenosis), endocrine hypertension(pheochromocytoma, Cushing’s disease, primary aldosteronism), conduction artery disease(aorta stenosis, takayasu arteritis), gestation hypertension. Emphasize the impact of deciding etiology on therapy.6. TherapyPoint out importance of early, long-term and active therapy.A. General therapy: proper balance between work and rest, avoidance of overstrain, salt restriction, physical exercise(eg. qigong, the shadowboxing), avoidance of tobacco, weight-reduction, proper use of sedative, etc..B. Antihypertensive drug therapy1) Brief introduction to the six types of antihypertensive drugsa) Diuretics: thiazides, related sulfonamide compounds, loop diuretics, potassium-sparing diuretics.b) Adrenergic blocking agent: propanolol and other β-blockers.c) Calcium channel blocker(CCB)d) ACE inhibitor(ACEI)e) ARBf) α-blocker2) Choice of drugsa) Individualized therapy: decide agents and dosage form according grading of the patient.b) Goal of antihypertensive drug therapy.c) Applying plan.3) Treatment with Chinese Medicinea) Determination of treatment based on differentiation of symptoms and signs-to treat the patient as the following principles: hyperactivity of liver-yang, deficiency of the liver-yin and kidney-yin;

deficiency of both yin and yang.b) A single Chinese herbal medicine: Clerodendri Trichotomi(chou wutong), Herba Apocyni Veneti(luobuma), etc..c) Acupuncture4) Treatment of hypertensive crisis and hypertensive encephalopathya) Gain adequate control of blood pressure immediately: sodium nitroprusside, nitroglycerin, short-acting dihydroprtidines, urapidil.b) Apply dehydrator or rapid diuretics on patients with hypertensive encephalopathy.c) Keep the patient quiet.7. PrognosisGood prognosis is expected in patients with benign hypertension when properly treated, whereas the contrary and excessive complications might be expected when not treated. Accelerated type is supposed to be bad prognostic.`8. PreventionFind out patients early by screening. Eliminate and avoid related risk factors.Teaching Method1. Patients with primary and secondary hypertension might be demonstrated to the students.2. Wall maps, X-rays, ECG and funduscopic examination pictures would be presented.

（修订人：曾锐 心脏内科）

消化系统疾病Disease of Digestive System

GastritisPurpose and Requirement1. Understand the clinical manifestation and main diagnosed points of gastritis, and be familiar

with differential diagnosis of gastritis.2. Understand the principle of treating gastritis.3. Know gastritis is a common disease, and be familiar with the causes and pathogenesis of

gastritis.Content1. Introduction: Understand that acute gastritis is referred as the acute inflammation in gastric

mucosa with congestion, edema, erosion, bleeding and etc. 2. Causes and Pathology: Be familiar with that the pathogenic causes including the acute stress,

drugs, chemical and physical irritations, infection, ischemia and bile reflux, and the pathologic feature is an acute inflammation with effusion, erosion, bleeding, and etc.

3. Clinical Manifestations: Understand the gastrointestinal and systemic symptoms. Understand the acute gastritis caused by drugs may accompany with gastric bleeding, and it should be considered in the differential diagnosis of upper gastrointestinal bleeding. Know that emergency gastrosopy can attribute to the conclusive diagnosis.

4. Diagnosis and Differential Diagnosis:A:Diagnosis: Understand that the diagnosis of this disease is mainly based on the history of

illness, symptoms and signs. Emergent gastroscopy within 24-48h after the onset of bleeding is essential for diagnosis.

B:Differential Diagnosis: acute cholecystitis, acute pancreatitis, stress ulcer,Mallory-weiss syndrome and etc.

Chronic GastritisPurpose and Requirement:1. Understand the clinical manifestation,classification, diagnosis and differential diagnosis of

chronic gastritis.2. Understand the causes and pathogenesis of this disease.3. Understand the principle of treating and preventing this disease.Content:

1.Introduction: Be familiar with the conception and incidence of chronic gastritis.Chronic gastritis can be classified into non-atrophic gastritis, atrophic gastritis and special forms of gastritis2.Causes and Pathogenesis: Be familiar with the pathogenic role of Hp, and know other probable causes such as acute gastritis, diet, alcoholic, bile reflux and immunological factors.3.Pathology: Understand the pathologic feature of chronic superficial gastritis and atrophic gastritis. 4.Clinical Manifestations: Know that a lot of patients have no typical symptoms and signs, and some patients can have no symptoms. 5.Laboratory Findings: A. Be familiar with the value of serologic test in the diagnosis of autoimmune gastritis.Be

familiar with the method and significance of detecting Hp (pyloric helicobacteria).B. Understand the main gastroscopic findings and their value in the diagnosis of chronic

gastritis.In addition, understand the value of biopsies in the diagnosis of chronic gastritis.6.Diagnosis and Differential Diagnosis:Understand the diagnostic methods and differential diagnosis.and know the conclusive diagnosis mainly depends on gastroscopic examination and gastric mucosal biopsy.7.Treatment:A. Treatment for the pathogenic factors, especially for Hp.B. Treatment for the symptoms.8.Prognosis:Know that the timely and correct treatment maycure this disease, a few of chronic atrophic gastritis may develop into gastric carcinoma, and the patients with gastric mucosal displasia should be strictly followed up.

Peptic UlcerPurpose and Requirement:1. Understand the clinical manifestation, diagnosis and differential diagnosis of peptic ulcer.2. Understand the causes and pathogenesis of this disease.3.Understand the principle of treating and preventing this disease.Content:1. Introduction: The concept, incidence, epidemiology.2. Causes and Pathogenesis: Know the pathogenesis of this disease is not completely clear yet. Be

familiar with that the basic pathogenesis is the imbalance between the pathogenic and defensive factors resulting in the mucosal damage in stomach and duodenum. The main factors are as follows:

A. Pathogenic Factors: Hp, NSAIDS, the digestive role of gastric acid and protease, genetic factor, the abnormal movement of stomach and duodenum,smoking, stress, psychologic factor, and other risk factors.

B. Impairment of Defensive Factors: the damage of the mucus and mucosal barrier, mucosal circulation and the epithelial turnover, and the bad influence of gastritis, duodenitis and smoking.

3. Pathology: Know the common location, number and size of ulcer, and the pathologic anatomy and development of ulcer.

4. Clinical Manifestation:A.Clinical Feature: chronic course, periodic onset and regular symptom.B.Symptoms:

1) Pain: the location, character, regularity and affecting factors.2)Other Gastrointestinal symptoms.3)Systemic Symptoms.

C.Signs: Know that there may be few signs in the patients without complications and no signs in the patients at the remission stage. Understand the various signs, including the signs of special type of ulcer such as ulcer without symptoms, peptic ulcer in the elderly people, post bulbar ulcer, and pyloric channel. ulcerD.Complications: massive bleeding, perforation, pyloric obstruction and canceration.

5. Laboratory Findings: Be familiar with the importance and findings of gastroscopy. Know the significance of detecting Hp. Understand the significance of gastric fluid assay and stool occult blood test, and the feature of barium meal.

6. Diagnosis and Differential Diagnosis:Understand the importance of history and the significance of various laboratory tests in the diagnosis of this disease. The disease should be distinguished from functional dyspepsia, chronic gastritis, gastrinoma, gastric carcinoma, chronic cholecystitis, cholelithiasis and hooker worm infection.

7. Treatment:Understand the purpose and principle of treatment.1) General Treatment: it covers the regulation of psychologic status, life ,diet and living

habits.2) Drug Treatment:

a) Treatment for eradicating Hp.b) Drugs for inhibiting gastric acid excretion: the antagonist to the second receptor of

histamine, antagonist to the H+-K+ proton pump and other antacids.c) Drugs for protecting the gastric mucosa: bismuth, sucralfate and prostaglandin.d) Prevention from the relapse of peptic ulcer.

3) The strategy for treating peptic ulcer.2. Prognosis: know the relapse rate, and understand the treatment of complications.3. Prevention: know the regulation of psychologic status and diet, prudence to using the durgs

causing ulcer, and the points for attention during the remission of the disease.

CirrhosisPurpose and Requirement:1. Understand the causes and pathogenesis of cirrhosis. 2. Understand the clinical manifestation and the main diagnosing points.3. Understand the differential diagnosis, complications and the principle of treatment.Content: It mainly covers portal cirrhosis.1. Introduction: Understand the concept and classification of this disease.2. Causes and Pathogenesis:

Be familiar with the common causes of cirrhosis, including viral hepatitis, malnutrition,

chronic alcoholic toxicity, chronic drug toxicity, impairment of circulation, metabolizing diseases, genetic disease and other unknown causes,. Understand that chronic hepatitis is the most common cause of the disease.

3. PathologyKnow the degenerative, necrotic hepatic cells give rise to the regeneration of hepatic cell, resulting in the regenerative nodular and the proliferative fibered tissue, which form hepatic pseudolobe. In addition, know that the portal hypertension results from the impaired circulation.

4. Clinical Manifestations:Understand the clinical manifestations in uncompensated compensated phase.

A. The appearances of damaged liver function include low albumin in serum, high γglobulin, hemorrhagic tendency, endocrinal disturbance, and jaundice ,etc.

B. The appearances of portal hypertension include the splenomegaly, hypersplenism, ascites, and development of portal systemic collateral veins.

5. ComplicationsThe common complications include massive upper gastrointestinal bleeding, infection, hepatic encephalopathy, primary hepatic carcinoma, hepatorenal syndrome hepatopulmonary syndrome and the disturbance of water, electrolyte, acid and alkaline.

6. Laboratory Tests:Understand the routine blood test, urobilirubin test, liver function test, prothrombin time assay, immunologic test, barium meal test for esophagus and gastroscopy. Know that the laparoscopy and liver puncture can be carefully done under strict indication. In addition, know the ultrasonic test and CT.

7. Diagnosis:The diagnosis is difficult at the compensated stage, and it should be based on the pathogenic factors, history, clinical appearances and laboratory findings.

8. Differential Diagnosis:If the liver enlarges, the disease should be distinguished from chronic hepatitis and hepatic carcinoma. If ascites exists, it should be distinguished from tuberculous peritonitis, carcinous ascites, and constrictive pericarditis. If upper gastrointestinal bleeding exists, it should be distinguished from peptic ulcer. In addition, hepatoencephalopathy should be distinguished from uremia, hypoglycemia, and diabetic acetonemic acidosis. Finally, the differential diagnosis should be made among all kind of cirrhosis.

9. Treatment:A. General Treatment:

It includes the rest, diet and drug. In the essential conditions, the patient should be infused liquid, blood, plasma or albumin.B. Treatment of ascites.C. Treatment of complications.D. Surgery is used to portal hypertension and liver transplantation.10. Prognosis:

Know the factors affecting prognosis and deadly factors.11. Prevention:

Prevention of various pathogenic factors.

Acute pancreatitisPurpose and Requirement1. Understand the different clinical manifestations of each type and main points of the diagnosis

of acute pancreatitis.2. Understand the prevention and integrated treatment methods combining traditional Chinese

medicine with Western medicine of acute pancreatitis.3. Be familiar with the etiology and comprehend the pathogenesis.4. Comprehend the occurrence rules of acute pancreatitis.Content1. Introduction: concept2. Etiology and Pathogenesis:

A. In most conditions , Acute pancreatitis is the result of auto-digestion of pancreas by activated pancreatic enzymes from all kinds of reasons leading to complete or partial obstruction of outlet of pancreatic duct . Interpret the pathogenesis of shock.B. Etiology: More common reasons: binge overeating, alcohol abuse and biliary system diseases; more rare reasons: tissue damage, circulation reasons, endocrinal and metabolic reasons and acute communicable diseases.

3. Pathology:A. Interstitial edema type,B. necrotic type, C. Brief introduction of fulminant pancreatitis.

4. Clinical manifestation: Point out that clinical manifestation is different according to different type and Interpretate the following items in detail.A. Symptoms:

1) the characteristic of abdominal pain,2) nausea and vomiting3) shock4) pyrexia, disbalance of electrolytes else manifestations.

B. Signs: tenderness, tense abdominal wall, paralysis of intestine, hemorrhagic patches on abdominal wall, hydrothorax, ascite and tetany.

C. Clinical progression.5. Complications: diabetes mellitus, chronic pancreatitis, pancreatic cyst and abscess, multiple

organ failure, etc.6. Laboratory findings:

A. Emphatic introduction of the measurements of amylase of blood,.urine, hydrothorax and ascite and the clinical significance of ratio of amylase to creatinine clearance rate.

B. Clinical significance of of WBC, blood lipases, blood glocuse, blood calcium, ultrasonography and x-film examinations.

7. Diagnosis and differential diagnosis:A. Clarify the main points of the diagnosis. put emphasis on the methods of making a

diagnosis of mild and severe type in early stage since it is not difficult to make a diagnosis according to symptom, signs and laboratory findings, while the type of shock is used to be misdiagnosis.

B. Differential diagnosis: the following diseases should be considered.1) Ascariasis biliary and acute cholecystitis,2) Perforation of peptic ulcer,3) Acute intestinal obstruction,4) Myocardial infarction,5) Embolism of mesentery vessels

8. TreatmentA. General treatment, monitoring and care.B. Suppression or decrease excretion of pancrease.

1) Modify diet regime and fasting, gastrointestinal decompression and intravenous infusion when necessity.

2) Somatostatin.3) Suppression of acid excretion

C. Suppression the activity of pancreatic enzymes.D. analgesia: pethidine Maintenance the balance of water and electrolytes.E. Rescue of shock.F. Usage of antibiotics.G. Emphasis the value of EST in the treatment of biliary pancreatitis.H. Evidence-based classification of Traditional Chinese medicine and qing-yi soup。I. Indications for operation.

9. Prognosis: better to edematous type and worse to hemorrhagic and necrotic type.10. Prevention: prevention and treatment of ascariasis, cholelithiasis, reasonable diet and

temperance.

Intestinal tuberculosis and tuberculous peritonitisPurpose and Requirement1. Understand the clinical manifestation, diagnosis, prevention and cure of intestinal tuberculosis

and tuberculous peritonitis. 2. Be familiar with pathogenesis and complications.ContentMorbidity, age of occurrence, gender. Point out that they are still not uncommon diseases despite the morbidity has decreased significantly after liberation.Ⅰ.intestinal tuberculosis1.Etiology and Pathogenesis: brief introductionA. Main primary tuberculous focus and invasion pathway of tuberculous bacillus.B. Most common occurrent sites of intestinal tuberculosis and pathogenesis, by self-study.2.Pathology: pathological typeA. ulcerative type,

B. proliferative type.Interpret the relationship among number of invasive tuberculous bacillus, toxicity and immune status of host.3.Clinical Manifestation: Point out different manifestation of different types and put

emphasis on ulcerative intestinal tuberculosis.A. General manifestation including toxemia of tuberculosis, malnutrition and extra-intestinal

manifestation. B. Diarrhea and constipation.C. Abdominal pain and abdominal signs ( mass, tenderness).D. Complications: tuberculous peritonitis, intestinal obstruction; rare conditions including

hemorrage , perforation of intestinal tract and fistula cannulas formation. 4.Laboratory findingsA. Routine examinations of blood and stool and significance of blood sedimentation rate; test of

tuberculin。B. Main signs of x-ray barium meal examination. C. Colonofibroscope examination.5.Diagnosis and differential diagnosisA. Diagnosis: according to age, clinical manifestation, extra-intestinal diseases especially

cavernous pulmonary tuberculosis and laryngeal tuberculosis, laboratory findings especially x-ray barium meal examination.

B. Differential diagnosis: Crohn’ s disease, right side cancer of colon, amebiasis, granulomatous schistosomiasis and other diseases.

6.Treatment: brief introduction the following items.A. General treatment: rest and nutritionB. Anti-tuberculosis drugs.C. Anti-symptomatic therapy.D. Surgery intervention.7.Prognosis: Factors influencing prognosis8.Prevention: Thorough treatment of primary focus.

Ⅱ.Tuberculous peritonitis1.Etiology and PathogenesisA. Primary focus of tuberculous peritonitis.B. Infection pathways of invasion of tuberculous bacillus to peritoneum and pathogenesis.2.Pathology: pathological typesA. exudative type,B. adhesive type,C. caseous type.3.Clinical Manifestation: Emphatic introduction the diversity of episode and clinical manifestation according to primary focus, infection pathway, response of host and histological type and introduction of following manifestations in detail.A. General manifestation including toxemia of tuberculosis and malnutrition.B. Combine pathological type to the introduction of related symptoms and signs

( abdominal pain and abdominal tenderness, ascites, dough kneading sensation,

mass and else.) C. Common complications are intestinal obstruction, acute perforation on the

proximity of obstrction; abdominal abscess and intestinal fistula are rare seen.4.Laboratory findingsA. Routine examinations of blood, blood sedimentation rate and test of tuberculin.B. Examination of ascites ( including animal inoculation).C. x-ray examination.D. Abdominal B ultrasonography.E. Laparoscope examination.5.Diagnosis and differential diagnosisA. Diagnosis: Brief introduction of main points of diagnosis according to age, clinical

manifestation, laboratory findings and diagnostic treatment of anti-tuberculosis when necessity.

B. Differential diagnosis: Make corresponding differential diagnosis from aspects of long-term pyrexia, ascites, abdominal pain, mass and etc.

6.Treatment: brief introduction the following items.A. General treatment.B. Anti-tuberculosis drugs.C. Anti-symptomatic therapy and indications and usages of adrenal corticoid hormones.D. Indications of surgery intervention.7. Prognosis: Factors influencing prognosis8.Prevention of intestinal tuberculosis and tuberculous peritonitis : prevention methods. Diagnosis in early stage and thorough treatment of pulmonary tuberculosis and other extra-peritoneum tuberculosis.

Reference books:[1]Andreoli and Carpenter’s Ceceil Essentials of Medicine, 7th Edition;[2]Sleisenger & Fordtran’s Gastrointestinal and Liver Disease 6th Edition[3]Davidson’s Principles and Practice of Medicine 18th Edition

（修订人：郭林杰 消化内科）

泌尿系统疾病Urinary System Diseases

General Introduction of intoxicationPurpose and Requirment1. Understand the classic clinical features, diagnostic basis, differential diagnoses and management principles for intoxications; Understand the cause, toxic tract and factors related to intoxications2. Be familiar with the diagnosis and therapy of organophosphorous insecticides intoxication, acute sedative-hypnotic poisoning, alcohol poisoning and venomous snake bite intoxication.

Content1. Introduction: concept for intoxication.2. Pathogenesis: including pathogens (industrial product, drug, pesticide, toxic animals and vegetable), toxic tracts (oral, iv, inhaling, skin) and varies factors related to intoxications(duration, acute or chronic, susceptibility), et al.3. Clinical manifestation:

A acute intoxications: 1) Skin and mucosa2) Eyes3) Neural system4) Respiratory system5)Cardiovascular system6) Urinary system7) Hematic system8) fever

B Chronic intoxication: neural system, digestive system, urinary system, hematic system and skeletal system.4. Clinical diagnosis: history of toxin contact, clinical manifestation, laboratory findings. 5. Treatment: A Principles of therapy B Therapy for acute intoxications: 1) Stop contacting with the toxin

2) Cleaning the unabsorbed toxin in body: vomiting inducing, emptying stomach, preventing absorption in the bowel (catharsis and clysis).

3) increase elimination of absorbed toxin: diuresis, oxygenation, dialysis, blood adsorbtion. 4) Therapy of special alexipharmic:

5) Symptomatic therapy and supportive care 6) Others: psychiatric and social assessment, prevention cautions. C Therapy for chronic intoxication6. Preventions8. Introduce the diagnosis and therapy of organophosphorous insecticides intoxication, acute

sedative-hypnotic poisoning, alcohol poisoning and venomous snake bite intoxication.

Glomerulonephritis

Purpose and Requirement1. Understand the definition and characteristics of glomerulonephritis,; understand the current clinical and pathologic typing methods for primary glomerulonephritis; understand the clinical features, diagnostic basis, differential diagnoses and management principles for glomerulonephritis syndrome.2. Be familiar with the causes, pathogenesis and pathology of acute and chronic glomerulonephritis. Be familiar with immunoreaction, inflammation and non-immunoreaction mechanisms in glomerulonephtitis. Be familiar with acute glomerulonephritis, chronic glomerulonephritis and acute progressive glomerulonephritis. Be familiar with genetic glomerulonephritis like Alport syndrome, Fabry syndrome and thin basement membrane disease. Content1. Introduction: concept and clinical classifications of glomerulonephritis: acute, acute progressive, chronic and insidious glomerulonephritis.2. Pathogenesis: Immunoreaction from kidney to pathogenic factors, procedures of immunity and inflammations. 3. Clinical types of glomerulonephritis

A acute glomerulonephritis: it will be discussed in detail in Pediatrics.B acute progressive glomerulonephritis:1) Causes and pathogenesis: classification of acute progressive glomerulonephritis2) Pathology: crescentic glomerulonephritis3) Clinical manifestation: It happens in a sudden with the symptoms similar to acute

glomerulonephritis but more severe. It is a rapid, persisting and progressive course with worsen renal function rapidly.

4) Clinical diagnosis and differential diagnosis: It should be distinguished with acute renal tubular necrosis and acute renal failure based on the chronic renal diseases with some inducing factors.

5) Treatment: a) Principles of therapy b) General therapy c) Symptomatic therapy d) Special therapy 1) Attentive plasma exchange therapy

2) Methylprednisolone impulse therapy3) Tetra-therapy: adenocortin, cyclophosphamide (CTX), anti-coagulation agents and

dipyridamole combined therapy.4) Hemodialysis on the condition of uremia.

C chronic glomerulonephritis:1) Causes and pathogenesis: the relationship between acute and chronic glomerulonephritis,

immunoreaction.2) Pathology: caused by various pathologic types.3) Clinical manifestation:

a) protein urine, edema, hypertension, renal function damage. It presents with various clinical manifestation because of pathologic variety.

b) Complications4) Clinical diagnosis and differential diagnosis: It should be distinguished with acute

glomerulonephritis, insidious glomerulonephritis, genetic glomerulonephritis (like Alport syndrome, Fabry syndrome and thin basement membrane disease), hypertension renal damage, interstitial nephritis, chronic pyelonephritis and other secondary glomerulonephritis.

5) Treatment: a) Principles of therapy b) General therapy: including dietetic control c) Symptomatic therapy d) Blood pressure control and avoiding the factors which damage the kidney.

6) Prognosis: The importance of residual renal function protection is emphasized.D Insidious glomerulonephritis (learn by yourself )1) It is glomerulonephritis without obvious symptoms or signs, without hypertension or obvious

renal damage. Patients could be divided into two groups: with haematuria only and with proteinuria only. 2) These patients should be distinguished with the patients suffering from urinary tract infection, SLE, genetic glomerulonephritis, physiologic hematuria or proteinuria.

Nephrotic SyndromePurpose and Requirment1. Understand the typic clinical features, diagnostic basis, differential diagnoses and management principles for nephrotic syndrome.2. Be familiar with the clinical features of the main five pathologic types of nephrotic syndrome.Content1. Introduction: concept for nephritic syndrome.2. Pathology: introduce the main five pathologic types of nephritic syndrome in brief.3. Clinical manifestation:

A large amount of urine protein (>3.5g/d) B hypoalbuminemia (serum Albumin<30g/l) C edema D hyperlipoproteinemia and hypercholesterolemia

E Various clinical features of nephritic syndrome with different pathologic types4. Complications: infections, embolism and thrombosis, acute renal failure, disorders of metabolism of protein and lipid.5. Clinical diagnosis and differential diagnosis: A Diagnostic basis of nephrotic syndrome: clinical manifestation and laboratory findings. B The main points for differentiation primary nephrotic symdrome from commom secondary nephrotic syndromes.6. Treatment: A Principles of therapy B General therapy C Symptomatic therapy D Special therapy 1) Medicines: glucocorticoid and cyclophosphamide (CTX) 2) Mechanism of glucocorticoid and cyclophosphamide 3) Indication of glucocorticoid 4) Adiministration of glucocorticoid and cyclophosphamide 5) Side effect of glucocorticoid and cyclophosphamide and related cautions7. Prognosis: Factors related to prognosis

Urinary Tract Infection (UTI)Purpose and Requirement1.Understand the classic clinical features, diagnostic criteria, differential diagnosis and

management principles for cystitis, acute and chronic pyelonephritis;

2. Be familiar with etiology, pathogenesis and risk factors for UTI;

3. Be familiar with the laboratory test for UTI;

4. Know about the difference between relapsing infection and recurrence of infection.

Content1.Review: routine laboratory test for diagnosis of UTI.

2.Introduction: definition ,etiology and epidemiology for UTI.

3. Pathogenesis: infection route, host defense and virulence in UTI.

4.Clinical features for urinary tract infections:

A. acute cystitis: clinical manifestation (bladder irritation), laboratory test,

imageology examination, pathologic changes; definition of relapsing and

recurrence of infection.

B. acute pyelonephritis: clinical manifestation (systematic symptom), laboratory test,

imageology examination, pathologic changes; differential diagnosis between upper and

lower UTI.

C. chronic pyelonephritis: clinical manifestation, laboratory test, imageology

examination, pathologic changes; It can be diagnosed only if there are some changes of

renal image and renal tubular dysfunction.

5. Complications: perirenal abscesses, papillary necrosis, septicaemia and renal

insufficiency.

6. Treatment:

A Therapy for acute cystitis and acute pyelonephritis:

1) general treatment

2) principles of antibiotics selection

3) period of antibacterial treatment

4) different antibiotic regimen for moderate and sever infection

5) criteria for cure

B Therapy for chronic pyelonephritis: treatment principles.

C Therapy for recurrent UTI

D Therapy for special UTI, like which in pregnant women and male.

E Therapy for asymptomatic bacteriuria

H Therapy for complications: perirenal abscesses, papillary necrosis

7. Prognosis.

Chronic Renal Failure (CRF)Purpose and Requirment1. Understand the pathogenesis mechanism, principles of diagnosis and treatment, the importance of renal failure prevention, dialysis with its indication and contraindication.2. Be familiar the pathogenic changes, the underline mechanism of various clinical symptoms, criteria for the stages of renal failure, risk factors leading to death and the urgent rescuing.3. Be familiar the causes, clinical manifestation and treatment principles of acute renal failure (ARF).4. Be familiar with the differential diagnosis of CRF and ARF.5. Be familiar with treatment of hyperkalemia and metabolic acidosis, be familiar with indications for emergent dialysis therapy.Content1. Introduction: concept for CRF and the criteria for stages. Definition of CKD and its stages.2. Pathogenesis: introduce the various cause factors for uremia, hypothesis of healthy-survived

renal units ，hypothesis of trade-off, hypothesis of uremic toxin. It is emphasized in uremia with the patholophysical changes, retention of metabolic product, metabolic acidosis, disbalance of water, electrolyte and endocrine function.3. Clinical manifestation:

A Symptoms1) Geneal symptoms

2) Manifestation in digestive system 3) Manifestation in mental and nervous system 4) Manifestation in cardiovascular system

5) Manifestation in hematic system6) Manifestation in respiratory system7) Manifestation on skin8) Mechanism of water and electrolyte disorder and their clinical manifestation.

B Criteria for the stages of renal failure: renal insufficiency compensating stage, renal insufficiency uncompensating stage, renal failure stage and uremia stage. Stage of CKD based on eGFR. C Risk factors leading to death in uremia: hypertension, left heart failure, severe acidosis, massive haemorrhage in brain or digestive tract, hyperkalaemia, et al. 4. Laboratory findings: features of blood and urine changes, renal function test, serum biochemical test and others.5. Clinical diagnosis and differential diagnosis: A Diagnostic basis of typical uremia, including basic diseases and inducement factors identification. The clinical features in atypical cases. The factors causing renal function worsen. B The main points for differential diagnosis with other diseases easily misdiagnosed with CRF: ARF, diabetic acidosis, hypertension encephalopathy, et al.6. Treatment: A Principles of therapy B General therapy: including previous intrinsic disease treatment and reducing the inducible (irreversible) factors, dietetic and water control. C Symptomatic therapy: blood pressure control and its importance, correcting the disorders of water, electrolyte, acid-base, Ca-P mentabolism. Mechanism and indication for ACEI and ARB therapy to slow the progression of CRF. D Special therapy 1) Dialysis by oral medicine 2) peritoneal dialysis 3) hemodialysis 4) renal transplantation

5) Indications and contraindication6) advantages and short points7) indications for emergent dialysis therapy

E Traditional Chinese Medicine treatment F Medicine election and dose adjustment in CRF patients G Therapy for complications: hyperkalaemia, heart failure, uremia related anemia, blooding, infection, et al.

7. Prognosis:

Acute Renal Failure

Purpose and Requirment1. Be familiar the causes, clinical manifestation and treatment principles of acute renal failure (ARF).4. Be familiar with the differential diagnosis of ARF.5. Be familiar with treatment of hyperkalemia and metabolic acidosis, be familiar with indications for emergent dialysis therapy.

Content1. Introduction: Definition of AKI and its stages.2. Pathogenesis: introduce the various cause factors for AKI, pathogensis of ATN3. Clinical manifestation:

A Symptoms B Criteria for the stages of acute kidney injury4. Laboratory findings: features of blood and urine changes, renal function test, serum biochemical test and others.5. Clinical diagnosis and differential diagnosis: A: The main points for differential diagnosis between AKI and CKD B: Differential diagnosis between ATN, AIN and RPGN6. Treatment: A Principles of therapy B Symptomatic therapy: blood pressure control and its importance, correcting the disorders of water, electrolyte, acid-base, Ca-P mentabolism. C Renal replacement treatment D Therapy for complications: hyperkalaemia, heart failure, uremia related anemia, blooding, infection, et al.7. Prognosis:

（修订人：秦伟 肾脏内科）

血液系统Hematology Disease

Introduction of AnemiaPurpose and Requirement1. Understand the basic definition of anemia, importance of pathogenic diagnosis and the

procedure and methods of diagnosis2. Understand the pathogenesis and classification of anemia and its therapeutic principle.3. Be familiar with the clinical features of anemia.Content1. Introduction: Definition of anemia and normal level of hemoglobin. Factors that can affect the

level such as age, sex, altitude of inhabitancy. Anemia is a common symptom caused by various diseases rather than a disease entity.

2. Classification: morphologic classification and pathogenic classification. Advantage and disadvantage of these two classifications and the significance in the clinical work.

3. Clinical manifestations: Including the manifestations of the primary diseases and the manifestations of various systems due to anemia. Explain the symptoms and signs in different systems considering pathophysiology and various factors affecting the symptoms (the speed of the occurrence, the degree of anemia, blood volume, and quality).

4. DiagnosisA: Steps of diagnosis

1) Identify the existence of anemia and its degree2) Identify the type of anemia3) Find the causes (especially important, should be emphasized)

B: Methods of diagnosis 1) History: History must be all-around and systemic. Based on a case, information on

anemia, such as nutrition status, reproduction, bleeding, drug taken, career, work types, family history; primary disease should be carefully sought. The importance of history-taking in etiologic diagnosis should be emphasized.

2) Physical examination: systemic PE; especially pay attention to the presence of enlarged liver, spleen, lymph nodes, signs of bleeding, nails deformation and abnormal sensation.

3) Peripheral blood test: Hb, RBC, HCT, Reticulocyte Count, Index of RBC (MCV, MCH, MCHC), morphology of RBC should be emphasized.

4) Bone marrow examination5) Special hematology test can identify the quality of anemia.6) Other tests to find the anemic causes: urinary and faecal test, blood biochemistry, radiology,

endoscopy5: Principles of therapyA. Eliminate the cause of anemia: treat the underlying diseases, which is the first principle.B. Drugs (Iron, vitamin B12, Folic acid, adrenal steroids, androgenic steroids etc.) can not be

abused, but be correctly focalized.

C. Splenectomy may be effective in cases with hereditary spherocytosis, abnormal hemoglobinopathies or autoimmune hemolytic anemia.

D. Blood transfusion is only applied in uncompensated and severe anemia.E. Marrow transplantation: It can be chosen to treat aplastic anemia and severe abnormal

hemoglobinopathies.F. Chinese herbal medicine.

Aplastic AnemiaPurpose and Requirement1. Understand the clinical and hematological features of the disease, and the diagnostic evidences and differential diagnosis.2. Be familiar with causes, pathogenesis and therapeutic methods.3. Know about etiology, pathology and prognosis.Content1. Introduction: Explain the characters of AA and introduce its etiology.2. Causes: Secondary AA: Drug, chemicals physical factors, infection etc. Primary AA: causes

unknown.3. Pathogenesis: Introduce the roles of the injury of hematopoietic stem cells, deficiency of bone

marrow micro-environment, abnormal immunity and hereditary factors in the pathogenesis of AA. Especially emphasize the importance of abnormal immunity.

4. Clinical features: Illustrate its clinical features and difference between acute severe type and chronic type (Onset, main symptoms, degree of symptoms and course.)

5. Laboratory features: Laboratory features of acute severe type and chronic type including: examination of the peripheral blood, bone marrow smear and biopsy, hematopoietic progenitor cell culture (CFU-GM,CFU-E, etc)

6. Diagnosis criteria:A. Pancytopenia, absolute number of reticulocytes decreasesB. Spleen is not enlarged.C. Evidences for reduction of hematopoietic cellsD. Exclude other diseases leading to pancytopenia.

7. Differential diagnosis: point out the gist in differentiating AA from the following diseasesA. Hypoplastic leukemia.B. Thrombocytopenic purpuraC. Paroxysmal nocturnal hemoglobinuriaD. Myelodysplastic syndromes.E. Other diseases with pancytopenia.

8. Therapy:A. Pathogenic treatment : remove and stop contacting any toxic agents to bone marrow.B. Supportive therapy: Prevent infection and bleeding. Blood component transfusion.C. Drugs to stimulate hematopoiesis: Adrenal steroids, androgen, securinine and

hematopoietic growth factors (GCSF, GM-CSF, Epo).D. Immunosuppressant: CysA, ALG, ATGE. Bone marrow transplantation.

F. Chinese herbal medicine 9. Prevention: Administrate carefully. Labor protection. Find toxic reaction early.10. Course and prognosis.

Introduction to hemorrhagic diseasesPurpose and requirement1. Understand the classifications of hemorrhagic disorders, the bleeding characters each

classification, laboratory findings and diagnosis.2. Understand the normal mechanism of hemostasis, coagulation and anticoagulation.3. Be familiar with principles of therapy.Content1. Introduction: Conception, features and classifications of hemorrhagic disorders

Classification:1). Hemorrhagic disorders due to vascular factors.2). Disorders of the quality or the quantity of platelets.3). Dysfunction of coagulation4) Disorder of anticoagulation or fibrinolysis5) Compound disorder of hemostasis

2 Normal hemostasis and coagulation: the important 3 points of hemostasis A: Construction and functions of vascularB: Attachment, release, agglutination of platelets and its roles in hemostasisC: Procedure of coagulation: every coagulation factor, intrinsic and extrinsic coagulation pathways and the dynamic balance between anticoagulation and fibrinolysis

2. Mechanism of anticoagulation and fibrinolysisA. AT-III: important anticoagulation factorB. Protein C system: composed of PC, PS and thrombomodulin (TM)C. Tissue factor pathway inhibitorD. Heparin. Combine with At-III to play its role in anticoagulationE. fibrinolysis system

4. DiagnosisA. History: Past history of bleeding, Family history, contacting history of drugs and

chemicals. Allergies, injures, primary illness.B. Signs: bleeding characters and position, etc.C. According to history and signs, clinical diagnosis can be done: bleeding due to vascular ,

platelet disorder or disorder of coagulationD. Laboratory test:1) Screening test: Capillary resistance test, platelet count, bleeding test, clot retraction test,

coagulation time (CT), prothrombin time (PT), activated partial thromboplastin time (APTT) and their clinical significance

2) Diagnostic test:a) Examinations for vascular disorders

b) Examinations for platelet disordersc) Examinations for coagulation disordersd) Anticoagulation disordere) Fibrinolysis disorder

3) Special tests5. Therapy principles A: Eliminate causes and prevent bleeding B: Adrenal steroids, vitamin k, or hemostatic.

The indication and effectiveness of platelet or fresh plasma transfusion and other plasma products.

Idiopathic Thrombocytopenic PurpuraPurpose and Requirement:1. Understand the common causes of thrombocytopenic purpura, clinical features of ITP,

essentials of diagnosis and therapeutic principles.2. Be familiar with pathogenesis and differential diagnosis of ITP.Content:1. Introduction: Normal platelet count, relationship between platelet count and bleeding signs.

According to the etiology, thrombocytopenic purpura can be divided into idiopathic and secondary

2. Etiology and pathogenesis: “Idiopathic” means the causes can not be identified. Autoimmunity (Antibody against platelet), spleen ( production of auto-antibodies against platelets, platelet sequestration), defect of platelet maturation and capillary factor play roles in the pathogenesis of ITP.

3. Clinical manifestation: A. Features of bleeding: cutaneous, mucous and visceral bleeding.B. The difference between acute and chronic ITP: onset, age, inducement, course and prognosis.4. Laboratory test: Except for reduction of platelet count, WBC and HB are normal, but the

patients with repeatedly bleeding of alimentary and urogenital tact can be anemia. Bleeding time, clot retraction test, and capillary resistance test. Bone marrow smear: megakaryocytic quantity and morphology.

5. Diagnosis: Important points of diagnosis. Differential diagnosis: Pure purpura; acute leukemia; aplastic anemia; hypersplenism, disorders of coagulation. Introduce five criteria of ITP

6. Therapy:A. Symptomatic therapy and supportive therapy, platelet transfusion (emphasize the

indication )B. Adrenal steroids: mechanism, indication, dosage, duration and effect.C. Splenectomy: indication and effect.D. Immunosuppressant: indication, dose and effect.E. Other choices.

LeukemiaPurpose and Requirement1. Understand the clinical manifestation, laboratory test features, diagnostic evidences, and the

principles of treatment.2. Be familiar with the current conception, pathogenesis, classification, epidemiology and

prognosis of this disease,Content 1. Acute leukemia:

A. Classification: Introduce FAB classification system and MIC classification system, their advantages and methods.

B. Clinical manifestations: Infection(fever), bleeding, anemia and the infiltration of leukemia cells.

C. Laboratory test: Blood test, bone marrow morphology and cytochemistry staining. Additional introduction of abnormality in chromosomes and fusion genes. Leukemia cell immunophenotype

D. Diagnosis: According to clinical features, blood test, bone marrow morphology, diagnosis can be made. Differential diagnosis of acute lymphocyte leukemia, acute granulocyte leukemia and acute monocyte leukemia. The value of cytochemistry staining and immunophenotype.

E. Therapy:1). Symptomatic and supportive therapy: Blood components transfusion, infection prevention (protecting environment, antibiotics, antifungal drugs); nursing, nutrition and psychological support.2). chemotherapy: therapeutic principles, common used drugs and chemotherapy regimens in ALL and ANLL, regimens of post remission maintenance and course.3). Prevention and treatment of central nerves system leukemia and testis leukemia.4).Hematopoietic stem cell transplantation: Allogeneic stem cells transplantation and autologous stem cells transplantation .Their advantages ,disadvantages and effectiveness.

F. Prognosis: Natural history, survival after chemotherapy.2. Chronic myeloid leukemia

A. Pathogenesis: BCR- ABL fusion gene and its role in the pathogenesis of CML.B. Clinical features: usual, unusual and occasional symptoms. Some patients are diagnosed

when they take routine physical examinations or go to hospital because other diseases.C. Laboratory features: Blood test (the features of WBC and differential count); Neutrophil

alkaline phosphatase activity reduce; other changes in CBC test; Bone marrow :cellularity; myeloid/erythroid ratio; differential count. Myelofibrosis can be found in the end stage. Chromosome change: ph` chromosome.

D. Differential diagnosis:1). Leukemoid reaction2). Myelofibrosis.

E. Illustrate the modern therapy methods simply:1). Chemotherapy: especially introduce hydroxyurea ( effect, toxicity and side effect)2). other treatment: Irradiation, leukapheresis. Indication and value.3). Hematopoietic stem cell transplantation.4). Interferon-alpha: mechanism, side effect and effect.5). Target to molecule therapy: P210 inhibitor (STI571 or Imatinib).6). Treatment to acute phase.

3. Chronic lymphocytic leukemiaA. Conception: CLL is a clonal disease of B lymphocyte. The leukemic cells are long life

and accumulating in the body, infiltrating bone marrow, lymph nodes etc. finally inducing hematopoietic failure.

B. Clinical manifestation: In the early stage there are no symptoms, in the advanced stages there are lymphadenopathy, splenomegaly, anemia, thrombocytopenia, infection, or some symptoms related with hypermetabolism.

C. Lab. Examination: leukocytosis, lymphocytosis, anemia or/and thrombocytopenia, the immunophenotype of CLL cells (CD5,CD19,CD20 positive); the characteristics of bone marrow smear and biopsy; Chromosome abnormality.

D. Diagnosis: According to blood picture and bone marrow smear and the immunophenotype of leukemic cells.

E. Clinical stage: Introduction of Binet staging.F. Management: According to patient condition and stage to make When and how to treat

1) Chemotherapy: Indication, dosage, course and effectiveness of chlorambucil, prednisone, cyclophosphamide, fludaraibine.

2) Radiotherapy: Indication3) Splenectomy: Indication4) Supportive care: Management of infection(antibiotics, human IgG infusion) immune

hemolytic anemia and immune thrombocytopenia.F. Prognosis: Natural history, survival after treatment, and causes of mortality (hemorrhage,

infection, organic failure). （修订人：侯理 朱唤玲 血液内科）

免疫系统疾病Rheumatic diseases

General introductionPurpose and Requirement1. Understand the conceptions, etiology, clinical features and laboratory characteristics.2. Be familiar with the classification criteria and treatment of rheumatic diseases.Teaching Methods: LecturesPeriod: 3 class hoursContent1. Introduction: To introduce the concept of rheumatic diseases, and to clarify the relationships

between rheumatic diseases and other similar concepts such as Rheumatic Fever, Rheumatoid Arthritis and Connective Tissue Diseases.

2. Etiology: Rheumatic diseases are results of multiple factors.3. Clinical manifestations of rheumatic diseases: A. Chronic courseB. Attacks followed by remissions repeatedly in the course of diseaseC. Clinical manifestations are diverse and varied even in one diseaseD. With complex abnormities of biochemistry and immunologyE. Treatment responses are varied individually4. Classification: Briefly introduce the clinical features of diffused connect tissue disease and

serology-negative spondyloarthritis.5. Laboratory findings: Elaborate on the clinical meanings of rheumatoid factor(RF), anti-nuclear

antibodies(ANA), anti-neutrophil cytoplasmic antibodies(ANCA), and anti-phospholipid antibodies(aPS), as well as the clinical meaning of HLA subtypes on diagnosis, and the significance of joint fluid analysis on arthritis.

6. Other examinations: Meanings of X-ray on the diagnosis of rheumatoid arthritis and gout arthritis, and labial gland biopsy on Sjogren’s syndrome.

7. Diagnosis: Rheumatic diseases contain numerous entities, and a correct diagnosis depends on careful history taking, physical examination, laboratory examination and other pertinent examinations. a. History taking: Arthralgia is a cardinal symptom in rheumatic diseases, mastering the key

points in history taking on arthralgia are requiredb. Physical examination: Master the techniques and key points of joint examinations (pay

more attention to find whether the joint is red, swollen, tender, limited motion, deformity and important signs related to arthritis diagnosis), malar rash, perlungual erythematosus, erythematosus on hands and feet, Raynaud phenomenon and skin sclerosis.

8. Treatment: Briefly introduce the general principles of treatment, symptomatic treatments, treatments that aiming at diseases improvement and relapse prevention, surgical treatments and other treatment options.

Rheumatoid ArthritisPurpose and Requirement1. Understand clinical manifestations, diagnosis, differential diagnosis and treatment of RA2. Be familiar with the etiology, pathogenesis and pathological features of RATeaching Method: Self learningContent1. Introduction: Concept and epidemiology of RA2. Etiology and Pathogenesis: The causes remain unknown. Comprehend the relationship between

pathogenesis and autoimmunity, and features of RF3. Pathology findings: Synovial hyperplasia, formation of pannus, cartilage and subchondral bone

destruction, subcutaneous nodules, and vasculitis.4. Clinical manifestations: How RA happens? Systemic symptoms (fever, fatigue, weight loss),

local symptoms and signs (joint pain, swelling, rigidity, ankylosis and deformity)5. Examinations:

A. Laboratory: anemia, increased erythrocyte sedimentation rate and C-reactive protein, presence of RF, anti-cyclic citrullinated peptide antibodies and other autoantibodies, joint fluid analysis

B. X-ray findings: joint space narrowing, bony structure destruction, severe osteoporosis6. Diagnosis and Differential diagnosis: Diagnosis mainly depends on clinical manifestations

(systemic and local) and examinations(X-ray, autoantibodies). Differential diagnosis including: rheumatic arthritis, degenerative arthritis, gouty arthritis and spondyloarthritis.

7. Treatment: Common treatment principles. Introduce general treatments (supportive treatments), drug treatments (Non-steroid anti-inflammatory drugs, steroids, disease-modifying anti-rheumatic drugs and bioagents), physical therapy, surgery and traditional Chinese medicine, etc.

8. Prognosis: Achieve early symptom-control and long-term remission.

Systemic Lupus Erythematosus Purpose and Requirement1. Understand clinical manifestations, laboratory examinations and classification criteria of SLE2. Be familiar with the treatment principles and medicationsTeaching period: 3 class hoursTeaching method: Lectures Content1. Introduction: Clinical features and epidemiology of SLE2. Etiology and Pathogenesis: SLE is an autoimmune disease. The causes remain unknown, but

we know it may be related with these factors:A. GeneticsB. Infections C. Drugs

D. Sex hormoneE. Others

3. Pathology: Briefly introduce the common pathological findings in SLE, and specific changes on skin, kidney or other organs involved

4. Clinical manifestations: Fever, musculoskeletal symptoms, skin lesions, involvement of kidney, cardiac-vascular system, pulmonary system, neurological and psychological system, gastrointestinal system, eyes, lymph nodes, spleen, and hematological system.

5. Laboratory examinations: A. Hematologic analysisB. Urine analysisC. Autoantibodies analysis1) Antinuclear Antibody (ANA)2) Anti-Sm antibody3) Anti-ds DNA antibody4) Antiphospholipid antibody5) Serum complement level6. Diagnosis and Differential diagnosis: Elaborate on the diagnosis of SLE (the American College

of Rheumatology diagnostic criteria). Differential diagnosis including RA, Rheumatic Fever, Chronic Glomerulonephritis, Idiopathic Thrombocytopenic Purpura (ITP), Autoimmune Haemolytic Anemia and other Connective Tissue Diseases such as Polymyositis, Dermatomyositis and Systemic Sclerosis.

7. TreatmentA. Introduce the treatment principlesB. Medications (the appropriate usage of glucocorticoids, immunosuppressive drugs,

traditional Chinese medicine), physical therapy, etc.C. Treatments of comorbiditiesD. Treatment of lupus crisis: neuro-psychological SLE, lupus nephritis, infections

（修订人：王润词 风湿免疫科）

内分泌代谢系统疾病Endocrine and metabolic disease

Introduction

Goals and objectives1. Learn about the physiological and biochemical basis of endocrine system.2. Learn about the scope of clinical endocrinology and the relationship with other clinical subjects.3. Learn about the development of endocrinology4.Master the common diagnostic and therapeutic principles of the common endocrine and metabolic diseases.Teaching time: three 45-min long sessionsTeaching contents[Brief introduction about the physiological function of the major endocrine hormones] Based on the physiological and biochemical basis of endocrine system, introduce briefly the concept and scope of endocrine system. The concept of endocrine system includes tissues, not only glands. Neuroendocrine system plays an important role in regulating the homeostasis of human internal environment. The hypothalamus-adenohypophysis-target gland axe is the major parts of endocrine system, playing feedback roles in regulating and controlling physiologically. Hormones experience interactions with substance metabolism.[Diagnostic basis and methods of endocrine and metabolic diseases. ]Emphasize that the main diagnostic evidence is based on clinical symptoms and signs, introduce briefly the common functional tests. Diagnosis including:Functional diagnosispathological (location) diagnosisetiological diagnosis[Therapeutic principles of endocrine diseases]Surgery, radiotherapy and drugs are used to inhibit the overproduction of hormones. Hormone replacement and etiological therapy are for hypofunction diseases.

Hypopituitarism

Purpose and Requirement Learn about etiology, pathogenesis, clinical manifestations, diagnosis methods and therapeutic principles of hypopituitarism.Teaching contents1.Introduction Definition of hypopituitarism.2.Etiology and pathogenesis

Different pathogenesis with different etiology.3.Clinical manifestationsMainly involved the hypofunction of the target organs (Gonad, thyroid gland and adrenal gland).Pituitary or suprasellar tumor could produce signs and symptoms due to their space-occupying characteristics and their location. 4.Laboratory testsEvaluate function of adenohypophysis by measuring pituitary and target organs' hormones. Assessment of pituitary-gonadal, pituitary-adrenal and pituitary-thyroid hormones levels. The stimulating tests involved in adenohypophysis such as GnRH, TRH, CRH, GHRH stimulating tests.

5.DiagnosisThe diagnosis of hypopituitarism must be based the history, clinical examination, Laboratory tests and imaging characteristics.6.Treatment Etiological therapy and hormone replacement therapy. Learn about the treatment principle of pituitary crisis

HyperthyroidismGoals and objectivesBe familiar with the etiology and pathogenesis of hyperthyroidism.Learn about pathophysiology of hyperthyroidism.Master Clinical manifestations of hyperthyroidism, including some specific manifestations, diagnosis and differential diagnosis.Master Drug therapeutic principles of hyperthyroidism, learn about Indications of radioiodine-131, as well as the treatment of thyroid storm.Teaching time: three 45-min long sessionsTeaching contents1.Introduction] Definition and classification of thyrotoxicosis. Focus on Graves' disease.[Etiology and pathogenesis] Autoimmune abnormality in the pathogenesis of Graves' disease will be emphasized in the lecture.[Clinical manifestations] Thyrotoxicosis plays an important role in nerve system, hypothalamus-adenohypophysis-target gland axes and other systems. Manifestations of the increased sympathetic excitability and hypermetabolic states will be emphasized in the lecture.[Specific manifestations] Emphasize the clinical manifestations of infiltrative ophthalmopathy, thyroid storm, thyrotoxic heart disease and thyrotoxic periodic paralysis.[Laboratory testing] Evaluation of thyroid function can be concluded the direct measurements of Thyroid hormones concentration and indirect ones of thyroid function.1.Direct measurements of Thyroid hormones concentration, such as TT3, TT4, FT3, FT4.2. TSH

3. Indirect measurements of thyroid function. Like Thyroid-related Imaging examinations.[Diagnosis and differential diagnosis] Many cases can be diagnosed by the manifestations and Thyroid hormones concentration, however, non-classic cases should be confirmed by necessary laboratory testing.[differential diagnosis] Diffused enlargement of thyroid gland, nodular goiter, Hashimoto's thyroiditis, thyroid cancer, enlargement of cervical lymph nodes[Treatment]Appropriate rest, pay attention to nutrition.Focus on mechanism of action, indication, usage, course and side effects of antithyroid drugs.Briefly introduce indications, contraindication and complication of radioiodine131 therapy. Indications, contraindications and complications of surgery Symptomatic treatment and support, including sedatives, Beta-blockers and vitamin B.Prevention of thyroid stormPrevention the causes of thyroid storm, early detection and treatment can prevent or stop the development of disease. Therapeutic strategyIlluminate the importance of high doses of thionamides, imidazole and iodine, Beta-blockers, glucocorticoids and other adjuvant therapy in the prevention of thyroid storm.8. Prevention of Graves' opohthalmopathy

Chronic adrenocortical hypofunctionGoals and objectivesBe familiar with the major etiology, pathophysiology, clinic manifestations and therapeutic strategy of chronic adrenocortical hypofunction1.Introduction Definition of chronic adrenocortical hypofunction, the difference of primary and secondary adrenocortical hypofunction.2.Etiology and pathogenesis The major etiology is adrenal tuberculosis in china, but idiopathic adrenal atrophy caused by autoimmunity in west.Other rare etiology, such as tumor, degeneration, vasculopathy, adrenalectomy.3.Pathophysiology and clinic manifestation Describe the substance metabolic disturbance and organ dysfunction caused by insufficient secretion of  Cortisol and aldosterone.4.Clinic manifestationsDescribe all the symptoms from different systems:  hyperpigmentation, fatigue, emaciation, symptoms of circulation, digestive system, nervous system.The clinic character of adrenocortical crisis.The clinic manifestations related with etiology, such as tuberculosis or other autoimmnue diseases.5.Laboratory testingMetabolic disorder, such as hypoglycemia, abnormal Oral glucose tolerance, hyponatremia, hyperkalemiaAdrenocortical functional tests

Decreased cortisol concentrations in blood and urine, and increased plasma ACTH levels.ACTH stimulation test, cortisol concentrations in blood and urine can show the adrenocortical reserve function reduction.6.Diagnosis and differential diagnosis Diagnosis basis Clinic manifestation, hyperpigmentation, fatigue, emaciation Laboratory testing, decreased cortisol concentrations in blood and urine and adrenocortical reserve function reduction. Etiology, such as tuberculosis or other autoimmnue diseases.2. Differential diagnosisDefinition of primary and secondary adrenocortical hypofunction Detect the disease which have the manifestations of hyperpigmentation, fatigue, emaciation7.TreatmentHormone replacement therapy, the doses of glucocorticoids and mineralocorticoid must be regulated by the patients’ condition.General treatment, including support, symptomatic treatmentEtiological therapy Treatment of adrenocortical crisis.

Hypercortisolism

（Cushing’s syndrome）Purpose and requirement:1. Understand the cause, pathogenesis, clinical features and laboratory findings of

hypercortisolism.2. Be familiar with treatment of hypercotisolism.

Teaching contents1.Introduction Introduce briefly the Clinical characteristics of Cushing's syndrome.2.Etiology and pathogenesis Adrenocortical tumor, the growth and secretion are autonomous and beyond the regulation of ACTH.pituitary adenomas or functional disorders of hypothalamus-pituitary axis, causing adrenalhyperplasia, many of which can be regulated by ACTH, it is also called Cushing syndromeIntroduce the other two Cushing's syndrome, heterologous ACTH syndrome and iatrogenic Cushing's syndrome3.Pathophysiology and clinic manifestationMetabolic disturbance caused by glucocorticoids excess:  such as fat, protein, glucose, blood electrolyte,

Hyperpigmentation and nervous system.4.Diagnosis1. DiagnosisIn diagnostic procedures, a stepwise evaluation is carried out in three phases: confirmation of hypercortisolism. Differentiation among the three forms of Cushing’s syndrome, and localization procedures.

A. Confirmation 1) Urinary steroid excretion

a) Urinary free-cortisol excretion (UFC) is the measurement of choice of the initial diagnosis of hypercortisolism. It represents a direct measurement of cortisol not bound to plasma protein and is the most reliable and useful test for assessing the cortisol secretion rate. UFC is elevated in approximately 95% of Cushing syndrome patients but only if several samples are assayed.b) Urinary 17-hydroxycoticosterioid (17-OHCS). This measures the metabolites of cortisol. The urinary 17-OHCS measurements are elevated in 76% to 89% of cases.

2) Diurnal variation of plasma cortisol. Plasma values are highest from 6 to 8 A.M., declining during the day to less than 50% to 80% of morning values from 10 P.M. to midnight. This rhythm is lost very early in the course of hypercortisolism in almost all patiens.

3) Overnight hexamethasone suppression test. This test is a practical screening test for hypercortisolism.

B. Differential diagnosis of Cushing syndrome1) The 8 mg dexamethasone suppression test. This test distinguishes pituitary Cushing

syndrome form other causes, which can be used in place of the 2-day dexamethasone suppression test as it probably has similar accuracy and specificity.

2) Measurement of ACTH. C. Localization procedures

1) CT scan of the adrenal is the initial test of choice and reliably identifies most tumors as the surrounding tissue is suppressed and atrophied.

2) abdominal ultrasonography is reasonably accurate in lateralizing an adrenal tumor but is rarely indicated.

3) MRI complements the CT in some cases but does not offer greater sensitivity for small adrenal lesions. A T2-weighted image may distinguish adrenal carcinoma and adenoma, helping in the surgical decision.

5.Differential diagnosissimple obesity, stress state6.Treatment

A. Pituitary Cushing’s syndrome1) Transsphenoidal adenomectomy or hypophysectomy is the treatment of choice of patients

with pituitary Cushing’s syndrome. Selective removal of pituitary microadenomas yields a remission rate of 85% (up to 93% for isolated tumors and less than 50% for invasive tumors).

2) Pituitary X-irradiation is and optional form of therapy for patients with pituitary Cushing’s syndrome and is particularly useful in younger individual.

B. Adrenal Cushing’s syndrome1) unilateral adrenal adenomas are removed by surgery and have a high remission rate.

Because the contralateral adrenal gland is suppressed, glucocorticoid replacement is necessary for several months until adrenal function returns.

2) Adrenal carcinomaSurgery is the treatment of choice.

C. Ectopic Cushing’s syndrome1) surgery2) adrenal enzyme inhibition

Diabetes mellitusGeneral introductionPurpose and Requirement 1. Understand the cause, pathogenesis and distinction of type 1 diabetes mellitus and type 2

diabetes mellitus.2. Understand the clinical manifestation, natural history and common complications of diabetes

mellitus.3. Understand diagnostic procedure and multiple treatment, be familiar with usage of insulin and

oral hypoglycemic agents, understand the benefits of long-term glucose control.4. Be familiar with diagnosis and treatment of diabetic ketoacidosis.Content1. IntroductionDiabetes is a multiple clinical syndrome mainly characterized by plasma hyperglycemia, as well as dyslipidemia and other metabolic disorders. There are many varieties in diabetes mellitus, including two major types (type 1 diabetes and type 2 diabetes).In China, morbidity of diabetes, especially type 2 diabetes mellitus has been increasing during past two decades. Disabilities, blindness, surgical amputation are mainly caused by diabetes.2. EtiologyThe origin of diabetes is multifactorial, including genetic and environmental factors. The genetic model of diabetes still doesn’t identified yet, but familiar studies and identical twin studies document the polygenetic model for diabetes mellitus. Environmental factors undoubtedly interact with genetic suscepitibility, such as obesity, diet, unhealthy lifestyle. For type 1 diabetic patients, infection and damage of islet beta cells by a number of human viruses is the main environmental cause, some of the viruses have the potential for contributing to the development of type 1 diabetes. Abundant evidence suggests that islet beta cell destruction is immunologically mediated. The exact immunologic mechanisms involved in the pathogenetic pathway have not yet been defined, even in animal models. For type 2 diabetes mellitus, obesity is the major environmental factor. 3 pathopathogenesis and pathology

A.Disorders of glucose, fat, protein as well as water and mineral metabolism due to absolute or relative I nsulin hyposecretion are main pathogenesis of diabetes mellitus.

B.Type 1 diabetes mellitusMononuclear cell infiltration of the islets (insulitis or isletitis) in pancreases is mainly the pathologic finding. Cell-mediated immune processes are responsible for the destruction of islet beta cells. Lymphocyte, NK cells, and macrophages/monocytes appear to be involved.

Cytokines produced by these cells mediate damage to beta cells and finally cause beta cells failure. A variety of antibodies to islet cells and islet cell marker can be detected at diagnosis of type 1 diabetes, and even several years prior to diagnosis. These include antibodies to islet cells, insulin, glutamic acid decarboxylase, islet tyrosine phosphatase and others.

C. Diminished insulin secretion and insulin resistance are the key metabolic features of type 2 diabetes mellitus. Insulin secretion is higher than normal during fasting, and in response to oral glucose or mixed meals, and blood glucose levels are mildly abnormal at the early stage. As the disease progresses, fasting blood glucose levels or the 2-hour postprandial glucose levels increase further, and insulin secretion increases substantially. The increase circulating insulin concentrations observed before and early in the course of type2 diabetes mellitus in the hallmark of insulin resistance. Insulin resistance results in diminished insulin activity in the liver as well as in fat and muscle tissue, resulting in both poor disposal of glucose peripherally and enhanced glucose production by the liver, leading to hyperglycemia. Combine insulin resistance with diminished insulin secretion and one has a setting for profound hyperglycemia.

4.Clinical manifestationsThe typical clinical manifestations of diabetes mellitus include polyuria, polydipsia, polyphagia, loss of weight, usually observed in type 1 diabetes mellitus. For type 2 diabetes, these classic manifestations are rare. For different patients, diabetes mellitus has great heterogeneity in clinical manifestations. For some patients, especially type 1 diabetes mellitus, clinical manifestation of polyuria, polydipsia, polyphagia and loss of weight are severe and ketoacidosis are usually occur spontaneously. Some type 2 diabetic patients have rare clinical manifestations for a long duration or visit doctor because of symptoms of chronic vascular or neurologic complications. Accompanied disease and complications include:

A diabetic ketoacidosis, nonketotic hyperosmolar coma, diabetic lactic acidosis B infections: including suppurating or fungus infection of skin, urinary infection, tuberculosis C vascular complication: including diabetic retinopathy and nephropathy due to microvascular diseases and coronary disease, cerebral arteriosclerosis, acra gangrene due to macrovascular diseases, and other eye vascular complications such as cataracts.D neuropathy. The most common manifestation of the peripheral neuropathy of diabetes is symmetrical sensory loss in the distal lower extremities.

5.Laboratory findingsA Plasma glucose test: the normal range of fasting blood glucose is 3.3mmoo/L~6.0mmol/L

and of 2h postprandial glucose below 7.8mmol/L. Glucose concentrations can be affected by some acute diseases, fever, some drugs, psychitric factors.

B Measurement of insulin and C-peptides. This test is helpful to know the islet secretion function of the patient’s, in order to evaluate the degree of the insulin resistance and direct management.

C Measurement of glycosylated hemoglobin A1c. Measurement of HbA1c provides an integrated assessment of antecedent glycemia over an extended period. An increase of HbA1c constitutes presumptive evidence of diabetes mellitus, although verification by standard procedures is required. 6. Diagnosis

A. Fasting blood glucose: if the value is than 7.0mmol/L on 2 or more separate days, the diagnosis of diabetes mellitus can be confirmed according to the latest diagnostic classification. Random bolld glucose values greater than 11.1mmol/L are also diagnostic.

B The 2 hour oral glucose tolerance test. If the diagnosis is still in doubt, then perform a 2 hours glucose tolerance test. If the postprandial glucose levels is higher than 11.1mmol/L, the diagnosis can be confirmed.

The OGTT is influenced by many factors other than diabetes, including age, diet, state of health, gastrointestinal function, medications, and emotional state.

C. The classification of Diabetes Mellitus: depends on the clinical manifestation, family history, present illness and laboratory test. Differentiation diagnosis should consider secondary Diabetes. 6.Treatment

The goal of the treatment is to tightly control blood glucose concentration and other metabolic disorders and prevent chronic complications. The goal of therapy usually are best achieved using a multidisciplinary approach, including diet therapy, exercise, modulating life style and oral hypoglycemic drugs.

A. Diet therapy: dietary prescriptions must take into account the individual and ethnic preferences as

well as the family habits of the child, teenager, or adult. Types and timing of food intak are probably more important with type 2 diabetes than total calories as long as obesity is not an associated problem.

1) Carbohydrates: the total carbohydrate content of the diabetic meal plan should be 50%~60% of total calories. Complex high-fiber carbohydrates are encouraged.

2) Protein: the total protein content of the diabetic meal plan should be 15%to 20%. It may be prudent to limit animal source protein rather than vegetable source protein.

3) Fat: total fat content should be no more than 25% to 30% of total calories. Saturated animal fat intake should be reduced whereas intake o unsaturated fats-particularly those from vegetable sources-should not necessarily be restricted.

B. Exercise: consistent daily activity is a very important content of diabetes management. In type 2

diabetic patients, exercise is helpful to reduce the body fat and maintain a healthy BMI. In type 1 diabetic patients, exercise should be well managed to prevent hypoglycemia.

C. Oral hypoglycemic agents (OHA): there are several kinds of OHA.1) Biguanide (Metformin): decrease hepatic glucose production and enhances hepatic

and muscle sensitivity. Metformin is the first recommended OHA for obese type 2 diabetic patients. This agent can also decrease the concentrations of LDL and triglycerides. It may also normalize ovulatory abnormalities in girls with PCOS. Side effects are usually gastrointestinal disturbance, but these usually diminish with time. Recommended dosage at beginning is 250~500mg per day, and can increase to 1500 mg per day maximum.

2) Sulfonylureas: promote insulin secretion. This agent is the first choice for non-obese type 2 patients. It is usually start at low dosage, such as 2.5~5mg per day for one week, and then titrate upward to 15mg maximum. Sulfonylureas can cause severe hypoglycemia, so it is not recommended in elder over 70 years. It also can cause

weight gain. 3) Glucosidase inhibitors: this kind of OHA can slow carbohydrate absorption and slow

the hydrolysis of complex carbohydrates, which decreases postprandial rise in glucose. Recommended daily dosage are from 25mg to 150mg. The main side effect is flatulence.

4) Meglitinide: this drug can cause short-term promotion of glucose stimulated insulin secretion. It can take place of sulfonylureas in type 2 diabetic patients in order to decrease

5) Triazolidenediones: this kind of OHA is also called insulin enhancer. It improve peripheral insulin sensitivity and reduce triglyceride concentration. The side effect includes liver dysfunction, edema, but these side effects all seldom occur.

D. Insulin therapy: including rapid or short-acting insulin, intermediate-acting insulin and long-term acting insulin. 1) For type 1 diabetic patients, insulin therapy is a replacement management.

Aggressive insulin therapy using four or five injections of rapid/short-acting plus intermediate-acting insulin daily is started as soon as possible in an attempt to “rest” the damaged islet cells.

2) For type 2 diabetes, insulin is used in patients whose islet secretion function is failure, especially in recently years, insulin is recommended using as early as possible in type 2 diabetic patients in order to protect islet function. In type 2 diabetic patients, insulin is also used in some acute states, such as acute diabetic complications, acute infection, pregnancy, myocardial infarction etc.

3) Side effects of insulin: the major side effects of insulin is hypoglycemia, especially in patients who received tight insulin therapy. Other side effects include edema, weight gain and allergy to insulin.

4)

Diabetic ketoacidosis1. Pathopathogenesis and clinical manifestations:.

A. Pathopathogenesis: Diabetic ketoacidosis is the most common endocrine emergency. Mortality rates from 1% to 10% related deaths. 1) Role of insulin: All of the abnormalities associated with DKA can be traced to and

absolute or relative lack of insulin that develops over several hours or days. In type 1 diabetes mellitus, insulin lack results from failure of endogenous insulin secretion or inadequate administration of exogenous insulin or from increased requirements for insulin caused by the presence of an underlying stressful condition. In type 2 diabetes, it usually occur in the presence of stress. The associated stress can be in the form of an intercurrent infection (pneumonia, urinary tract infection, upper respiratory tract infection, meningitis, cholecystitis, pancreatitis), a vascular disorder (myocardial infarction, stroke), an endocrine disorder (hyperthroidism, Cushing syndromer, acromegaly etc.), trauma, pregnancy, or emotional stress.

2) Role of counterregulatory hormones: the increased secretion of the counterreglatory hormones (hormones antagonistic to the action of insulin, such as epinephrine, cortisol, glucagons, and growth hormone) might explain the additional insulin

requirements in such disorders. 3) The insulin deficiency activates glycogenolysis and gluconeogenesis, resulting

hyperglycemia and osmotic diuresis that leads to dehydration and electrolyte depletion. In addition, lipolysis results in production of free fatty acids as well as glycerol, which further helps fuel new glucose production. Contributing further to the hyperglycemia are the decreased peripheral glucose utilization and the volume depletion that reduce renal blood flow and consequently the amount of glucose filtered and excreted by the kidney. Free fatty acids are delivered to the liver where ketone bodies are produced with resultant ketonemia, which is intensified by decreased peripheral utilization. This leads to ketonuria, which further depletes electrolytes by and associated obligatory loss of cations. The hypersecretion of epinephrine, glucagons, cortisol, and growth hormone contributes to ketoacidosis by inhibiting insulin-mediated glucose uptake by muscle, activating glycogenolysis and gluconeogenesis, activating lipolysis and inhibiting residual insulin secretion.

B. Clinical manifestations: 1) Polydipsia, polyuria and weakness are the most common presenting complaints: the

severity depends on the degree of hyperglycemia as well as the duration of illness. 2) Anorexia, nausea, vomiting, and abdominal pain may be present and may mimic an

abominal emergency. 3) Ileus and gastric dilatation may occur and predispose to aspiration. 4) Kussmaul breathing is present as respiratory compensation for the metabolic acidosis

and is usually apparent when the pH is less than 7.2.5) Neurologically, 20% of patients are without any sensorial changes at all, whereas

10% are actually comatose. 6) Signs: hypothermia is common in DKA. A fever should be taken as strong evidence

of infection and vigorously pursued. Hyperpneaor Kussmaul respirations, tachycardia, poor skin turgor hyporeflexia are often present in DKA.

2. Diagnosis and differential diagnosis. Diagnosis in early stage of DKA is very important in treatment and secure life. A. Diagnosis：

1) Glucose: serum glucose is usually elevated above 300mg/dL, although levels range from almost normal to very high levels characteristic of hyperosmolar coma.

2) Ketones: the three principal ketone bodies are β-hydroxybutyric acid, acetoacetate, and acetone. The total ketone concentration is usually greater than 3 mM/L and can go as high as 30 mM/L.

3) Acidosis: the metabolic acidosis is characterized by a serum bicarbonated of less than 15mEq/L and an arterial pH of less than 7.3.

4) Electrolytes: the serum sodium level may be low, normal, or high. The presence of the elevated serum glucose results in the obligatory movement of water from the intracellulat to the extracellular space. This redistribution of body water can contribute to apparent hyponatremia despite dehydration and hyperosmolality. Serum potassium levels can be low, normal or high. An initial low potassium concentration attests to severe depletion and should be managed aggressively.

B. Differential diagnosis: DKA should be differentiated with hypoglycemic coma, diabetic

lactic coma, hyperosmolar hyperglycemic syndrome(HHS). HHS occurs in middle-aged and elderly patients. Most have mild type 2 diabetes or no prior history of diabetes. Patients who suffering from HHS tent to have a serum osmolality greater than 340mOsm/kg. Various neurologic deficits such as coma, transient hemiparesis, hyperreflexia, and generalized areflexia are commonly present and altered states of consciousness from lethargy to coma are observed in HHS. In hypoglycemic coma, glucose levels are usually lower than 2.8mmol/L. Lactic acids increase significantly in diabetic lactic acidosis.

3. TreatmentA. General management technique: the patients should be placed in an intensive care unit.

Initially, laboratory data should be obtained every 1 to 3 hours and then less frequently once clinical improvement is noted. Frequent assessment of potassium status and careful observation of neurologic status are vital. If the patients is tin shock, stupor, or coma, use of a nasogastric tube, especially if vomiting is present, and urinary catheter is recommended.

B. Hydration and electrolyte therapy: 1) Fluid replacement: 2) Electrolytes therapy:

C. Insulin therapy: insulin can be administered by subcutaneous, IM, or IV routes, depending on the clinical situation. Low dose insulin infusion is the mode of insulin administration that is now generally accepted. The dosage of insulin is about 0.1IU/kg/h. The benefits derived from continuous low dose insulin infusion are: avoiding the potential hazards of rapid and erratic serum glucose and somolar fluctuations, avoiding a greater extent episodes of late hypoglycemia and hypokalemia, and, with a constant amount of insulin infused, a steady linear fall in glucose can be expected and appropriate changes in IV solution anticipated.

D. Bicarbonate: can be administrated when pH is lower than 7.0.

Metabolic bone diseases and osteoporosisPurpose and requirement:

1.Master the definition and clinical manifestations of primary osteoporosis and diagnosis and treatment of primary osteoporosis.2.Be familiar with the basic principles and process of bone mass.3.Learn about common causes of metabolic bone diseases and endocrine regulatory factors of primary osteoporosis.

Teaching time: three 45-min long sessionsTeaching contents 1.Introduction Etiologies of metabolic bone diseases, currency of treatment and prevention of primary osteoporosis.Etiologies and pathogenesis of primary osteoporosis. Describe that primary osteoporosis is caused by multiple factors, focusing on variation of endocrine hormone as the main factor. Clinical manifestations of primary osteoporosis. Focus on features of bone pain and low-

traumatic fracture.2.Common assistant examinations:

（1）Measuring bone mass: Emphasize on the indications and clinical significance. (2) X-ray: introduce characteristics of low bone-density, bone fracture line, bone deformity and soft tissue swelling. (3) Biochemical examination: introduce the possible biochemical variations and diagnostic values of them.3.Diagnosis and differential diagnosisWHO diagnostic criteria about osteoporosis will be emphasized in the lecture. Pay attention to exclude the possible diseases caused by variation of bone mass.4.Treatment：(1) Therapeutic goals are based on calcium and Vitamin D replacement. Action mechanism, classification and indication of anti-osteoporosis. (2) Non-surgery treatment of bone fracture caused by osteoporosis. (3) Anti-symptomatic treatment

（修订人：卢春燕 范翩翩 谭惠文 内分泌代谢科）