Pathophysiology
(Course Code:1001001)
Guideline
I. Course Introduction
80classes comprise 56 for lecturing,24for experimental training.
3.5 credits; 5thsemester
II. Lecturing section
Department of Pathophysiology
III. Attribution
Pathophysiology is a science concerning the etiology and pathogenesis of disease, as well as the mechanisms of functional and metabolic alternations in diseases. In the course of pathophysiology, students will learn the alternations of function, metabolism and underlying mechanism in diseases. The pathophysiology is a crucial bridge course between basic medical science and clinical medicine, which enables medical students to use the knowledge of basic medical science for the diagnosis and treatment of diseases.
IV. Requirements
Pathophysiologyis an important basic course of medicine. Through the study of this course, students are required to master basic law of disease onset and progress,the alternations of function, metabolism and underlying mechanism in diseases.In addition, students are required to master basic experimental skills and know new developments of the subject.
V. Compulsory subject
Pathology and physiology
VI. Teaching arrangement of pathophysiology
Contents |
Lecturing |
Class discussion |
Self-study |
Experimental training |
Chaper 1,2 Introduce and conspectus of disease |
2 |
|||
Chaper 3 Disorders of water and electrolyte metabolism |
6 |
|||
Chaper 4 Acid-base balance and disturbance |
6 |
|||
Chaper 5 Hypoxia |
4 |
|||
Chaper 6 Fever |
2 |
Chaper 7 Dysfunction of cell signaling in diseases |
2 |
|||
Chaper 8 Cell proliferation, disferentiation, apoptosis and the related diseases |
2 |
|||
Chaper 9 Stress |
2 |
|||
Chaper 10 Coagulation and Anti-coagulation Disturbance |
2 |
|||
Chaper 11 Shock、MODS |
6 |
|||
Chaper 12 Ischemia-reperfusioninjury |
2 |
|||
Chaper 13 Heart failure |
4 |
|||
Chaper 14 respiratory failure |
4 |
|||
Chaper 15 hepatic failure |
2 |
|||
Chaper 16 Renal failure |
6 |
|||
Chaper 17 Brain dysfunction |
2 |
|||
Cell proliferation, disferentiation |
2 |
|||
Experiment 1 HemorrhagicShock |
4 |
|||
Experiment 2 ExperimentalAcute Right Heart Failure |
4 |
|||
Experiment 3 RespiratoryFailure |
4 |
|||
Experimet 4 Acute Toxic RenalDysfunction |
4 |
|||
Experimental 5 Acute RightHeart Failure |
4 |
|||
Experiment 6 Experimentaldesign and discussion |
4 |
|||
Total |
54 |
2 |
24 |
VII . References
1. Textbook
(1）Wang Jianzhi editor-in-chief《pathophysiology》Second edition，People's Medical Publishing House
(2) Pathophysiology concepts and altered health states Seventh edition,Lippincott Williams and wilkins
2. Website:http://www.icourses.cn/coursestatic/course_6169.html
Ⅷ. Assessment method
Final examination 80%，formative evaluation 20%
ⅠRequirement
Chapter 1 Introduction
1. Master basic concept including ①pathophysiology ②pathological process
2. Understand the mission, position and main studying method of pathophysiology
3. Understand briefly concept of evidence-base medicine and history of pathophysiology
"Key and difficult points
1. Definition of pathophysiology and pathological process
2. The main studying method of pathophysiology
ⅢThe keylecturing content and points
1. Concept of pathophysiology and pathological process
2. The main studying method of pathophysiology as well as the mission and position of pathophysiology in medical science.
ⅣThe of self-learning content
1．The history of pathophysiology
ⅤQuestion
1．What is pathophysiology and pathological process？2．What is main method of studying pathophysiology？3．What is evidence-base of medicine？
ⅠRequirements
Chapter 2 Conspectus of Diseases
1.Master concepts including Health, disease, death, brain death and thecriteria of brain death；
2. Understandetiology of disease
3. Understand briefly significance of brain death in medicine
"Key and difficult points
The etiology and mechanism of disease
ⅢLecturing main contents
1. Health and disease
(1) Concept of health
(2) Concept of disease
2. Etiology
(1) Causes of diseases
(2) Predisposing factors
3. Pathogenesis
(1) General rule for pathogenesis of diseases
(2) Fundamental mechanisms for diseases
4. Outcome of disease
(1) Complete recovery and incomplete recovery
(2) Brain death including concept, the criteria of diagnosis and significance
ⅣQuestion
1. Please explainreversal role of cause and resultusing serious bleeding caused by damage
2. What is brain death and thecriteria of brain？
Chapter 3 Disorders ofWaterand Electrolyte Metabolism
ⅠRequirements
1. Tounderstand the regulation of water and electrolyte metabolism.
2. Tounderstand the concepts, pathogenesis and manifestation of hypovolemic hyponatremia and hypovolemic hypernatremia.
3. Tounderstand the effects ofhypokalemia andhyperkalemia.
4. Tounderstand the effects of hypomagnesemia and hypermagnesemia.
5. Tounderstand normal calcium and phosphorus metabolism and disorders of calcium and phosphorus metabolism.
6. To understand briefly the body fluid distribution and electrolyte contents.
7. To understand briefly the function and balance of electrolytes.
8. To understand briefly hypervolemic hyponatremia and hypovolemia with a normal serum sodium concentration.
9. To understand briefly the etiology and pathogenesis ofhypokalemia andhyperkalemia.
10. To understand briefly the pathophysiological basis of prevention and treatment ofhypokalemia andhyperkalemia.
11. To understand briefly the etiology and pathogenesis of hypomagnesemia and hypermagnesemia.
12. To know water and electrolyte exchanges among different fluid compartments.
13. To know the function and balance of water.
14. To know the concepts, pathogenesis, manifestation and pathophysiological basis of normovolemic hyponatremia, normovolemic hypernatremia, hypervolemic hypernatremia and edema.
15. To know the pathophysiological basis of hypomagnesemia and hypermagnesemia.
"Main and difficult points
1. The regulation of water and electrolyte metabolism.
2. The effects ofhypokalemia andhyperkalemia.
3. The effects of hypomagnesemia and hypermagnesemia.
ⅢTeaching content
1. The function and balance of body fluid
(1).The concept and distribution of body fluid, the main points are the concepts of intracellular and extracellular fluids.
(2).The regulation of body fluid, the main points are the mechanisms for regulating body fluid and electrolyte balance.
2. The categories and manifestation of disorders of water and sodium metabolism (1). The etiology, pathogenesis and manifestation of hypovolemic hyponatremia and
hypovolemic hypernatremia, the main points are the pathogenesis.
(2). The etiology, pathogenesis and manifestation of edema, the main point is the pathogenesis. (3). The etiology, pathogenesis and manifestation of hypokalemia and hyperkalemia, the main
points are the effects on the skeletal and smooth muscle and cardiac muscle.
(4). The etiology, pathogenesis and manifestation of hypomagnesemia and hypermagnesemia.
ⅣSelf-study content
1. Hypervolemic hyponatremia and hypovolemia with a normal serum sodium concentration.
2. Normovolemic hyponatremia, Normovolemic hypernatremia, Hypervolemic hypernatremia.
3. Disorders of calcium and phosphorus metabolism.
ⅤReferences and websites
Texbook：Pathophysiology
ⅥQuestions
1. Which typeofdehydrationisthe most common? Which typeofdehydrationisthe most dangerous?Why?
2. What are the main mechanisms of disorders of potassium metabolism induced cardiac arrhythmia?
3. Which organ dysfunctionsare inducedbyhypokalemia? What arethemainalterations?
4. What is the most severe outcome of hyperkalemia? What is the mechanism?
Chapter 4 Acid-base Balance and Disturbances
ⅠRequirements
1. Tounderstand the clinical tests for acid-base disturbances
2. Tounderstand the reasons and mechanisms of simple acid-base disturbances
3. Tobe familiar with the regulation of acids and bases
4. Tobe familiar with the compensations for simple acid-base disturbances
5. Tobe familiar with the clinical classifications of mixed acid-base disturbances
6. Tobe familiar with the pathophysiological basis of prevention and treatment of simple acid-base disturbances
7. Toknow the reasons of mixed acid-base disturbances
8. Toknow the acid-base map and expectation value of compensation for acid-base disturbances
"Main points
1. Definition and clinical manifestation of pH, PaCO2, Standard bicarbonate (SB), Actual bicarbonate (AB)
2. Etiology,mechanisms and compensation for simple acid-base disturbances
3. Etiology,clinical classification and discrimination of mixed acid-base disturbances
ⅢTeaching contents
1. Concept and generation of acid and base, regulation of acid-base balance.Concept of acid and base, especially volatile acid and nonvolatile acid. Sources and generation of acid and base. Body regulation of acid-base balance
2. Typesof acid-base disturbances, clinical tests for acid-base disturbancesTypesof acid-base disturbance and its classification standard Definition, clinical manifestation and normal value of pH, PaCO2, standard bicarbonate (SB), actual bicarbonate (AB) and anion gap (AG)
3. Simple acid-base disturbances. Reasons, mechanisms of simple acid-base disturbance. The
influence of simple acid-base disturbances on the body. Treatment principles
4. Mixed acid-base disturbances.Typesand features of mixed acid-base disturbances
Ⅳ Self-studying content
Expect compensatory formula of mixed acid-base disturbance
ⅤQuestions
1. How the body maintains acid-base balance? What are the features of these regulations?
2. Please describe the definition, clinical manifestation and normal value of pH, PaCO2, standard bicarbonate (SB), actual bicarbonate (AB) and anion gap (AG).
3. Please list the reasons of metabolic alkalosis.
4. How the body compensates after metabolic acidosis?
5. What are the influences of respiratory alkalosis on body?
Ⅰ Requirement
Chapter 5 Hypoxia
1. Master basic concept including①Definition of hypoxia②Significance of common blood oxygen parameters③Hypoxia classification, cause and blood oxygen change characters④Mechansims of hypoxia.
2. Understand the metabolic and fucnitonal alterations under hypoxia.
3. Understand briefly treatment of hypoxia.
"Key and difficult points
1. Definition of hypoxia.
2. Definition and significance of blood oxygen parameters.
3. Hypoxia causes and blood oxygen changes. 4.Blood oxygen changes of anemia.
ⅢThe key lecturing content and points
1. Definition and significance of hypoxia and common blood oxygen parameters: hypoxia, PO2,CO2max, CO2,SO2,P50.
2. Classification, Etiology and Pathogenesis of Hypoxia: Hypotonic hypoxia, Hemic hypoxia, Circulatory hypoxia and Histogenous hypoxia.
3. Alterations of Function and Metabolism.
ⅣThe self-learning content
Oxygen therapy and oxygen intoxication.
ⅤQuestion
1．What is the definition of P50？
2．What are alterations of blood oxygen parameters for hypotonic hypoxia？
3．How many types of hypoxia？
Chapter 6 Fever
ⅠRequirement
1. Master basic concept including①fever②endogenous pyrogens；③central mediators of fever
2. Master the mechanisms of fever
3. Understand the alterations of metabolism and function during fever
4. Understand briefly the pathophysiological basis of prevention and treatment for fever
"Key and difficult points
The mechanisms of fever
ⅢThe key lecturing content and points
1. Concept of fever
2. Regulation of normal body temperature
3. Etiology of fever
4. Pathogenesis of fever
5.Alterations of metabolism and function during fever
6. Pathophysiological basis of prevention and treatment
ⅣThe self-learning content
Cassification of high body- temperature.
ⅤQuestions
1．What is fever？
2．What are the main differences between fever and hyperthermia？3．How does body temperature rise during fever？
4. What are the beneficial effets of fever?
Chapter 7 SignalTransductionand Diseases
I. Requirements
1．Understand the basic procedure and mechanisms of the cellular signal transduction,theconcept of nuclear receptor, membraneous receptor and the basic regulation module for cellular signa transduction;；
2．Know the abnormalities in the cellular signal transduction; Know the signal transduction mechanisms for the insulin-resistant diabetes；
3．Understand briefly the reason for the cellular signal transduction, the multiple abnormalities in the tumor and hypertensivecardiomyopathy
II. Key points and difficult points
Keypoints：Thebasic procedure and mechanisms of the cellular signaltransduction；Theconcept of nuclear receptor, membraneous receptor；The basic regulation module for cellular signa transduction；The abnormalities in the cellular signal transduction
Difficult points：The mechanisms for multiple abnormalities in the cellular signal transduction in some diseases.
III. Detail requirements for sections
Section 1, Basic knowledge for cellular signal transduction.Understand the basic procedure and mechanisms of the cellular signal transduction,theconcept of nuclear receptor, membraneous receptor and the basic regulation module for cellular signa transduction；Know the cellular signal transduction mediated by G protein coupled receptor.
Section 2, The reasons and mechanisms for cellular signal transduction abnormalities. Understand briefly the reason for the cellular signal transduction；Know the abnormalities in the cellular signal transduction。
Section 3, The abnormalities of cellular signal transduction and diseases.Understand briefly the types for the cellular signal transduction abnormalities induced diseases. Know the two types signal aberrant (Primary: signal excess, signal insufficiency; Secondary: stimulatoryantibody,blocking antibody) and their representative diseases; Know two types of receptor aberrant (Primary: receptor gene mutation; Secondary: receptor downregulation or desensitization) and their representative diseases;Know the aberrant G-proten in cell signaling and related diseases(Acromegaly or Gigantism, cholera); Know the mechanisms for phorbolester induced cancer; the sympathetic deregulation in heart failure; Know the mechanisms for infections shock inducedcoldshockandwarmshock;Knowthecrosstalkofcellularsignaltransductionin
Myocardial Hypertrophy
IV. Self learning points
The abnormalities in the cellular signal transducton during the inflammation
Chapter 8 Apoptosis
I. Requirements：
Understand the conception of apoptosis, the differences between apoptosis and necrosis; Know the mechanisms for apoptosis
Understand the apoptosis and disease
Know the significance of apoptosis in the disease therapy
II. Key points and difficult points
Key points
1, The main differences between apoptosis and necrosis
2, The three theories in apoptosis: oxidativeinjury,calcium imbalance, mitochondrial injury 3, The relationship of apoptosis withtumor,auto-immune disease, AD, heart failure, and AIDs
Difficult points
1, The main differences between apoptosis and necrosis 2, The biochemical changes of apoptosis
3, Roles of related genes (Bcl-2, p53, Fas) in the apoptosis regulation 4, The mitochondrial injury theory for apoptosis
III. Detail requirements for sections
Section 1, The findings of apoptosis and its physiological significance.Apoptosis is different to the necrosis, especially in the stimulatory factors, morphology, biochemical changes, inflammatory changes;
Section 2, the procedure for the apoptosis.The morphological changes of apoptosis, biochemical parameters, the concept of caspases, how the caspases affect the apoptosis and how they be activated. The regulators for the apoptosis (Bcl-2, p53, Fas, c-myc);
Section 3, the mechanisms for apoptosis.The three theories in apoptosis: oxidative injury, calcium imbalance, mitochondrial injury
Section 4, the apoptosis and diseases.The relationship of apoptosis with tumor, auto-immune disease, AD, heart failure, and AIDs
ⅠRequirement
Chapter 9 Stress
1. Master basic concept including①stress;②stressor；③general adaptation syndrome;④stress-related disease
2. Master the neuroendocrine responses underlining stress condition
3. Master the mechanisms of stress ulcer
4. Understand cellular and humoral responses during stress
5. Understand functional and metabolic responses during stress
6. Understand briefly the stress-related disease
7. Understand briefly the pathophysiological basis of prevention and treatment for stress
"Key and difficult points
1.The compositions and the functions of Locus Ceruleus-norepinephrine
neurons-sympathetic/adrenal medulla axis and Hypothalamus-pituitary-adrenal cortex axis
2. The mechanisms of stress ulcer
ⅢThe key lecturing content and points
1. Concept of stress, Stressor and general adaptation syndrome
2. Neuroendocrine responses during stress
3. Cellular and humoral responses during stress
4. Functional and metabolic responses
5. Stress-related disease during stress
6. Pathophysiological basis of prevention and treatment
ⅣThe self-learning content
Three stages of .general adaptation syndrome
ⅤQuestions
1．What are stress and Stress-related disease？
2．What are Locus Ceruleus-norepinephrine neurons-sympathetic/adrenal medulla axis and Hypothalamus-pituitary-adrenal cortex axis? How do they response during stress？
3．What are the mechanisms of stress ulcer？
Chapter 10 Coagulation and Anti-coagulation Disturbance
ⅠRequirement
1.Master basic concept including①disseminated intravascular coagulation (DIC) concept, etiology and pathogenesis and therapeutic priciple②DIC influencing factors and metabolic/funcitonal alterations.
2.Understanding coagulation/anti-coagulation components and their functions. 3.Understanging briefly pathlogical process of coagulation/anti-coagulation disorders.
"Key and difficult points
1 DIC concept, etiology and pathogenesis.
2 DIC influencing factors and metabolic/functional alterations.
ⅢThe key lecturing content and points
1.DIC concept.
2.DIC causes and pathogenesis.
3.Influncing factors for DIC
4.DIC developing processes and clasification.
5.DIC metabolic and fucntional alterations.
6.DIC treatment priciple.
ⅣThe self-learning content
1. Coagulation/anti-coagulation components and their functions.
ⅤQuestion
1. Describe briefly DIC stages and their characteristics.
2. Describe the relationships between shock and DIC.
3. Why severe infection causes DIC?
ⅠRequirement
Chapter 11 Shock
1. Master basic concept including①shock②auto blood transfusion； ③auto fluid transfusion;④bloodredistribution;⑤multipleorgandysfunctionsyndrome;⑥systemic
inflammatory response;⑦compensatory anti-inflammatory response syndrome;⑧mixed antagonist response syndrome
2. Master the etiology and classification of shock and multiple organ dysfunction syndrome
3. Master three stages of shock and their pathological changes
4. Master the mechanisms of multiple organ dysfunction syndrome
5. Understand roles of humoral factors in pathogenesis of shock
6. Understand functional and metabolic responses during shock
7. Understand briefly the pathophysiological basis of prevention and treatment for shock and multiple organ dysfunction syndrome
"Key and difficult points
1. Alterations of microcirculations during ischemic hypoxia stage and stagnant hypoxia stage
2. Compensatory mechanisms for blood pressure recovery during ischemic hypoxia stage of shock
3. Interactions between DIC and shock during organic failure stage
4. The mechanisms of multiple organ dysfunction syndrome
ⅢThe key lecturing content and points
1. Concept of shock and multiple organ dysfunction syndrome
2. Etiology and classification of shock
3. Three stages of shock and their pathological changes
4. Roles of humoral factors in pathogenesis of shock
5. Functional and metabolic changes of shock
6. The mechanisms of multiple organ dysfunction syndrome
7. Pathophysiological basis of prevention and treatment for shock and multiple organ dysfunction syndrome
ⅣThe of self-learning content
The history of shock and multiple organ dysfunction syndrome
ⅤQuestions
1．What are the difference between ischemic hypoxia stage and stagnant hypoxia stage？2．How to compensate blood pressure to reaching normal level during ischemic hypoxia stage of
shock
3．How do DIC and shock interact with each other during organic failure stage？
4. What is multiple organ dysfunction syndrome? What are the main mechanisms of multiple organ dysfunction syndrome?
ⅠRequirement
MODS
1.Master the concept of MODS，SIRS,CARS,MARS 2.Master the mechanism of MODS and SIRS
"Key and difficult points
1.The concept and etiology of MODS
2.The pathogenesis of SIRS, CARS and MARS
ⅢLecturing content and key points
1. The concept of SIRS anditsetiology and pathogenesis
2. The concept of MODS and its etiology and pathogenesis
ⅣQuestion
1. How does severe trauma induce MODS?
2. How to define SIRS?
Chaper 12 Ischemia-reperfusion Injury
ⅠRequirement
1. Master①basic concepts of ischemia-reperfusion (I/R) injury, free radicle, calcium overload and myocardial stunning.②I/Rinjury mechanisms including freee radical induction, calcium overload and inflamatory cell infiltration.
2. UnderstandingI/Rinjury causes and influencing factors.
3. Understanding briefly effects ofI/Rinjury on body and therapeutic priciple ofI/Rinjury.
"Key and difficult points
1. Mechanisms of free radical induction during I/R.
2. Calcium overload mechanism and its role inI/Rinjury.
3. Role of inflamatory cells in I/Rinjury.
ⅢThe key lecturing content and points
1. Concept ofI/Rinjury
2. I/Rinjury mechansims: role of free radicals, calcium overload and wite blood cells after I/R.
3. I/Rinjury therapeutic principle.
ⅣThe of self-learning content
I/R injury-caused metablolic and functional alterations
Ⅴ Question
1. What areI/Rinjury mechanisms?
2. What are functional and structure changes in heart after I/R?
ⅠRequirement
Chaper 13 Heart Failure
1. Tounderstand the general concept of heart failure
2. Tobe familiar with the etiology and the classification of heart failure
3. Tocomprehensively understand the pathogenesis of heart failure
4. Tobe familiar with the cardiac compensation and its underlying mechanism
5. Tobe familiar with the systemic compensation and the clinical manifestations
6. Toknow the pathophysiological basis of prevention and treatment of heart failure
"Key and difficult points Key points
1. Definition of heart failure
2. Identification of the difference among heart failure, shock and pericarditis
3. Disorders in energy production and utilization
4. Dysfunction of excitation-contraction coupling
5. Diastolic dysfunction
6.Asynergic myocardial contraction and dilation
7. Pathophysiologic basic of clinical manisfestation
Difficult points
1. Identification of the difference among heart failure, shock and pericarditis
2. The mechanism of the excitation-contraction coupling dysfunction
3. The mechanism of the systolic and diastolic dysfunction
4. Compensation to decompensation of myocardial hypertrophy
ⅢTeaching content
1. Concept of heart failure
2. Causes and predisposing factors of heart failure
3. Classification of heart failure
4. Mechanisms for heart failure
Decrease of contractility; Injury of myocardium; Disorders in energy metabolism;Dysfunction of excitation-contraction (EC) coupli; Diastolic dysfunction; Delayed calcium restoration; Impaired dissociation of the actin-myosin complex; Decreased diastolic potential energy of ventricles; Decrease of ventricular compliance; Asynergia of ventricular contraction and relaxation
5. Compensatory and adaptive response; Cardiac compensation; Systemic compensation
6. Clinical Manifestations
7.Treatment principles
ⅣQuestions
1. Briefly describe the mechanism and significance of myocardial hypertrophy after heart pump dysfunction.
2. Briefly describe the types of myocardial hypertrophy and their characteristics.
3. Please describe the influence of acidosis on excitation-contraction coupling and its mechanism.
4.Please describe the classification of heart failure.
5.Which symptom firstly occurs in left heart failure patients? Briefly describe its mechanism.
6. Explain the mechanisms of depressed myocardial contractility in heart failure.
7.Please describe the mechanisms of diastolic dysfunction in heart failure.
8.Please describe the cardiac compensation in the early stages of heart failure.
9.Please describe the pathogenesis of heart failure induced by essential hypertension.
10. Please describe the pathogenesis of heart failure induced by myocardial infarction.
ⅠRequirement
Chapter 14 Respiratory Failure
1.Tounderstand the concept and classification of respiratory failure
2. Tocomprehensively understand the etiology and mechanisms of respiratory failure caused by ventilatory disorders
3. Tocomprehensively understand the etiology and mechanisms of respiratory failure caused by gas exchange dysfunction
4.Tounderstand the concept，characteristics and mechanisms of ARDS
5.Tobe familiar with the alternations of metabolism and function in respiratory failure
6.Toknow the pathophysiological basis of prevention and treatment of respiratory failure
"Key and difficult points
1. Definition and classification of respiratory failure
2.The etiology and blood gas alteration in restrictive and obstructive hypoventilation
3.The concept of equal pressure point of airway
4.The different type of dyspnea occurred in obstructive hypoventilation
5.Theetiology,mechanism and blood gas alteration in diffuse disorder
6.Theetiology,mechanism and blood gas alteration in ventilation-perfusion disorders
7.The underlying mechanism of ARDS
8. The difference in oxygen therapy between type I respiratory failure and type II respiratory failure
ⅢTeaching content
1. Concept of respiratory failure
2. Classification of respiratory failure
Hypoxemic respiratory failure, Type I respiratory failure Hypercapnic respiratory failure, Type II respiratory failure
3. Etiology and mechanisms for respiratory failureVentilatorydisorder
Restrictive hypoventilation Obstructive hypoventilation Gas exchange dysfunction Diffusion disorder
Ventilation and perfusion imbalance Functional shunt
Dead space like ventilation Anatomic shunt
4.ARDS
5. Metabolic and functional alterations
6. Treatment principles
ⅣQuestions
1. Why does PaCO2sometimes decrease, sometimes increase during ventilation-perfusion imbalance?
2. Which kind of ventilation-perfusion imblance is easy tobe compensated? Why? How to be compensated?
3. What are the true shunt and functional shunt? How to identify them?
4. What are the differences in manifestation forms of dyspnea when the airway obstruction occurs at different positions? Why?
5. Please describe the pathogenesis and blood gas changes of acute respiratory distress syndrome (ARDS).
6. What is the difference of oxygen therapy between type I and type II respiratory failure? Why?
Chapter 15 Hepatic Insufficiency
ⅠPurpose and requirement
1. Master the concept of hepatic insufficiency;
2. Understand the causes and classification of hepatic insufficiency;
3. Master the concept of hepatic encephalopathy;
4. Master the pathogenesis of hepatic encephalopathy: ammonia intoxication hypothesis, false neurotransmitter hypothesis, amino acid imbalance hypothesis, GABA hypothesis;
5. Understand the precipitating factors of hepatic encephalopathy;
6. Know the principles of prevention and treatment of hepatic encephalopathy.
"Key and difficult points
1. The concept of hepatic encephalopathy;
2. The pathogenesis of hepatic encephalopathy: ammonia intoxication hypothesis, false neurotransmitter hypothesis, amino acid imbalance hypothesis, GABA hypothesis; the relationship of the four hypotheses.
ⅢThe key lecturing content and points
Section 1 The concept of hepatic insufficiency, etiology and classification (25 minutes)
1. Review the function of normal liver: metabolism, secretion, synthesis, detoxification,immunity.The concept of hepatic insufficiency is discussed based on the normal function ofliver.
2. Causes and classification of hepatic insufficiency: different causes induce acute or chronic liverseparately.The liver has a strong compensatorycapacity,only strong and violent damage which leads to massive loss of functional hepatic cells in a short period of time can lead to acute hepatic failure.
Section 2 The concept and pathogenesis of hepatic encephalopathy (50 minutes)
1. Almost all patients with hepatic insufficiency in the terminal stage are manifested as hepatic encephalopathy and hepatorenal syndrome. From this point, start the discussion on the concept of hepatic encephalopathy. Briefly introduce the staging of hepatic encephalopathy. Emphasize that thereisnospecificmorphologicalchangeinthebraintissueofpatientswithhepatic
encephalopathy, thus brain metabolism and dysfunction are the main mechanisms.
2. Discuss the four hypotheses of hepatic encephalopathy from the main arguments, laboratory and clinical basis, to the detailed mechanism. Analyze the relationship among the four hypotheses, lead to comprehensivetheory. Finally,use a diagram to review again.
Section 3 The precipitating factors of hepatic encephalopathy (10 minutes)
Give examples of some precipitating factors which can lead to hepatic insufficiency especially in patients with chronic liver dysfunction. Discuss with the student why they can induce encephalopathy based on the mechanisms of hepaticencephalopathy.
Section 4 The prevention and treatment of hepatic encephalopathy (5 minutes)
1. Treatment ofetiology,removal of primary disease, difficult in general;
2. Prevention and control the precipitating factors;
3. Therapeutic treatment: reduce blood ammonia, application of L-dopa or combined amino acid solution;
4. Alternative therapy: artificialliver,liver transplantation
ⅣThe self-learning content
1. Common causes and mechanisms of liver disease:
2. Hepatic cells, liver dysfunction;
3. Theetiology,type and pathogenesis of hepatorenal syndrome.
V Reference books, literature, website
Textbook:《Pathophysiology》eighth edition, editor-in-chief:WangJian-zhi Reference book:《Human pathophysiology》
Ⅵ Questions
1. Brief introduce the pathogenesis of hepatic encephalopathy.
2. What are the precipitating factors that can promote the occurrence of hepatic encephalopathy, why?
Chapter 16 Renal Insufficiency
Ⅰ Purpose and requirement
1. Know the basic pathogenesis of renal dysfunction: renal unit injury; renal endocrine dysfunction;
2. Master the concept, classification and causes of acute renal insufficiency; Master the concept, cause and pathogenesis of acute renal tubule necrosis;Master the mechanism of the metabolic changes of the acute functional renal insufficiency; Know the prevention and control of acute renal insufficiency;
3. Master the concept of chronic renal insufficiency and its development stage; Master the etiology and pathogenesis of chronic renal insufficiency: Intact nephron hypothesis; Glomerular hyperfiltration hypothesis; “Trade-off" hypothesis; Master the metabolic changes and mechanisms of chronic renal insufficiency;
4. Understand the concept of uremia; Understand uremic toxins; Understand the metabolic changes in uremia; Know the principles of prevention and treatment of chronic renal insufficiency and uremia.
"Key and difficult points
Key points:
1. The mechanism of glomerular filtration rate reduction in acute renal failure
2. The effect of acute renal failure on the body
3. Mechanism of progressive reduction of nephrons in chronic renal failure
4. The effect of chronic renal failure on the body
Difficult points:
1. The different effect of oliguic and non-oliguric acute renal failure on the body
2. The similarities and differences of acute renal failure and chronic renal failure, and the underlying mechanisms.
3. The characteristics and mechanism of urinary function changes and disorders of water and electrolytes in chronic renal failure
Ⅲ The key lecturing content and points
Section 1 The basic etiology and pathogenesis of renal dysfunction
1. Kidney damage
2. Disturbance of renal hormones
Section 2 Acute renal failure
1. The concept and cause of acute renal failure
2. The concept, cause and classification of acute tubular necrosis
3. The mechanism of functional and metabolic changes in (oliguric) acute functional renal failure
4. The mechanism of urinary dysfunction in (oliguria) acute functional renal failure
5. Prevention and treatment of acute functional renal failure
Section 3 Chronic renal failure
1. The concept and development stage of chronic renal failure
2. Etiology and pathogenesis of chronic renal failure
①Intact nephron hypothesis;
②Glomerular hyperfiltration hypothesis;
③“Trade-off" hypothesis
3. Metabolic changes and mechanisms in patients with chronic renal failure
Section 4 Uremia
1. The concept of uremia
2. Uremic toxins
3. Metabolic changes in uremia
4. Prevention and treatment of chronic renal failure and uremia
Ⅳ The self-learning content
1. Mechanism of cell injury and mechanism of cell proliferation and repair in acute renal failure
2. Common independent risk factors for chronic renal failure
3. Uremia
①The concept of uremia;
②Uremic toxins
4. Metabolic changes in uremia
V Reference books, literature, website
References
1. Richard E Gilbert, et al. Novel approaches to the treatment of progressive renal disease. Current Opinion in Pharmacology 2001; 1: 183-189
2. Ricardo Rocha and CharlesT.Stier,Jr.Pathophysiological effects of aldosterone in cardiovascular organizations TRENDS in Endocrinology & Metabolism 2001; 12 (7): 308-314
3. Mai Ots, et al. Characteristics of progressive renal disease. Clinica Chimica Acta 2000; 297: 29-41
4. Naveen Singri, et al. Acute renal failure. JAMA 2003; 289 (6): 747-751
5. Leon F. Ferder, et al. Effects of renin-angiotensin system blockade in the agingkidney.
Experimental Gerontology 2003; 38: 237-244
Ⅵ Questions
1. What is the mechanism of oliguria and polyuria in acute renal tubular necrosis? What are the manifestations of dyshomeostasis and the underlying mechanism?
2. What is the mechanism of hypocalcemia in chronic renal insufficiency? What is the impact on the body? Why do some patients show tetany after the correction of acidosis?
3. What is the mechanism of polyuria in chronic renal insufficiency?
4. Why does NPN increase in chronic renal insufficiency? And why are potassium, phosphorus and sodium normal?
5. What is the“Trade-off" hypothesis? What is the role of PTH in anti-injury and injury in chronic renal insufficiency?
6. What is the consequence of chronic kidney failure due to the dysfunction of renal endocrine function? And what is the mechanism?
Ⅰ Requirement
Chaper 17 Brain Dysfunction
1．Master etiology and pathogenesis of cognitive disorder 2．Master consciousness disorder and its pathogenesis 3．Understand performance characteristics of brain diseases 4．Understand manifestation of cognitive disorder 5．Understand hazard caused by consciousness disorder
6．Understand briefly principles of prevention and therapy for brain dysfunction
"Key and difficult points
1．The etiology and pathogenesis of cognitive disorder 2．The etiology and pathogenesis of consciousness disorder
Ⅲ The key lecturing content and points
1. Performance characteristics of brain diseases
2. The concepts of brain dysfunction, cognitive disorder and consciousness disorder
3. The brain structure of cognition and consciousness
4. The etiology and pathogenesis of cognitive disorder and consciousness disorder
5. Principles of prevention and therapy for brain dysfunction
Ⅳ Question
1．What is mechanism of protein aggregation in brain? 2．What is the pathogenesis of consciousness disorder?
3. Please introduce major manifestations in consciousness disorders?
Chinese