肝胆系疾病
肝胆胰疾病学知识点
肝胆胰疾病学知识点肝胆胰疾病是指发生在肝脏、胆囊和胰腺等器官上的各种疾病。
这些疾病涉及到多个方面的知识，包括病因、发病机制、临床表现、诊断和治疗等。
本文将介绍肝胆胰疾病的常见知识点。
一、肝疾病1. 肝硬化肝硬化是由于肝脏组织的长期损伤和修复过程中纤维组织增生、结构改变而引起的一种慢性进行性疾病。
常见的肝硬化病因有乙型肝炎病毒感染、酒精性肝炎以及自身免疫性疾病等。
2. 脂肪肝脂肪肝是指肝细胞内积聚大量脂肪颗粒，导致肝脏功能异常的一种疾病。
主要包括酒精性脂肪肝和非酒精性脂肪肝。
常见的病因包括饮食不当、肥胖、高血脂等。
3. 肝癌肝癌是恶性肿瘤的一种，通常发生在肝脏组织中。
主要有原发性肝癌和转移性肝癌两种类型。
原发性肝癌的主要病因包括乙型肝炎病毒感染和丙型肝炎病毒感染。
4. 肝炎肝炎是肝脏组织发生炎症反应的疾病，主要有急性肝炎和慢性肝炎两种形式。
最常见的肝炎病毒有甲型、乙型、丙型、丁型和戊型，其中乙型和丙型是导致慢性肝炎的主要病因。
5. 肝衰竭肝衰竭是指肝脏功能严重受损或丧失的病理状态，往往是一些慢性肝疾病发展到晚期的结果。
肝衰竭可分为急性和慢性两种类型，临床表现多样化，包括黄疸、腹水、肝性脑病等。
二、胆囊疾病1. 胆囊炎胆囊炎是指胆囊受到感染和炎症反应的一种疾病，常见的类型有急性胆囊炎和慢性胆囊炎。
常见的病因是胆囊内结石导致胆汁淤积，继而使细菌感染。
2. 胆囊结石胆囊结石是胆囊内形成的各种类型的结晶体，常常与胆囊炎并存。
胆囊结石的形成与胆汁成分异常有关，如胆固醇过高、胆固醇酸盐过低等。
3. 胆管炎胆管炎是指胆管受到感染和炎症反应的一种疾病，常见的类型有急性胆管炎和慢性胆管炎。
常见的病因是梗阻或狭窄引起的胆汁淤积，继而使细菌感染。
4. 胆道结石胆道结石是指胆管或胆囊内形成的结石，与胆道炎症密切相关。
胆道结石的形成与胆汁成分异常、胆囊排空功能障碍等因素有关。
三、胰腺疾病1. 胰腺炎胰腺炎是指胰腺受到感染和炎症反应的一种疾病，主要有急性胰腺炎和慢性胰腺炎两种形式。
肝胆疾病
PART 14 Disorders of the Gastrointestinal SystemC HAPTER301Approach to the PatientWith Liver DiseaseM arc GhanyJ ay H.HoofnagleA diagnosis of liver disease usually can be made accurately by acareful history, physical examination, and application of a fewlaboratory tests. In some circumstances, radiologic examinationsare helpful or, indeed, diagnostic. Liver biopsy is considered thecriterion standard in evaluation of liver disease but is now neededless for diagnosis than for grading and staging of disease. This chap-ter provides an introduction to diagnosis and management of liverdisease, briefly reviewing the structure and function of the liver; themajor clinical manifestations of liver disease; and the use of clinicalhistory, physical examination, laboratory tests, imaging studies, andliver biopsy.L IVER STRUCTURE AND FUNCTIONⅥT he liver is the largest organ of the body, weighing 1–1.5 kg andrepresenting 1.5–2.5% of the lean body mass. The size and shapeof the liver vary and generally match the general body shape—longand lean or squat and square. The liver is located in the right upperquadrant of the abdomen under the right lower rib cage againstthe diaphragm and projects for a variable extent into the left upperquadrant. The liver is held in place by ligamentous attachments tothe diaphragm, peritoneum, great vessels, and upper gastrointesti-nal organs. It receives a dual blood supply; ~20% of the blood flowis oxygen-rich blood from the hepatic artery, and 80% is nutrient-rich blood from the portal vein arising from the stomach, intestines,pancreas, and spleen.T he majority of cells in the liver are hepatocytes, which constitutetwo-thirds of the mass of the liver. The remaining cell types areKupffer cells (members of the reticuloendothelial system), stellate(Ito or fat-storing) cells, endothelial cells and blood vessels, bileductular cells, and supporting structures. Viewed by light micros-copy, the liver appears to be organized in lobules, with portal areasat the periphery and central veins in the center of each lobule.However, from a functional point of view, the liver is organized intoacini, with both hepatic arterial and portal venous blood enteringthe acinus from the portal areas (zone 1) and then flowing throughthe sinusoids to the terminal hepatic veins (zone 3); the interven-ing hepatocytes constituting zone 2. The advantage of viewing theacinus as the physiologic unit of the liver is that it helps to explainthe morphologic patterns and zonality of many vascular and biliarydiseases not explained by the lobular arrangement.P ortal areas of the liver consist of small veins, arteries, bile ducts,and lymphatics organized in a loose stroma of supporting matrixand small amounts of collagen. Blood flowing into the portal areasis distributed through the sinusoids, passing from zone 1 to zone 3of the acinus and draining into the terminal hepatic veins (“centralveins”). Secreted bile flows in the opposite direction, in a counter-current pattern from zone 3 to zone 1. The sinusoids are lined byunique endothelial cells that have prominent fenestrae of variablesize, allowing the free flow of plasma but not cellular elements. Theplasma is thus in direct contact with hepatocytes in the subendothe-lial space of Disse.H epatocytes have distinct polarity. The basolateral side of thehepatocyte lines the space of Disse and is richly lined withmicrovilli; it demonstrates endocytotic and pinocytotic activity,with passive and active uptake of nutrients, proteins, and othermolecules. The apical pole of the hepatocyte forms the canalicularmembranes through which bile components are secreted. Thecanaliculi of hepatocytes form a fine network, which fuses into thebile ductular elements near the portal areas. Kupffer cells usually liewithin the sinusoidal vascular space and represent the largest groupof fixed macrophages in the body. The stellate cells are located inthe space of Disse but are not usually prominent unless activated,when they produce collagen and matrix. Red blood cells stay in thesinusoidal space as blood flows through the lobules, but white bloodcells can migrate through or around endothelial cells into the spaceof Disse and from there to portal areas, where they can return to thecirculation through lymphatics.H epatocytes perform numerous and vital roles in maintaininghomeostasis and health. These functions include the synthesis ofmost essential serum proteins (albumin, carrier proteins, coagula-tion factors, many hormonal and growth factors), the production ofbile and its carriers (bile acids, cholesterol, lecithin, phospholipids),the regulation of nutrients (glucose, glycogen, lipids, cholesterol,amino acids), and metabolism and conjugation of lipophilic com-pounds (bilirubin, anions, cations, drugs) for excretion in the bileor urine. Measurement of these activities to assess liver function iscomplicated by the multiplicity and variability of these functions.The most commonly used liver “function” tests are measurementsof serum bilirubin, albumin, and prothrombin time. The serumbilirubin level is a measure of hepatic conjugation and excretion,and the serum albumin level and prothrombin time are measuresof protein synthesis. A bnormalities of bilirubin, albumin, andprothrombin time are typical of hepatic dysfunction. Frank liverfailure is incompatible with life, and the functions of the liver aretoo complex and diverse to be subserved by a mechanical pump;dialysis membrane; or concoction of infused hormones, proteins,and growth factors.L IVER DISEASESW hile there are many causes of liver disease (T able 301-1), they gen-erally present clinically in a few distinct patterns, usually classified ashepatocellular, cholestatic (obstructive), or mixed. In h epatocellulardiseases(such as viral hepatitis or alcoholic liver disease), features ofliver injury, inflammation, and necrosis predominate. In c holestaticdiseases(such as gallstone or malignant obstruction, primary biliarycirrhosis, some drug-induced liver diseases), features of inhibitionof bile flow predominate. In a mixed pattern, features of both hepa-tocellular and cholestatic injury are present (such as in cholestaticforms of viral hepatitis and many drug-induced liver diseases). Thepattern of onset and prominence of symptoms can rapidly suggesta diagnosis, particularly if major risk factors are considered suchas the age and sex of the patient and a history of exposure or riskbehaviors.2520CHAPTER 301 Approach to the Patient With Liver DiseaseT ypical presenting symptoms of liver disease include jaundice, fatigue, itching, right upper quadrant pain, nausea, poor appe-tite, abdominal distention, and intestinal bleeding. A t present, however, many patients are diagnosed with liver disease who have no symptoms and who have been found to have abnor-malities in biochemical liver tests as a part of a routine physical examination or screening for blood donation or for insurance or employment. The wide availability of batteries of liver tests makes it relatively simple to demonstrate the presence of liver injury as well as to rule it out in someone suspected of liver disease.E valuation of patients with liver disease should be directed at(1) establishing the etiologic diagnosis, (2) estimating the disease severity (grading), and (3) establishing the disease stage (staging).TABLE 301-1 Liver Diseases2521PART 14 Disorders of the Gastrointestinal System D iagnosis should focus on the category of disease such as hepato-cellular, cholestatic, or mixed injury, as well as on the specific etio-logic diagnosis. G rading refers to assessing the severity or activity ofdisease—active or inactive, and mild, moderate, or severe. S tagingrefers to estimating the place in the course of the natural historyof the disease, whether acute or chronic; early or late; precirrhotic,cirrhotic, or end-stage.T he goal of this chapter is to introduce general, salient conceptsin the evaluation of patients with liver disease that help lead to thediagnoses discussed in subsequent chapters.C LINICAL HISTORYⅥT he clinical history should focus on the symptoms of liver disease—their nature, patterns of onset, and progression—and on potentialrisk factors for liver disease. The symptoms of liver disease includeconstitutional symptoms such as fatigue, weakness, nausea, poorappetite, and malaise and the more liver-specific symptoms of jaun-dice, dark urine, light stools, itching, abdominal pain, and bloating.Symptoms can also suggest the presence of cirrhosis, end-stage liverdisease, or complications of cirrhosis such as portal hypertension.Generally, the constellation of symptoms and their patterns of onsetrather than a specific symptom points to an etiology.F atigue is the most common and most characteristic symptomof liver disease. It is variously described as lethargy, weakness,listlessness, malaise, increased need for sleep, lack of stamina, andpoor energy. The fatigue of liver disease typically arises after activ-ity or exercise and is rarely present or severe in the morning afteradequate rest (afternoon versus morning fatigue). Fatigue in liverdisease is often intermittent and variable in severity from hour tohour and day to day. In some patients, it may not be clear whetherfatigue is due to the liver disease or to other problems such as stress,anxiety, sleep disturbance, or a concurrent illness.N ausea occurs with more severe liver disease and may accom-pany fatigue or be provoked by odors of food or eating fatty foods.Vomiting can occur but is rarely persistent or prominent. Poorappetite with weight loss occurs commonly in acute liver diseasesbut is rare in chronic disease, except when cirrhosis is present andadvanced. Diarrhea is uncommon in liver disease, except withsevere jaundice, where lack of bile acids reaching the intestine canlead to steatorrhea.R ight upper quadrant discomfort or ache (“liver pain”) occurs inmany liver diseases and is usually marked by tenderness over theliver area. The pain arises from stretching or irritation of Glisson’scapsule, which surrounds the liver and is rich in nerve endings.Severe pain is most typical of gallbladder disease, liver abscess, andsevere venoocclusive disease but is an occasional accompanimentof acute hepatitis.I tching occurs with acute liver disease, appearing early inobstructive jaundice (from biliary obstruction or drug-inducedcholestasis) and somewhat later in hepatocellular disease (acutehepatitis). Itching also occurs in chronic liver diseases, typically thecholestatic forms such as primary biliary cirrhosis and sclerosingcholangitis where it is often the presenting symptom, occurringbefore the onset of jaundice. However, itching can occur in any liverdisease, particularly once cirrhosis is present.J aundice is the hallmark symptom of liver disease and perhapsthe most reliable marker of severity. Patients usually report dark-ening of the urine before they notice scleral icterus. Jaundice israrely detectable with a bilirubin level <43 μmol/L (2.5 mg/dL).With severe cholestasis there will also be lightening of the colorof the stools and steatorrhea. Jaundice without dark urine usuallyindicates indirect (unconjugated) hyperbilirubinemia and is typicalof hemolytic anemia and the genetic disorders of bilirubin conjuga-tion, the common and benign form being Gilbert’s syndrome andthe rare and severe form being Crigler-Najjar syndrome. Gilbert’ssyndrome affects up to 5% of the population; the jaundice is morenoticeable after fasting and with stress.M ajor risk factors for liver disease that should be sought in theclinical history include details of alcohol use, medications (includ-ing herbal compounds, birth control pills, and over-the-countermedications), personal habits, sexual activity, travel, exposure tojaundiced or other high-risk persons, injection drug use, recentsurgery, remote or recent transfusion with blood and blood prod-ucts, occupation, accidental exposure to blood or needlestick, andfamilial history of liver disease.F or assessing the risk of viral hepatitis, a careful history of sexualactivity is of particular importance and should include the numberof lifetime sexual partners and, for men, a history of having sex withmen. Sexual exposure is a common mode of spread of hepatitis Bbut is rare for hepatitis C. A family history of hepatitis, liver disease,and liver cancer is also important. Maternal-infant transmissionoccurs with both hepatitis B and C. Vertical spread of hepatitis Bcan now be prevented by passive and active immunization of theinfant at birth. Vertical spread of hepatitis C is uncommon, butthere are no reliable means of prevention. Transmission is morecommon in HIV-co-infected mothers and is also linked to pro-longed and difficult labor and delivery, early rupture of membranes,and internal fetal monitoring. A history of injection drug use, evenin the remote past, is of great importance in assessing the risk forhepatitis B and C. Injection drug use is now the single most com-mon risk factor for hepatitis C. Transfusion with blood or bloodproducts is no longer an important risk factor for acute viral hepa-titis. However, blood transfusions received before the introductionof sensitive enzyme immunoassays for antibody to hepatitis C virus(anti-HCV) in 1992 is an important risk factor for chronic hepatitisC. Blood transfusion before 1986, when screening for antibody tohepatitis B core antigen (anti-HBc) was introduced, is also a risk fac-tor for hepatitis B. Travel to an underdeveloped area of the world,exposure to persons with jaundice, and exposure to young childrenin day-care centers are risk factors for hepatitis A. Hepatitis E isone of the more common causes of jaundice in Asia and Africa butis uncommon in developed nations, although mild cases have beenassociated with eating raw or undercooked pork or game (deer andwild boars). Tattooing and body piercing (for hepatitis B and C) andeating shellfish (for hepatitis A) are frequently mentioned but areactually quite rare types of exposure for acquiring hepatitis.A history of alcohol intake is important in assessing the causeof liver disease and also in planning management and recommen-dations. In the United States, for example, at least 70% of adultsdrink alcohol to some degree, but significant alcohol intake is lesscommon; in population-based surveys, only 5% have more thantwo drinks per day, the average drink representing 11–15 g alcohol.Alcohol consumption associated with an increased rate of alcoholicliver disease is probably more than two drinks (22–30 g) per dayin women and three drinks (33–45 g) in men. Most patients withalcoholic cirrhosis have a much higher daily intake and have drunkexcessively for ≥10 years before onset of liver disease. In assessingalcohol intake, the history should also focus on whether alcoholabuse or dependence is present. A lcoholism is usually defined bythe behavioral patterns and consequences of alcohol intake, noton the basis of the amount of alcohol intake. A buse is defined bya repetitive pattern of drinking alcohol that has adverse effects onsocial, family, occupational, or health status. D ependence is definedby alcohol-seeking behavior, despite its adverse effects. Many alco-holics demonstrate both dependence and abuse, and dependence isconsidered the more serious and advanced form of alcoholism. Aclinically helpful approach to diagnosis of alcohol dependence andabuse is the use of the CAGE questionnaire (T able 301-2), which isrecommended in all medical history-taking.25222523CHAPTER 301Approach to the Patient With Liver DiseaseFamily history can be helpful in assessing liver disease. Familial causes of liver disease include Wilson’s disease; hemochromatosis and α 1antitrypsin (α 1 A T) deficiency; and the more uncommon inherited pediatric liver diseases of familial intrahepatic cholestasis, benign recurrent intrahepatic cholestasis, and A lagille syndrome. Onset of severe liver disease in childhood or adolescence with a family history of liver disease or neuropsychiatric disturbance should lead to investigation for Wilson’s disease. A family history of cirrhosis, diabetes, or endocrine failure and the appearance of liver disease in adulthood should suggest hemochromatosis and lead to investigation of iron status. Adult patients with abnormal iron stud-ies warrant genotyping of the H FE gene for the C282Y and H63D mutations typical of genetic hemochromatosis. In children and ado-lescents with iron overload, other non-HFE causes of hemochro-matosis should be sought. A family history of emphysema should provoke investigation of α 1 A T levels and, if low, for Pi genotype. P HYSICAL E XAMINATION ⅥT he physical examination rarely demonstrates evidence of liver dysfunction in a patient without symptoms or laboratory findings, nor are most signs of liver disease specific to one diagnosis. Thus, the physical examination complements rather than replaces the need for other diagnostic approaches. In many patients, the physi-cal examination is normal unless the disease is acute or severe and advanced. Nevertheless, the physical examination is important in that it can be the first evidence for the presence of hepatic failure, portal hypertension, and liver decompensation. In addition, the physical examination can reveal signs that point to a specific diag-nosis, either in risk factors or in associated diseases or findings.T ypical physical findings in liver disease are icterus, hepato-megaly, hepatic tenderness, splenomegaly, spider angiomata, pal-mar erythema, and excoriations. Signs of advanced disease include muscle wasting, ascites, edema, dilated abdominal veins, hepatic fetor, asterixis, mental confusion, stupor, and coma. In males with cirrhosis, particularly when related to alcohol, signs of hyperestro-genemia such as gynecomastia, testicular atrophy, and loss of male-pattern hair distribution may be found. I cterus is best appreciated by inspecting the sclera under natural light. In fair-skinned individuals, a yellow color of the skin may be obvious. In dark-skinned individuals, the mucous membranes below the tongue can demonstrate jaundice. Jaundice is rarely detectable if the serum bilirubin level is <43 μmol/L (2.5 mg/dL) but may remain detectable below this level during recovery from jaundice (because of protein and tissue binding of conjugated bilirubin).S pider angiomata and palmar erythema occur in both acute and chronic liver disease and may be especially prominent in persons with cirrhosis, but they can occur in normal individuals and are frequently present during pregnancy. Spider angiomata are super-ficial, tortuous arterioles and, unlike simple telangiectases, typically fill from the center outward. Spider angiomata occur only on thearms, face, and upper torso; they can be pulsatile and may be dif-ficult to detect in dark-skinned individuals.H epatomegaly is not a very reliable sign of liver disease, because of the variability of the size and shape of the liver and the physical impediments to assessing liver size by percussion and palpation. Marked hepatomegaly is typical of cirrhosis, venoocclusive dis-ease, infiltrative disorders such as amyloidosis, metastatic or pri-mary cancers of the liver, and alcoholic hepatitis. Careful assess-ment of the liver edge may also demonstrate unusual firmness, irregularity of the surface, or frank nodules. Perhaps the most reliable physical finding in examining the liver is hepatic tender-ness. Discomfort on touching or pressing on the liver should be carefully sought with percussive comparison of the right and left upper quadrants.S plenomegaly occurs in many medical conditions but can be a subtle but significant physical finding in liver disease. The availabil-ity of ultrasound (US) assessment of the spleen allows for confirma-tion of the physical finding.S igns of advanced liver disease include muscle-wasting and weight loss as well as hepatomegaly, bruising, ascites, and edema. A scites is best appreciated by attempts to detect shifting dullness by careful percussion. US examination will confirm the finding of ascites in equivocal cases. Peripheral edema can occur with or with-out ascites. In patients with advanced liver disease, other factors frequently contribute to edema formation, including hypoalbumin-emia, venous insufficiency, heart failure, and medications.H epatic failure is defined as the occurrence of signs or symptoms of hepatic encephalopathy in a person with severe acute or chronic liver disease. The first signs of hepatic encephalopathy can be subtle and nonspecific—change in sleep patterns, change in personality, irritability, and mental dullness. Thereafter, confusion, disorienta-tion, stupor, and eventually coma supervene. In acute liver failure, excitability and mania may be present. Physical findings include asterixis and flapping tremors of the body and tongue. F etor hepati-cus refers to the slightly sweet, ammoniacal odor that can occur in patients with liver failure, particularly if there is portal-venous shunting of blood around the liver. Other causes of coma and dis-orientation should be excluded, mainly electrolyte imbalances, sed-ative use, and renal or respiratory failure. The appearance of hepatic encephalopathy during acute hepatitis is the major criterion for diagnosis of fulminant hepatitis and indicates a poor prognosis. In chronic liver disease, encephalopathy is usually triggered by a medi-cal complication such as gastrointestinal bleeding, over-diuresis, uremia, dehydration, electrolyte imbalance, infection, constipation, or use of narcotic analgesics.A helpful measure of hepatic encephalopathy is a careful mental status examination and use of the trail-making test, which consists of a series of 25 numbered circles that the patient is asked to con-nect as rapidly as possible using a pencil. The normal range for the connect-the-dot test is 15–30 seconds; it is considerably delayed in patients with early hepatic encephalopathy. Other tests include drawing abstract objects or comparison of a signature to previous examples. More sophisticated testing such as with electroencepha-lography and visual evoked potentials can detect mild forms of encephalopathy, but are rarely clinically useful.O ther signs of advanced liver disease include umbilical hernia from ascites, hydrothorax, prominent veins over the abdomen, and c aput medusa , which consists of collateral veins seen radiating from the umbilicus and resulting from the recanulation of the umbilical vein. Widened pulse pressure and signs of a hyperdynamic circu-lation can occur in patients with cirrhosis as a result of fluid and sodium retention, increased cardiac output, and reduced peripheral resistance. Patients with long-standing cirrhosis and portal hyper-tension are prone to develop the hepatopulmonary syndrome,defined by the triad of liver disease, hypoxemia, and pulmonary∗One “yes” response should raise suspicion of an alcohol use problem, and more than one is a strong indication that abuse or dependence exists.PART 14 Disorders of the Gastrointestinal System arteriovenous shunting. The hepatopulmonary syndrome is char-acterized by platypnea and orthodeoxia, representing shortnessof breath and oxygen desaturation that occur paradoxically uponassuming an upright position. Measurement of oxygen saturationby pulse oximetry is a reliable screening test for the presence ofhepatopulmonary syndrome.S everal skin disorders and changes occur commonly in liver dis-ease. Hyperpigmentation is typical of advanced chronic cholestaticdiseases such as primary biliary cirrhosis and sclerosing cholangitis.In these same conditions, xanthelasma and tendon xanthomataoccur as a result of retention and high serum levels of lipids andcholesterol. A slate-gray pigmentation to the skin also occurs withhemochromatosis if iron levels are high for a prolonged period.Mucocutaneous vasculitis with palpable purpura, especially on thelower extremities, is typical of cryoglobulinemia of chronic hepatitisC but can also occur in chronic hepatitis B.S ome physical signs point to specific liver diseases. Kayser-Fleischer rings occur in Wilson’s disease and consist of a golden-brown copper pigment deposited in Descemet’s membrane at theperiphery of the cornea; they are best seen by slit-lamp examination.Dupuytren contracture and parotid enlargement are suggestive ofchronic alcoholism and alcoholic liver disease. In metastatic liverdisease or primary hepatocellular carcinoma, signs of cachexia andwasting may be prominent, as well as firm hepatomegaly and ahepatic bruit.L ABORATORY TE STINGⅥD iagnosis in liver disease is greatly aided by the availability of reli-able and sensitive tests of liver injury and function. A typical batteryof blood tests used for initial assessment of liver disease includesmeasuring levels of serum alanine and aspartate aminotransferases(ALT and AST), alkaline phosphatase (AlkP), direct and total serumbilirubin, and albumin and assessing prothrombin time. The patternof abnormalities generally points to hepatocellular versus cholestaticliver disease and will help to decide whether the disease is acute orchronic and whether cirrhosis and hepatic failure are present. Basedon these results, further testing over time may be necessary. Otherlaboratory tests may be helpful, such as γ-glutamyl transpeptidase(gGT) to define whether alkaline phosphatase elevations are due toliver disease; hepatitis serology to define the type of viral hepatitis;and autoimmune markers to diagnose primary biliary cirrhosis (anti-mitochondrial antibody; A MA), sclerosing cholangitis (peripheralantineutrophil cytoplasmic antibody; P-A NCA), and autoimmunehepatitis (antinuclear, smooth-muscle, and liver-kidney microsomalantibody). A simple delineation of laboratory abnormalities andcommon liver diseases is given in T able 301-3.T he use and interpretation of liver function tests is summarizedin Chap. 302.D IAGNOSTIC IMAGINGⅥT here have been great advances made in hepatic imaging, althoughno method is suitably accurate in demonstrating underlying cirrho-sis. There are many modalities available for imaging the liver. US,CT, and MRI are the most commonly employed and are comple-mentary to each other. In general, US and CT have a high sensitivityfor detecting biliary duct dilatation and are the first-line optionsfor investigating the patient with suspected obstructive jaundice.A ll three modalities can detect a fatty liver, which appears brighton imaging studies. Modifications of CT and MRI can be used toquantify liver fat, which may ultimately be valuable in monitoringtherapy in patients with fatty liver disease. Magnetic resonancecholangiopancreatography (MRCP) and endoscopic retrogradecholangiopancreatography (ERCP) are the procedures of choicefor visualization of the biliary tree. MRCP offers several advantagesover ERCP; there is no need for contrast media or ionizing radia-tion, images can be acquired faster, it is less operator dependent,and it carries no risk of pancreatitis. MRCP is superior to US andCT for detecting choledocholithiasis but less specific. It is useful inthe diagnosis of bile duct obstruction and congenital biliary abnor-malities, but ERCP is more valuable in evaluating ampullary lesionsand primary sclerosing cholangitis. ERCP allows for biopsy, directvisualization of the ampulla and common bile duct, and intraductalultrasonography. It also provides several therapeutic options inpatients with obstructive jaundice such as sphincterotomy, stoneextraction, and placement of nasobiliary catheters and biliary stents.Doppler US and MRI are used to assess hepatic vasculature andhemodynamics and to monitor surgically or radiologically placedvascular shunts such as transjugular intrahepatic portosystemicshunts. CT and MRI are indicated for the identification and evalu-ation of hepatic masses, staging of liver tumors, and preoperativeassessment. With regard to mass lesions, sensitivity of hepaticimaging continues to increase; unfortunately, specificity remainsa problem, and often two and sometimes three studies are neededbefore a diagnosis can be reached. Recently, methods using elastog-raphy have been developed to measure hepatic stiffness as a meansof assessing hepatic fibrosis. US and MR elastrography are nowAbbreviations: HAV, HBV, HCV, HDV, HEV: hepatitis A, B, C, D, or E virus; HBsAg,hepatitis B surface antigen; anti-HBc, antibody to hepatitis B core (antigen); HBeAg,hepatitis e antigen; ANA, antinuclear antibodies; SMA, smooth-muscle antibody;P-ANCA, peripheral antineutrophil cytoplasmic antibody.2524。
【课题申报】肝胆系统疾病的流行病学调查
肝胆系统疾病的流行病学调查课题申报书一、课题名称：肝胆系统疾病的流行病学调查二、课题背景和意义：肝胆系统疾病是临床常见的重大疾病之一，其包括肝炎、肝硬化、肝癌、胆囊结石等。
这些疾病给患者带来巨大的身体和心理负担，严重影响其生活质量甚至生命安全。
而肝胆系统疾病的发病率呈现出区域性差异，并且与环境、饮食习惯、遗传等因素有关。
因此，进行一次全面的肝胆系统疾病的流行病学调查对于深入了解其发病机制、制定针对性的预防和控制策略具有重要意义。
三、研究目的：1. 揭示肝胆系统疾病的流行病学特征和分布规律；2. 探究肝胆系统疾病的危险因素和影响因素；3. 分析肝胆系统疾病与环境、遗传和饮食等因素之间的关系；4. 为肝胆系统疾病的预防和控制提供科学依据。
四、调查内容和方法：1. 调查内容：（1）收集目标区域肝胆系统疾病的基本信息，包括发病率、性别分布、年龄分布等；（2）调查危险因素和影响因素，如饮酒、吸烟、饮食习惯、职业暴露等；（3）采集目标区域环境因素数据，如大气污染指数、水质、土壤质量等；（4）收集家庭和个人遗传因素数据，包括家族病史、基因检测等。
2. 调查方法：（1）问卷调查：针对居民的一般状况、饮食习惯、生活方式等进行问卷调查；（2）体格检查：对参与调查的个体进行体格检查和生物学标本采集；（3）实验室检测：对生物学标本进行肝胆功能指标分析、病毒感染检测等；（4）环境检测：采集目标区域的环境数据，包括空气质量、水质、土壤质量等；（5）数据统计与分析：使用统计软件对收集的数据进行统计分析，探究肝胆系统疾病的流行病学特征和相关因素。
五、预期成果及应用前景：1. 预期成果：（1）肝胆系统疾病的患病率、发病率、死亡率等基本信息；（2）肝胆系统疾病的流行病学特征和分布规律；（3）肝胆系统疾病的危险因素和影响因素；（4）肝胆系统疾病与环境、遗传、饮食等因素的关系；（5）肝胆系统疾病的预防和控制策略。
2. 应用前景：（1）为制定肝胆系统疾病的预防和控制策略提供科学依据；（2）为进行个体化预防和治疗提供参考；（3）为肝胆系统疾病的流行趋势预测和预警提供依据；（4）为其他相关疾病的研究提供借鉴。
《肝胆疾病课件》
胆囊癌
探索罕见但严重的胆囊癌， 包括早期症状和有效的治 疗选择。
胆管疾病
胆管结石
深入了解胆管结石的病因、症 状以及治疗方法。
胆管炎
了解胆管炎的分类、症状以及 如何预防和治疗。
胆管癌
探索胆管癌的发展过程、治疗 选择以及提供支持和指导的机 构。
脂肪肝
1 原因和类型
了解脂肪肝的不同原因和类型，如何 预防和减轻症状。
肝癌
1
早期检测
了解肝癌的早期检测方法，包括常见
治疗选择
2
的医学检查和筛查项目。
介绍肝癌的治疗选择，包括手术、化
疗、放疗等，以及可能的并发症和风
险。
3
康复与心理支持
探索肝癌患者的康复过程，以及提供 心理支持的重要性。
胆囊疾病
胆结石
深入了解胆结石的形成原 因、症状以及常见的治疗 方法。
胆囊炎
了解胆囊炎的病因、症状 以及如何预防和治疗。
肝胆疾病课件
欢迎来到《肝胆疾病课件》！本课件将为您详细介绍肝胆疾病的概述、各种 类型以及预防与治疗方法，帮助您更好地了解和保护肝脏健康。
肝炎
病毒பைடு நூலகம்肝炎
探索不同类型的病毒性肝炎， 了解其传播途径、症状和预防 措施。
酒精性肝炎
深入了解酒精性肝炎的成因、 影响及如何减少风险。
自身免疫性肝炎
探索自身免疫性肝炎的病因、 症状和治疗方法。
预防病毒性肝炎
了解如何预防病毒性肝炎的传 播，保护自己和他人的健康。
肝硬化
1 病因与症状
2 并发症
探索导致肝硬化的原因以及常见症状， 了解如何预防和提早检测。
了解肝硬化可能引发的并发症，以及 如何有效管理和减轻不适。
中医内科学如何诊治肝胆系统疾病的症状
中医内科学如何诊治肝胆系统疾病的症状中医内科学对于诊治肝胆系统疾病的症状有着独特的理论和方法。
肝胆系统疾病在临床上较为常见，包括胆囊炎、胆结石、肝炎、肝硬化等，给患者带来了诸多不适。
中医通过辨证论治，从整体观念出发，综合考虑患者的症状、体质、情志等多方面因素，制定个性化的治疗方案。
中医认为，肝胆互为表里，在生理功能上相互协调。
肝主疏泄，调畅气机，促进胆汁的分泌和排泄；胆附于肝，贮藏和排泄胆汁。
当肝胆功能失调时，就容易出现各种疾病症状。
常见的肝胆系统疾病症状包括胁痛、黄疸、口苦、眩晕等。
对于胁痛，中医认为其病因主要有肝郁气滞、瘀血阻络、肝胆湿热等。
肝郁气滞型胁痛，多因情志不舒，肝气郁结所致，表现为胁肋胀痛，走窜不定，疼痛每因情志变化而增减，常伴有胸闷、嗳气等症状。
治疗上以疏肝理气为主，常用方剂如柴胡疏肝散。
瘀血阻络型胁痛，多因久病入络，瘀血停滞所致，表现为胁肋刺痛，痛有定处，入夜尤甚，舌质紫暗。
治疗以活血化瘀、通络止痛为主，常用方剂如血府逐瘀汤。
肝胆湿热型胁痛，多因感受湿热之邪，或嗜食肥甘厚味，湿热内生，蕴结肝胆所致，表现为胁肋胀痛，口苦口黏，胸闷纳呆，恶心呕吐，小便黄赤，大便不爽。
治疗以清热利湿为主，常用方剂如龙胆泻肝汤。
黄疸也是肝胆系统疾病常见的症状之一。
中医将黄疸分为阳黄和阴黄两大类。
阳黄多因湿热蕴蒸所致，表现为黄色鲜明如橘色，伴有发热、口渴、小便短赤、大便秘结等症状。
治疗以清热利湿、通腑退黄为主，常用方剂如茵陈蒿汤。
阴黄多因寒湿阻遏所致，表现为黄色晦暗如烟熏，伴有脘腹痞满、畏寒肢冷、神疲乏力等症状。
治疗以温中化湿、健脾和胃为主，常用方剂如茵陈术附汤。
口苦这一症状，在肝胆系统疾病中也较为常见。
中医认为，口苦多由肝胆郁热或肝胆湿热所致。
肝郁化火者，常伴有烦躁易怒、失眠多梦、头晕头痛等症状，治疗以清肝泻火为主，常用方剂如丹栀逍遥散。
肝胆湿热者，除口苦外，还常伴有口中黏腻、舌苔黄腻等症状，治疗以清热利湿为主，方剂如龙胆泻肝汤加减。
肝胆外科疾病知识点
肝胆外科疾病知识点在肝胆外科领域中，有许多常见的疾病和相关知识点，下面我将为大家详细介绍一些重要的肝胆外科疾病知识点。
一、肝脏解剖结构肝脏是人体最大的腺体器官，位于腹腔右上腹部。
它主要由肝细胞组成，具有重要的生物功能，如合成蛋白质、代谢脂肪和糖类等。
肝脏的解剖结构包括肝叶、肝小叶、肝实质、门脉系统、肝动脉和肝静脉等组成部分。
二、肝脏疾病1. 肝炎：肝炎是指肝脏发炎引起的一类疾病，常见的有病毒性肝炎、药物性肝炎和酒精性肝炎等。
肝炎的症状包括恶心、食欲不振、乏力、发热等。
2. 肝硬化：肝硬化是慢性肝炎、酒精性肝病、自身免疫性肝病等引起的疾病，其特点是肝脏纤维化，肝功能受损并最终发展为肝功能衰竭。
3. 肝癌：肝癌是最常见的恶性肿瘤之一，早期症状不明显，晚期患者可出现腹水、黄疸、体重下降等症状。
肝癌的治疗方法主要有手术切除、化疗、放疗等。
三、胆囊疾病1. 胆结石：胆结石是胆囊内胆汁成分异常而形成的固体结晶体，患者可出现右上腹绞痛、恶心、呕吐等症状，严重者需手术治疗。
2. 胆囊炎：胆囊炎是胆囊发炎引起的疾病，主要症状包括右上腹绞痛、发热、黄疸等，常需抗生素治疗或胆囊切除手术。
3. 胰腺疾病1. 胰腺炎：胰腺炎是指胰腺发炎引起的一类疾病，可分为急性胰腺炎和慢性胰腺炎。
患者常表现为上腹剧痛、恶心、呕吐等症状，严重者可出现休克、多器官功能障碍等。
2. 胰腺癌：胰腺癌是一种常见的恶性肿瘤，症状不具体，易被忽视。
胰腺癌的治疗方式主要包括手术切除、化疗和放疗等。
四、结语以上就是肝胆外科疾病的一些重要知识点，希望对大家有所帮助。
在日常生活中，要注意保持健康的生活方式，及时就医治疗，才能有效预防和控制肝胆外科疾病的发生。
祝大家身体健康！。
中医诊断学问中的肝胆系统疾病与中医诊断技术研究
实验室检查方法（肝功能、免疫学等）
肝功能检查
通过检测血清中的谷丙转氨酶、 谷草转氨酶、总胆红素等指标， 评估肝脏的合成、代谢、解毒等 功能状态。
免疫学检查
检测肝炎病毒标志物、自身免疫 性肝病相关抗体等，用于诊断病 毒性肝炎、自身免疫性肝病等。
肿瘤标志物检查
检测血清中的甲胎蛋白、癌胚抗 原等肿瘤标志物，辅助诊断肝癌 等恶性肿瘤。
02
中医对肝胆系统疾病认识
中医理论体系下的肝胆概念
肝主疏泄
肝具有疏泄功能，能够调节人体气机，维持 气血运行畅通。
肝藏血
肝有贮藏血液和调节血量的功能，对人体各 部位的血液供应起到重要作用。
胆主决断
胆具有决断功能，能够影响人的精神和情绪 活动。
肝胆相表里
肝胆在生理和病理上密切相关，肝病常影响 胆，胆病也常波及肝。
04
中医诊断技术在肝胆系统疾病中 应用
望闻问切四诊合参
望诊
观察患者面色、舌苔、舌质等，判断病情轻重和 病邪性质。
问诊
详细询问患者病史、症状、治疗经过等，了解病 情全貌和辨证依据。
ABCD
闻诊
听患者语音、呼吸、咳嗽等声音，以及嗅出患者 口气、体气等异味，判断病位和病因。
切诊
通过脉诊和触诊，了解患者脉象、腹部肿块、压 痛等情况，判断病机和证候类型。
为了提高中医诊断的客观性和可重复性， 未来将加强对客观化指标的研究与应用， 如生物标志物、影像学检查等。
中西医结合诊疗模式的创新
国际化交流与合作的加强
未来中医肝胆系统疾病诊疗将更加注重中 西医结合，发挥各自优势，形成综合诊疗 模式，提高治疗效果和患者生活质量。
随着中医在国际上的认可度不断提高，未来 将加强与国际医学界的交流与合作，共同推 动中医诊断技术的发展和进步。
常见肝胆疾病的预防和治疗
常见肝胆疾病的预防和治疗肝胆疾病是指发生在肝脏和胆囊等部位的疾病，这类疾病在生活中十分常见，如果不及时预防和治疗，就有可能会给人们的健康带来不可逆转的损害。
因此，了解肝胆疾病的预防和治疗方法是非常重要的。
一、肝胆疾病的预防措施1.饮食上的预防。
经常接触较高温度的热饮、烤肉、煎炸和油腻等食物都有可能引起肝胆道疾病，因此，为了预防这些疾病的发生，人们应该多吃蔬菜和水果，减少摄入过多的脂肪、胆固醇和糖分。
此外，多喝水和少量多餐的习惯也能帮助胆囊排空，预防胆石症等疾病的发生。
2.保持健康的生活方式。
有规律的作息、减少烟酒的摄入、坚持适量的运动和保持心理上的平衡等都是有效的预防肝胆疾病的措施。
注意避免过度劳累和压力过大，这些因素同样会影响肝脏和胆囊的健康。
3.定期体检。
对于肝胆疾病的早期发现和治疗十分重要，因此，建议人们每年至少进行一次体检，这样有利于及时发现并预防疾病的发生。
二、肝胆疾病的治疗方法1.药物治疗。
常见的肝胆疾病，例如乙肝、轻度脂肪肝、淤胆等，可以通过合理的药物治疗控制病情。
但是，需要注意的是，肝脏是人体的器官之一，服药时间和剂量不得超标，否则会对肝脏造成损伤，使病情更加恶化。
2.手术治疗。
如果药物治疗无效，会出现一些肝胆疾病的严重并发症，医生就需要考虑手术治疗。
例如胆囊切除术和肝移植术等的实施，这种治疗方式只能在医生确诊的情况下进行，在手术后也需要注意术后的恢复。
3.中药治疗。
中药治疗在治疗肝胆疾病方面也有一定的好处，例如绿茶、蒲公英等中草药有助于通胆和保肝，饮用GCG草药类也可以刺激胆囊的收缩和排出胆石，对于治疗胆石症、胆囊炎等疾病有一定的帮助。
总之，肝胆疾病是很常见的疾病。
对于预防和治疗这类疾病非常重要，人们可以通过改善饮食习惯、保持健康的生活方式、定期体检等措施预防疾病的发生。
对于已经患病的人，药物治疗、手术和中药治疗等都可以起到一定的治疗作用。
需要注意的是，在治疗肝胆疾病的过程中不要擅自服用药物，一定要遵照医生的建议进行治疗。
- 1、下载文档前请自行甄别文档内容的完整性，平台不提供额外的编辑、内容补充、找答案等附加服务。
- 2、"仅部分预览"的文档,不可在线预览部分如存在完整性等问题,可反馈申请退款(可完整预览的文档不适用该条件!)。
- 3、如文档侵犯您的权益，请联系客服反馈,我们会尽快为您处理(人工客服工作时间：9:00-18:30)。
第四章肝胆病证一、名词解释1．黄疸2．黄胖3．胁痛4．积聚5．鼓胀6．萎黄7．头痛8、眩晕9、中风一、填空题：1.胁痛常见的病因病机包括有、、、和。
2胁痛病位主要责之于，有与及有关。
3.鼓胀后期多因出现、或等危候，使病情恶化，必须及时抢救。
4.鼓胀的病机多由于、、三脏受损，、、互结腹中，以腹部胀大为主，四肢肿不甚明显。
5《金匮要略·黄疸病》指出：“黄家所得，从得之。
”又对治疗提出“诸病黄家，但”。
6.黄疸的病理因素有湿邪、热邪、寒邪、疫毒、气滞、瘀血六种，但其中以为主，黄疸形成的关键是湿邪。
7.眩晕病位在，其病变脏腑与、、之脏关系密切。
8.眩晕的治疗原则是、。
9.中风病急性期是指发病后以内，中脏腑类最长病期可；恢复期是发病两周或1个月至半年以内；后遗证期系发病以上者。
10.中风基本病机总属，。
病位在，与密切相关。
11. 头痛的治疗原则当为、。
二、单项选择题：1.胁肋刺痛，痛有定处，入夜更甚，胁下有徵块，舌质紫暗，脉象沉涩，治疗选用()A.龙胆泻肝汤B.血府逐瘀汤C.丹栀逍遥散D.柴胡疏肝散2.胁痛一证，其病位主要在()A.肝脾B.脾胃C.肝胆D.肝肾3. 黄疸最重要的特征是A．目黄B．小便黄C．身黄D．齿垢黄４.水湿困脾型鼓胀的治法是()疏肝理气，祛湿散满 B.温中健脾，行气利水温补脾肾，攻下逐水 D.温阳化气，解表行水５.首载胆胀医案的书是A．《内经》B．《伤寒论》C．《症因脉治》D．《临证指南医案》６.鼓胀的病位在()肺脾胃 B.心肝肾 C.心脾肾 D.肝脾肾7.患者腹部胀大半年余，胁下胀痛不适，纳减，食后腹胀，尿少，下肢微肿。
检查：面色暗晦，周身皮肤发黄，腹胀大，胁下可触及痞块，双下肢按之微肿，脉弦细，舌苔腻，应诊断为()A.水肿B.黄疸C.积聚 C.鼓胀8.患者面目及肌肤淡黄，甚则晦暗不泽，肢软无力，心悸气短，大便溏薄，舌质淡苔薄，脉濡细。
属何病何证。
()热重于湿型黄疸 B.湿重于热型黄疸脾虚湿滞型黄疸 D.气滞血瘀型黄疸9.下列哪项不属阳黄与阴黄的鉴别要点()小便黄与不黄 B.病程较长与较短黄色鲜明与晦暗 D.虚证与实证10.黄疸发病涉及的脏腑是()肝胆 B.肝脾 C.肝胆脾胃 D.肝胆脾肾11.身目俱黄，右胁疼痛，牵引肩背，恶寒发热，大便色淡灰白，宜用()大柴胡汤 B.柴胡疏肝散 C.逍遥散 D.乌梅丸12.下列哪项不符合阴黄的临床特征()身目俱黄 B.黄色晦暗 C.纳少脘闷 D.发热口渴13.肝阳上亢型眩晕宜选用()镇肝熄风汤 B.大定风珠 C.天麻钩藤饮 D.龙胆泻肝汤14.下列哪项不是眩晕实证治疗原则()平肝潜阳 B.清肝泻火 C.化痰行瘀 D.疏肝理气15.中风中经络中脏腑的鉴别要点是：()神识昏蒙否 B.半身不遂否 C.语言流利否 D.口眼歪斜否16.中风风痰入络证主方是()大秦艽汤 B.真方白丸子 C.镇肝熄风汤 D.指迷茯苓丸三、多项选择题：1.柴胡疏肝散可用于下列哪些病证的治疗()鼓胀(气滞湿阻) B.胃痛(肝气犯胃)癃闭(肝郁气滞) D.胁痛(肝郁气滞) E.呕吐(肝气犯胃)2.胁痛的发生与下列何脏有关()脾 B.胃 C.肝 D.胆 E.肾3. 与肝、脾、肾三脏均有关的病证是()A．眩晕B．头痛C．水肿D．鼓胀E．泄泻4. 鼓胀的辨证要点主要辨()A．缓急B．虚实的主次C．气滞、血瘀、水停的主次D．寒热的偏盛E．阴阳的盛衰5. 阳黄的临床特点是()A．起病急B．色黄鲜明如橘皮C．伴有湿热症候D．身热不扬E．恶寒发热6.眩晕主要由哪些原因导致()风 B.火 C.痰 D.虚 E.瘀7.中风发病的先兆症状有()言语不利 B.肢体麻木 C.视物昏花 D.晕厥 E.心悸8.中风病常见的诱因为()气候骤变 B.烦劳过度 C.时行戾气 D.跌仆努力 E.情志相激9、积证日久可出现()痉厥出血黄疸鼓胀胁痛10、癥结的特征是()有形可征病属血分固定不移痛有定处病情较重11、积聚的病因有()情志失调饮食所伤感受寒湿黄疸、胁痛病后12、痰浊头痛的主症为()头痛如裹胸脘满闷纳呆呕恶舌苔白腻脉象弦滑13、血虚头痛的主症有()头痛而晕痛处固定头痛昏蒙心悸失眠头痛且空四、是非题1肝气犯胃的治法是疏肝解郁，理气止痛，方选香苏散和良附丸。
()2胃痛和腹痛的鉴别要点主要依据是病机。
()3肝气疏泄失常影响脾胃主要有两种情况，一为疏泄不及，一为疏泄太过。
()4对呕吐不止的病人服药方法应是少量频服，以减轻胃的负担。
()5食滞内停证的呕吐若因肉食而吐者，可重用山楂，因米食而吐者，可加谷芽。
() 6噎膈是食不得入，多为阳虚有寒;反胃是是入反出，多为阴虚有火。
()7膈之病名，首见于《内经》。
()8呃逆是以气逆上冲，呕吐痰涎，令人不能自制为主的病症。
()9呃逆治疗原则主要是和胃降气兼肃降。
（010腹痛是指胃脘以下，耻骨毛际以上的部位发生疼痛为主要变得病证。
()11腹部循行之经脉，包括手足三阴经、冲、任、带脉等。
()12治泻九法出自《医学心悟》。
()13对于痢疾的治疗，刘河间有“调气便脓自愈，行血则后重自除”之说。
()14寒湿痢以下痢稀薄或白冻，食少身疲，肢冷腰酸，或滑脱不禁为特点。
()15冷秘是由于外感寒邪，阴寒内盛，凝滞肠胃，失于传导，糟粕不行而成。
()四、论述题1.试述胁痛的病因病机。
2.临床上如何鉴别鼓胀与水肿?3.鼓胀病的预后与证的关系如何?4.如何理解湿邪在黄疸发病过程中的重要意义?5.瘀血阻窍型眩晕的症状、治法、主方是什么?6.中风与痫证、厥证的异同点是什么?7.中风脱证的主证、治法、方药是什么?六、病例分析[要求：写出诊断（包括证型诊断）、证候分析、治法、方药。
]病案1. 李某，男，12岁，5天前无明显诱因出现恶寒发热，头身重痛，食欲不振等症，自服感冒药无效。
2天来发现目白睛黄染，前来就诊。
现症：目白睛色黄，小便黄赤，脘腹满闷，不思饮食，恶心呕吐，发热微恶风寒，头身困重，舌苔黄腻，脉浮弦。
病案2. 张某，男，45岁。
“慢性肝炎”病史6年余。
近来食欲不振加重，自觉神疲畏寒，腹胀便溏，口不渴。
查体：身月俱黄，黄色晦暗无光泽，舌质淡，苔白腻，脉濡缓。
病案3. 张某，男性，30岁，98年11月24日就诊。
主诉：身黄，目黄，小便黄3天，伴发热1天。
病史：患者3天前因饮酒过度而致巩膜黄染，小便黄赤急来就诊。
现证见身目发黄色泽鲜明如橘皮，右胁疼痛而拒按，壮热口渴，口干口苦，恶心呕吐，脘腹胀满，大便秘结，小便黄赤，舌红苔黄腻，脉弦滑数。
病案4. 方某，女，32岁。
因与邻居发生口角，近２天出现两胁肋胀痛，伴胸闷脘胀，善太息，纳呆食少，舌苔薄白，脉弦病案5. 李某，男性，48岁。
主诉：胁痛2年。
患者于2年前患有乙型肝炎，口服多种药物，病情未见明显好转，胁痛反复发作。
近日因劳累过度而感胁痛加重，故来诊治。
现右胁隐痛绵绵不休，口干咽燥，两目干涩，心中烦热，头晕目眩，舌红少苔，脉弦细数。
病案6. 郑某，男，45岁。
饮酒史二十余年。
主诉腹部胀大半年余，伴胁下胀痛不适，纳减，食后腹胀，尿少，下肢微肿。
查体：腹胀大，皮色苍黄，按之不坚，双下肢按之轻度凹陷，舌苔白腻，脉弦细。
病例7. 李某，男，5l岁。
主诉腹胀大2个月，加重5天。
患者10年前诊断为乙型肝炎未正规治疗。
2个月前因劳累出现乏力，腹胀大，B超检查诊断为“肝硬化腹水”，近5天病情加重，腹胀大而坚满，按之较硬，腹部青筋怒张，胁腹刺痛拒按，面色晦暗，头面胸颈部可见红丝赤缕，大便色黑，肌肤甲错，口干不欲饮，舌质紫暗，苔白，脉细涩。
查：腹部叩诊移动性浊音阳性。
B超示肝硬化腹水、脾大。
病例8．张某，男，63岁。
平素多痰，昨日突发头晕，视物旋转，不能起床，不能睁眼视物，伴有头重昏蒙，胸闷身困，已呕吐数次，吐出皆为痰涎，舌淡苔白腻，脉弦滑。
病案9．张某，男，63岁，素体虚弱。
晨起时发现右半身不能活动，语言謇涩。
遂送医院就诊，查：面色恍白，口角流涎，手足肿胀，身体有汗，舌暗淡，苔薄白，脉沉细。
病案10．王某，男，46岁。
高血压病史2年，近来失眠、眩晕、耳鸣、手足心热；晚上观看电视时，突感头晕头痛，视物昏花，站起后跌倒在地，神识恍惚，半身不遂，不能言语。
家人呼唤，掐人中许久，渐渐醒来，但仍喎僻不遂。
查舌红绛无苔，脉细弦数。
病案11．赵某，男，45岁，干部。
主诉头痛五年，加重月余。
l年来，头痛时发时止，发作时胀痛较剧，每兼眩晕，血压偏高。
平时工作紧张，性情急躁，夜寐欠安。
此次连续头痛已有月余，服用西药疗效不显，舌质红，苔薄黄，脉弦。