Health Worlds

Chapter VIII of the biliary and pancreatic diseases
Section cholecystitis, and cholelithiasis are common diseases of abdominal surgery. Second only to acute appendicitis in the acute abdomen, intestinal obstruction door to third. If done properly, the cure rate of up to 85%, but some still not satisfied, worth studying. Cholecystitis and cholelithiasis close, inflammation may promote stone formation, and stone obstruction can be inflammation, the two are often in combination. In the case of cholecystitis, 90% or more is a calculus, and I are non-calculous cholecystitis, the clinical processes between the two have much in common, recent development of the diagnostic techniques, especially B-type ultrasonic inspection used for clinical diagnosis than in the past between the two is easy, to reduce duplication of its content, so the narrative along with it.
From the point of the incidence of gallstone disease in people over 20 years of age will be gradually increased, women peak around age 45, men are also significantly increased after the menopause, children's rare, usually middle-aged were more common. Females, male and female incidence rate ratio of 1:1.9 to 3, the maternal or obese is also more common. Primary bile duct stones in 20 to 40 years for the incidence peak, young adults more common, no gender differences. From the geographical point of , in China, Japan, primary stones, especially the high incidence of intrahepatic stones, is more common in rural areas i


n southern China, but rare in Europe and America and other Western countries. Stones in the gallbladder, the north and northwest China is more common when compared with the south. In addition, some stones have no symptoms so-called "stationary stone", or few symptoms, or only in the autopsy stumbled upon B-inspection, so the actual incidence of this disease is higher than the clinic.(A) of the bile duct system within the bile duct by the multi-level merge into the left and right hepatic duct. The left hepatic duct length is 1.5cm, right hepatic duct length is 1cm, between the diameter of about 0.3cm. Left, right hepatic duct in the liver hepatic duct merged into the door, about 3 ~ 5cm, diameter of about 0.4 ~ 0.6cm, and sometimes from the lobe of the liver (segments) with extrahepatic biliary duct confluence somewhere, namely, hepatic duct. Note intraoperative identification. When the common bile duct and cystic duct confluence Serve, about 7 ~ 9cm, diameter 0.6 ~ 0.8cm. Normal thin wall were days when the blue, the right edge of the hepatoduodenal ligament, right in front of the portal vein, hepatic artery right down, the duodenal rear, behind the pancreatic duct ditch, after the second paragraph of oblique medial wall into the duodenum, 70% of the people here and the pancreatic duct merged into the swollen ampulla (Vater ampulla), the common opening in the duodenal papilla, diameter of about 0.9cm, the confluence of a sphincter around (called Oddi sphincter) can control the bile, pancreatic juice excretion (Figure 2-68). Incarcerated offenders are usually prone to this stone.Figure 2-68 extrahepatic biliary anatomy(B) of the gallbladder was pear-shaped length 7 ~ 9cm, width of 2.5 ~ 3.5cm, its volume is 30 ~ 50ml, into the end of the body, neck three. The bottom of the free, body in the liver in the gallbladder bed dirty face, neck, cystic and cystic duct was connected to, said Hartmann (Hartmann)'s bags, stones often incarcerated here. Cystic duct length 2 ~ 4cm, diameter of about 0.3cm, the spiral within the mucosal folds, known as Hai Shite (Heister)'s valve, have a moderating effect of bile out. Variation of the cystic duct and its opening more, surgery should be attention. Cystic artery from the right hepatic artery, vein quoted directly from the gallbladder into the intrahepatic portal vein bed.
(C) of the triangle by the cystic duct gallbladder, hepatic duct and liver formed the lower edge of the triangle (Calot triangle), including gallbladder lymph nodes, through the cystic artery. Cholecystectomy, the need to carefully recognizable anatomy of this triangle is important.
(D) of the gallbladder and bile ducts in normal physiological conditions, the liver cells secrete bile daily 600-1000ml. Which, among water, mainly containing bile salts, bile pigments, cholesterol, lecithin, fatty acids, proteins, salts and so on. Gallbladder bile can be concentrated in the 4 to 17 times for digestion purposes. Gallbladder emptying is being affected by neural and endocrine regulation of gallbladder bile from the abdominal nerve plexus of vagus and sympathetic, sympathetic stimulation can inhibit the cholecystokinin, Oddi's sphincter contraction; vagus nerve stimulation of cholecystokinin, Oddi's sphincter relaxation, the bile into the intestine. When the acidic food into the duodenum, causing small intestinal secretion of cholecystokinin (CCK), the gallbladder, Oddi's sphincter is relaxed and coordinated the bile into the intestine. The bile salts of bile to help digest fats and fat-soluble vitamins and absorption. Back to absorb most of the bile salts in the ileum, and then into the liver to be used to form bile salt enterohepatic circulation. In addition gallbladder mucus daily 20ml, the grease to protect the biliary mucosa is not impaired. The presence of the gallbladder, bile duct pressure may play a role in regulation.
The role of bile duct motility still, once the gallbladder is removed, bile will expand compensation in lieu of some of the features of gallbladder, without specific symptoms; if for some reason can not make a timely opening of common bile duct sphincter, leading to accumulation of bile duct and acute expansion may give rise to biliary colic, when the common bile duct pres 40.0kPa (300mmH2O), then stop the secretion of hepatic bile. Therefore, the role of the bile duct from the conveyor.
(E) cross in the pancreas of pancreatic retroperitoneal space behind the stomach, the surface was slightly yellow strip of small nodular glands, soft, flat first and second lumbar vertebra. About 12.5 ~ 15cm, width of 3 ~ 4cm, thickness 1.5 ~ 2.5cm, and weighs about 60 ~ 100g. Is divided into head, neck, body, tail four. Head large, surrounded by the concave curve for the duodenum, the superior mesenteric vein in the lower edge of the right to form a gully behind the conflict surrounding the mesenteric vessels. Wide neck, the dark side is the superior mesenteric vein and portal vein at the junction. The right side of the head and neck in the spine. Pancreatic body and tail at the right side of the spine, the two lines is unclear, and the greater curvature of stomach, spleen and left kidney door adjacent to the door. Do not hurt when splenectomy pancreatic tail. The blood supply of the pancreas and duodenum from the pancreas, the artery and the splenic artery, vein and artery accompanying imported superior mesenteric vein and splenic vein.
With pancreatic exocrine and endocrine function. Exocrine tissues, including acinar and duct (main pancreatic duct and sub duct), about 70% of the merged into the main pancreatic duct and common bile duct ampulla, bile and pancreatic juice into the "common channel" opening in the duodenal . A few cases were the two openings in the duodenum. Vice-duct openings in the main pancreatic duct opening at the top of about 2.5cm. (Figure 2-69).Figure 2-69 of the front, in front of the pancreas organs (stomach, transverse colon and its mesentery) has been removed
Pancreatic acinar secretion of pancreatic juice per day up to 1000-2000ml, is a colorless, odorless, transparent alkaline liquid. pH value of 7.8 ~ 8.4, contains a variety of digestion of protein, fat and carbohydrate enzymes and a variety of inorganic salts, food plays a major role in digestion. Its secretion is also affected by nerves, food, drugs. Vagus nerve, the secretion increased; Afghanistan, including articles, Propantheline, belladonna anti-acetylcholine drugs etc., can inhibit the secretion, so the treatment for acute inflammation. Acidic food into the duodenum, upper small intestine mucosa can stimulate the secretion of secretin, the pancreatic juice increased, mainly to increase bicarbonate to neutralize stomach acid. Food containing large amounts of amino acids, fat, fatty acids, intestinal secretion of CCK - PZ promoting that pancreatic juice digestive enzyme content increased, while gallbladder, Oddi sphincter relaxation discharge of bile, pancreatic juice to digest food.
Endocrine pancreas, derived from islets. By the , , are three cells, which secrete insulin, the largest number of cells, islet cells represents about 75%; , followed by only 20% of the cells, secretion of glucagon; cells only small 5%, to gastrin secretion.Currently on cholecystitis and cholelithiasis lack of uniform classification, but according to etiology and clinical manifestations, and can be divided into:1. Acute cholecystitis (calculus and non-calculus) more than a stones occur in the gallbladder, bile duct stones can also occur in systemic or biliary infection, biliary parasitic disease and trauma and shock can cause acute gallbladder purulent infection.
2. Chronic cholecystitis (calculus and non-calculus) 90% were caused by stones, which may be obstructive factors, physical and chemical factors, infection factors, vascular factors cause, can also be evolved for acute cholecystitis, or the onset is chronic process.
3. Calculous cholecystitis in all cases stones are all caused by mechanical stimulation of the gallbladder and obstruction of acute and chronic inflammation. Sometimes stones did not cause clinical symptoms, the so-called stationary stones are also included in this class.
4. Acalculous cholecystitis refers to some of the causes of non-stone gallbladder caused by acute or chronic infection, relatively few such cases, treatment can sometimes be less satisfactory.1. Gallbladder stones to the local pathological changes of gallbladder means in terms of calculi in the gallbladder.
2. Bile duct stones in the bile duct system means. Gallbladder stones can fall to as secondary bile duct stones, in essence, the complications of gallstones; primary pigment in bile duct stones, gallbladder stones in many non-called primary bile duct stones, stones in the liver, bile duct in; can only exist in the intrahepatic bile duct, intrahepatic bile duct stones that is, as a special type of primary bile duct stones. Because the presence of stones, and change is often associated with varying degrees of cholangitis, but this clinic is sometimes ignored. Its extent, there are acute cholangitis and chronic cholangitis of the points.(A) the cause of cholecystitis
1. The obstruction is due to the cystic duct or gallbladder neck of mechanical obstruction, the gallbladder is expansive, full of concentrated bile, where high concentrations of bile salts that have a strong proinflammatory role in the formation of early chemical inflammation, secondary bacterial infection after , resulting in cystic purulent infection, caused by mostly by stones, large stones difficult to complete obstruction, mainly for mechanical stimulation, showing a chronic inflammatory. Sometimes the cystic duct is too long, twisting, compression and fibrosis, adhesion is the obstruction can not be ignored. A few cases there may be fleeing into the bile duct gallbladder roundworm, in addition to causing mechanical stimulation, the attendant into the pathogen, causing infection. Also be due to gallbladder, Oddi sphincter dysfunction, motor function disorders, can cause bile duct emptying, bile, so that by chemical stimulation of the gallbladder and bacterial infection is possible.
2. Infective factors of systemic infection or localized disease, bacteria blood lines, lymph, bile duct, intestine, or adjacent organ invasion of inflammatory proliferation of channels, into the parasite's invasion of cholecystitis caused by bacteria and so is an important reason. Common pathogens mainly E. coli, other streptococci, staphylococci, Salmonella typhi, gas bacillus, Pseudomonas aeruginosa, and sometimes may have Clostridium perfringens, the formation of gas cholecystitis.
3. Chemical retention in the gallbladder bile of factors, including high concentrations of bile salts or pancreatic juice reflux into the gallbladder, with activity of trypsin, can stimulate significant inflammatory changes in the gallbladder wall occurred. In some severe dehydration, elevated concentrations of bile salts in bile, can also cause acute cholecystitis.
4. Other factors such as vascular factors, due to severe trauma, burns, shock and multiple fractures, such as after major surgery due to hypovolemia, vascular spasm, slow blood flow, thrombosis of the cystic artery, causing ischemic necrosis of the gallbladder, or perforation; Sometimes food allergies, diabetes, peripheral nodular arterial inflammation, such as pernicious anemia, are related to the pathogenesis of cholecystitis.
(B) the reasons for gallstone formation has not yet completely clear, which may be a combination of factors.(1) metabolic factors in gallbladder bile of normal bile salt, lecithin, cholesterol in proportion to coexist in a stable group in the micelle. Normal cholesterol and bile salt ratio of between 1:20 to 1:30, such as certain metabolic causes bile salt, lecithin reduced, or cholesterol increased, while the proportion of less than 1:13, the cholesterol will precipitate precipitation, the polymer to form larger stones. Such as late pregnancy, older adults, significantly increased blood cholesterol levels, so many pregnant women and the elderly easy to contracting this disease. Another example is the impaired liver function, bile acid secretion is also easy to reduce the formation of stones. Patients with congenital hemolytic, due to large quantities of red blood cell destruction, can produce courage primality stones.
(2) documented a large number of biliary tract infection, from gallstones have developed a core of Salmonella typhi, Streptococcus, Clostridium Bacillus, Actinomyces monocytogenes, which shows the bacterial infection has an important role in stone formation. In addition to bacterial infection caused by cholecystitis, its colonies, exfoliated epithelial cells can become heart of stone, gallbladder inflammatory exudate of protein composition, can be a stone of the stent.
(3) others such as bile stasis, bile pH is too low, a lack of vitamin A, also one of the reasons are stone formation.(1) Department of gallbladder stones secondary to gallbladder stones move down for some reason the common bile duct, is called secondary bile duct stones. Occurred within the Cholecystitis long course, expansion of the cystic duct, stones smaller cases. The incidence was 14%.
(2) primary bile duct stones may be associated with biliary infection, biliary strictures, biliary parasites, especially roundworm infection. When the biliary tract infection, E. coli produce -glucuronidase enzyme, high activity can be combined with bile and bilirubin (direct response) hydrolyzed into free bilirubin (room to be), which then calcium and bile ions as insoluble calcium bilirubin, a bile pigment after precipitation of calcium stones. Secondary biliary ascariasis caused by biliary tract infection, more likely to have such a stone, which is due to Ascaris debris, horn skin bacteria into the eggs and the subsequent inflammatory products could become the core of stone. Bile duct stricture is bound to affect smooth flow, resulting in bile, bile pigments and cholesterol more precipitate to form stones. When combined with chronic inflammation, the more rapidly the process of stone formation. In short, the biliary tract infections, obstruction in the formation of stones, on each other and promote each other.(A) of the pathological changes of gallbladder
According to gallbladder infection, obstruction of the extent and duration of different stages can be divided into two kinds.
1. Pathologic changes of acute cholecystitis by the degree of inflammation is divided into:
(1) simple cholecystitis, gallbladder wall shows congestion, mucosal edema, epithelial loss, leukocyte infiltration, no adhesions surrounding the gallbladder, anatomy clear, easy surgical procedure. An early stage of inflammation, can be absorbed recovered.
(2) pyogenic cholecystitis, the gallbladder was enlarged, congestion and edema, hypertrophy, the surface may be accompanied by fibrinous purulent discharge, inflammation of the gallbladder has been affected floors, large amounts of neutral polynuclear cell infiltration, a sheet hemorrhage, mucous membrane occurs ulcers, gallbladder cavity filled with pus, and with the bile into the common bile duct, sphincter of Oddi spasm caused by, resulting in cholangitis, biliary complications. At this point severe adhesion around the gallbladder and, anatomy is unclear, difficult surgery, bleeding having.
(3) excessive swelling of gangrenous cholecystitis gallbladder, resulting in blood circulation disorders of gallbladder, gallbladder wall with scattered hemorrhage, focal necrosis, small abscess formation, or full-thickness necrosis, gangrene was changed.
(4), gallbladder perforation in (3), based on the bottom or neck of gallbladder perforation occurs, usually three days after the onset of illness occurred, the occurrence rate of about 6 to 12%, can be formed after perforation with diffuse peritonitis, subphrenic infection, inside or outside the biliary fistula, liver abscess, but more and greater omentum was wrapped around the organs, the formation of gallbladder abscess, peritonitis showing signs of limitations. At this time very difficult surgery and had to line cholecystostomy.
2. Pathologic changes of chronic cholecystitis often evolved from acute cholecystitis, or the onset of the chronic process. After several episodes, or chronic inflammation, mucosal destruction was polypoid change, gallbladder wall thickening, fibrosis, chronic inflammatory cell infiltration, muscle fiber atrophy, gall bladder dysfunction, severe atrophy of small gallbladder, the gallbladder lumen narrowing , or full of stones, forming the so-called atrophic cholecystitis. Often dense adhesions with the surrounding tissues and organs, the course 90% of elderly patients with stones. If the gallbladder neck (tube) for the oppression caused by stones or inflammatory adhesion obstruction, persistent retention of bile, bile, bile pigment is absorbed the original, replaced by mucus secreted by the gallbladder, is a colorless and transparent liquid, known as "white bile "swell as gallbladder hydrops of gallbladder.1. Pathologic changes of acute cholangitis in biliary obstruction when stones (liver) Explorer, bile will be stasis, biliary tract infection consequential, biliary pressure, increased bile duct dilatation, high pressure in the bile duct from the capillary overflow back into the blood, causing obstruction jaundice. Acute cholangitis, the bile duct mucosal congestion and edema, bile was purulent, severe luminal empyema, the majority of ulcers on the wall, or even cause hemobilia. Apart from a few cases of gallbladder contraction, a number significantly increased, and there is a change of acute cholecystitis. As bile reflux, infection spto the blood flow, a large number of bacteria and endotoxin into the blood circulation through the liver sinusoids, causing systemic toxic reactions, such as sepsis and multiple organ damage.
2. Pathologic changes of chronic acute cholangitis after bile duct ulcer scar repair, fibrosis, scar ring causing bile duct stenosis. Proximal bile duct stricture is more expansion, wall thickening, cavity filled with pigment stones. In severe cases, the expansion of the bile ducts like the small intestine. Because the lack of smooth muscle fibers bile duct, difficult to return to normal after the expansion diameter. Changes in intrahepatic bile duct also showed similar changes. Long-term obstructive jaundice, lack of intestinal bile salts, absorption of fat-soluble vitamin K, etc., while often impaired liver function, prothrombin synthesis reduced, often clotting mechanism, bleeding tendency.When acute cholangitis, purulent bile duct often in very high pressure, easy to Bile reflux in the liver, a large number of bacterial and endotoxin retention in the liver, some into the bloodstream, causing liver infection, usually diffuse increase , congestion and edema, with varying degrees of hepatic necrosis, such necrotic centrilobular degeneration from the visible to the multiple liver abscess (the so-called biliary liver abscess). Severely impaired liver, liver failure may occur. Chronic cases the bile duct caused by repeated infection, resulting in cholangitis, stenosis, proximal expansion, stone formation, liver, bile stasis and focal necrosis, fibrosis, culminating in biliary cirrhosis, as well as portal hypertension, or even gastrointestinal bleeding, hepatic coma. If the side of lesions involving the liver, the disease side of atrophy, contralateral compensatory hyperplasia, liver enlargement was asymmetry.Its ingredients can be divided into three categories:
1. Cholesterol, cholesterol-based stones, mostly oval-shaped (single person) or surface shape (multiple), with the surface smooth or slightly nodular, light gray, hard, lined radial section, X-ray chip does not develop. Such stones in the gallbladder and more.
2. The courage to bilirubin primality stones as the main component, mostly muddy, soft and brittle, some, such as mud pie-like, some, such as sand, to dark brown or brownish red. Vary in size, due to less calcium, X-ray imaging is not on the number. More than in the liver, bile duct in the.
3. Mixed stones from cholesterol, bile pigments and calcium salts such as the interval from. Different shape, for the multi-faceted form of particles, the surface smooth, blunt the edge of garden, was dark green or brown, cut surface layer ring. Contains more calcium because, in some cases of X-ray imaging (that is called positive stone.) More bile in the gallbladder can also be found in the.



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