Hepatobiliary Flashcards
(8 cards)
Cirrhosis
Cirrhosis (Greek kirrhos = yellow) implies irreversible liver damage. Histologically, there is loss of normal hepatic architecture with bridging fibrosis and nodular regeneration.
Causes
Most often chronic alcohol abuse, HBV, or HCV infection.
.
Signs
May be none (just raisedLFT) or decompensated end-stage liver disease.
Chronic liver disease:
Leuconychia: white nails with lunulae undemarcated, from hypoalbuminaemia; Terry’s nails—white proximally but distal ⅓ reddened by telangiectasias; clubbing; palmar erythema; hyperdynamic circulation; Dupuytren’s
contracture; spider naevi; xanthelasma; gynaecomastia; atrophic testes; loss of body hair; parotid enlargement; hepatomegaly, or small liver in late disease.
Complications Hepatic failure:
Coagulopathy (low levels factors II, VII, IX, & X causes high INR); encephalopathy—ie liver fl ap (asterixis) + confusion/coma; hypoalbuminaemia (oedema, leuconychia); sepsis (pneumonia; septicaemia); spontaneous bacterial peritonitis (SBP); hypoglycaemia. Portal hypertension: Ascites; splenomegaly; portosystemic shunt including oesophageal varices (± life-threatening upper GI bleed) and caput medusae (enlarged superficial periumbilical veins).
Tests Blood:
LFT: raised or decr bilirubin, high AST, high ALT, high alk phos. Later, with loss of synthetic function, look for low albumin ± incr PT/INR. low WCC & low level platelets indicate hypersplenism.
Find the cause:
Ferritin, iron/total iron-binding capacity; hepatitis
serology; immunoglobulins; autoantibodies; alpha-feto
protein; caeruloplasmin in patients 250/mm3 indicates spontaneous bacterial peritonitis.
Liver biopsy confirms the clinical diagnosis.
Management
General: Good nutrition is vital. Alcohol abstinence. Avoid NSAIDS, sedatives, and opiates.
Specific: For hepatitis-induced cirrhosis. High-dose ursodeoxycholic acid in PBC may normalize LFT, but may have no effect on disease progression.
Penicillamine for Wilson’s disease.
Ascites: Bed rest, f uid restriction (
Liver Tumours
The commonest (90%) liver tumours are secondary (metastatic) tumours, eg from breast, bronchus, or the gastrointestinal tract. Primary hepatic tumours are much less common and may be benign or malignant.
Symptoms
Fever, malaise, anorexia, weight decr, RUQ pain (incr liver capsule stretch). Jaundice is late, except with cholangiocarcinoma. Benign tumours are often asymptomatic. Tumours may rupture causing intraperitoneal haemorrhage.
Signs
Hepatomegaly (smooth, or hard and irregular, eg metastases, cirrhosis, HCC).
Look for signs of chronic liver disease and evidence of decompensation (jaundice, ascites). Feel for an abdominal mass. Listen for a bruit over the liver (HCC).
Tests
Blood: FBC, clotting, LFT, hepatitis serology, -fetoprotein 1 (low in 50–80% of HCC, though it is an uncertain prognostic indicator 174 may be normal if tumour 2.3≈104 virions/mL; this is quite a low level so most are at risk. HCV; AIH; cirrhosis (alcohol, haemochromatosis,
PBC); non-alcoholic fatty liver; aflatoxin; Clonorchis sinensis; anabolic steroids.
Treatment:
Resecting solitary tumours 3cm, and intrinsic liver disease and mets are often present).
Prognosis: ~5 months.
Benign tumours
Haemangiomas are the commonest benign liver tumours. They are often an incidental finding on ultrasound or CT and don’t require treatment. Avoid biopsy!! Adenomas are common.
Causes:
Anabolic steroids, oral contraceptive pill; pregnancy. Only treat if symptomatic, or >5cm.
Acute Viral Hepatitis
Acute viral hepatitis can be caused by five hepatitis viruses and probably other as yet unidentified viruses. Hepatitis A virus is the most common cause, followed by hepatitis B virus. Engaging in certain activities, such as getting a tattoo or body piercing, sharing needles to inject drugs, or having several sex partners, increases the risk of developing hepatitis.
Symptoms
Acute viral hepatitis can cause anything from a minor flu-like illness to fatal liver failure. Sometimes there are no symptoms. The severity of symptoms and speed of recovery vary considerably, depending on the particular virus and on the person’s response to the infection. Hepatitis A and C often cause very mild symptoms or none at all and may be unnoticed. Hepatitis B and E are more likely to produce severe symptoms. Infection with both hepatitis B and D (called coinfection) may make the symptoms even more severe.
Symptoms usually begin suddenly. They include a poor appetite, nausea, vomiting, and often a fever and pain in the upper right part of the abdomen (where the liver is located). In people who smoke, a distaste for cigarettes is a typical symptom. Occasionally, especially with hepatitis B, infected people develop joint pains and itchy red hives on the skin (wheals or urticaria).
Typically, after 3 to 10 days, the urine becomes dark, and jaundice develops. Both of these symptoms occur because bilirubin builds up in the blood. Bilirubin is the main pigment in bile, the greenish yellow digestive fluid produced by the liver. Most symptoms usually disappear at this point, and people feel better even though the jaundice may worsen. The jaundice usually peaks in 1 to 2 weeks, then fades over 2 to 4 weeks. Symptoms of cholestasis (a reduction or stoppage of bile flow)—such as pale stools and overall itchiness—may develop, particularly in people with hepatitis A.
Rarely, symptoms become extremely severe and liver failure develops (called fulminant hepatitis). Fulminant hepatitis is more likely to develop in people with hepatitis B, particularly if they also have hepatitis D. Fulminant hepatitis can progress very quickly. Toxic substances normally removed by the liver build up in the blood and reach the brain, causing hepatic (portosystemic) encephalopathy (see page Hepatic Encephalopathy). Fulminant hepatitis may be fatal, especially in adults.
People with acute viral hepatitis usually recover in 4 to 8 weeks, even without treatment. However, people infected with hepatitis C may become carriers of the virus. People infected with hepatitis B are less likely to become carriers. Carriers have no symptoms but are still infected and can transmit the virus to others. Carriers may develop chronic hepatitis even though the disease is not apparent. Carriers may eventually develop cirrhosis (severe scarring of the liver—see page Cirrhosis of the Liver) or liver cancer (see page Primary Liver Cancers).
Diagnosis
Doctors suspect acute viral hepatitis on the basis of symptoms. During the physical examination, a doctor presses on the abdomen above the liver, which is tender and somewhat enlarged in about half of the people with acute viral hepatitis.
Blood tests to determine how well the liver is functioning and whether it is damaged (liver function tests) are done. They can indicate whether the liver is inflamed and often help doctors distinguish hepatitis due to alcohol abuse from that due to a virus. Blood tests are done to help doctors identify which hepatitis virus is causing the infection. These tests can detect parts of the viruses or specific antibodies produced by the body to fight the viruses.
Occasionally, if the diagnosis is unclear, a biopsy is done: A sample of liver tissue is removed with a needle and examined.
If acute hepatitis seems likely, the cause is identified if possible. To help identify the cause, a doctor usually asks about activities that can increase the risk of getting viral hepatitis (see Table: The Hepatitis Viruses). To determine whether the cause may be something other than a virus, the doctor may ask whether people take any drugs that can cause hepatitis (such as isoniazid, used to treat tuberculosis) and how much alcohol they drink.
Prevention
Vaccines, given by injection into muscle, are available to prevent hepatitis A, B, and E infections.
Hepatitis A vaccine is recommended for all children (see Figure: Vaccinating Infants and Children) and for adults likely to be exposed to the virus, such as travelers to areas where hepatitis A is common (see page Hepatitis A Vaccine).
Hepatitis B vaccine is recommended for all people under age 18 (starting at birth—see page Hepatitis B Vaccine and Vaccinating Infants and Children)
Hepatitis E vaccine, a new vaccine, is most likely to be used in areas where hepatitis E is common.
As with most vaccines, protection requires allowing a number of weeks for the vaccine to reach its full effect as the immune system gradually creates antibodies against the particular virus.
If people who have not been vaccinated are exposed to hepatitis A virus, they can be given an injection of an antibody preparation called standard immune globulin. It prevents infection or decreases its severity. However, the amount of protection it provides varies, and the protection is only temporary.
If people who have not been vaccinated are exposed to hepatitis B virus, they are given hepatitis B immune globulin and are vaccinated. Hepatitis B immune globulin contains antibodies to hepatitis B, which help the body fight the infection. This preparation prevents symptoms or decreases their severity, although it is unlikely to prevent infection. Some people, such as those with a weakened immune system or those being treated with hemodialysis, may need a booster dose of the vaccine.
No vaccines against hepatitis C or D virus are available. However, vaccination against hepatitis B virus also reduces the risk of infection with hepatitis D virus.
Chronic Hepatitis
Chronic hepatitis, although much less common than acute hepatitis, can persist for years, even decades. In many people, it is quite mild and does not cause significant liver damage. However, in some people, continued inflammation slowly damages the liver, eventually resulting in cirrhosis (severe scarring of the liver—see Cirrhosis of the Liver), liver failure (see Liver Failure), and sometimes liver cancer ( Primary Liver Cancers).
Causes
Chronic hepatitis is usually caused by one of the hepatitis viruses
Hepatitis C virus causes about 60 to 70% of cases, and at least 75% of acute hepatitis C cases become chronic.
About 5 to 10% of hepatitis B cases, sometimes with hepatitis D coinfection, become chronic. (Hepatitis D does not occur by itself. It occurs only as a coinfection with hepatitis B.)
Rarely, hepatitis E virus causes chronic hepatitis in people with a weakened immune system, such as those who are taking drugs to suppress the immune system after an organ transplant, who are taking drugs to treat cancer, or who have HIV infection.
Hepatitis A virus does not cause chronic hepatitis.
Certain drugs can cause chronic hepatitis, particularly when they are taken for a long time. They include isoniazid, methyldopa, and nitrofurantoin.
Other causes include alcoholic hepatitis and fatty liver disease not related to alcohol use (nonalcoholic steatohepatitis). Less often, chronic hepatitis results from alpha1-antitrypsin deficiency (a hereditary disorder), celiac disease, a thyroid disorder, or, in children and young adults, Wilson disease—a rare hereditary disorder involving abnormal retention of copper in the liver.
In many people with chronic hepatitis, no obvious cause can be identified. In some of these people, the chronic inflammation resembles inflammation caused by the body attacking its own tissues. This type of inflammation, called autoimmune hepatitis, is more common among women than men.
No one knows exactly why a particular virus or drug causes chronic hepatitis in some people but not in others or why the degree of severity varies.
In about two thirds of people, chronic hepatitis develops gradually, often without causing any symptoms of a liver disorder until cirrhosis occurs. In the remaining one third, it develops after a bout of acute viral hepatitis that persists or returns (often several weeks later).
Symptoms often include a vague feeling of illness (malaise), poor appetite, and fatigue. Sometimes affected people also have a low-grade fever and some upper abdominal discomfort. Jaundice is rare.
Often, the first specific symptoms are those of chronic liver disease or cirrhosis. They can include an enlarged spleen, small spiderlike blood vessels visible in the skin (called spider angiomas), redness of the palms, and accumulation of fluid within the abdomen (ascites). Liver malfunction may lead to deterioration of brain function, called hepatic (portosystemic) encephalopathy and a tendency to bleed (coagulopathy). Brain function deteriorates because toxic substances build up in the blood and reach the brain. The liver normally removes them from the blood, breaks them down, then excretes them as harmless by-products into the bile or blood. The damaged liver is less able to remove them.
A few people have jaundice, itchiness, and stools that are greasy and foul-smelling (called steatorrhea) and light-colored. These symptoms develop because the flow of bile out of the liver is blocked.
Autoimmune hepatitis may cause other symptoms that can involve virtually any body system, especially in young women. Such symptoms include acne, cessation of menstrual periods, joint pain, scarring of the lungs, inflammation of the thyroid gland and kidneys, and anemia.
In many people, chronic hepatitis does not progress for years. In others, it gradually worsens. The outlook depends partly on which virus is the cause:
Chronic hepatitis C, if untreated, causes cirrhosis in about 20 to 30% of people. However, cirrhosis may take decades to develop. The risk of liver cancer is increased only if cirrhosis is present.
Chronic hepatitis B tends to worsen, sometimes rapidly but sometimes over decades, leading to cirrhosis. Chronic hepatitis B also increases the risk of liver cancer.
Chronic coinfection with hepatitis B and D, if untreated, causes cirrhosis in up to 70%.
Autoimmune hepatitis can be effectively treated in most people, but some develop cirrhosis.
Chronic hepatitis caused by a drug may completely resolve once the drug is stopped.
Diagnosis
Doctors may suspect chronic hepatitis when people have typical symptoms, when blood tests (done for other reasons) detect abnormally high liver enzymes, or when people have had acute hepatitis before. Also, everyone born between 1945 and 1965, regardless of whether symptoms are present, should be tested once for hepatitis C. Such testing is recommended because hepatitis C is common among this age group and is often unrecognized.
Blood tests to determine how well the liver is functioning and whether it is damaged (liver function tests) are done. They may help establish or exclude the diagnosis, identify the cause, and determine the severity of liver damage. Blood tests are also done to help doctors identify which hepatitis virus is causing the infection. If no virus is identified, other blood tests are needed to check for other causes, such as autoimmune hepatitis. However, a liver biopsy is essential to confirm the diagnosis. The liver biopsy also enables a doctor to determine how severe the inflammation is and whether any scarring or cirrhosis has developed. The biopsy may help identify the cause of hepatitis.
If people have chronic hepatitis B, ultrasonography is done every 6 months to screen for liver cancer. Levels of alpha-fetoprotein—a protein normally produced by immature liver cells in fetuses—may increase when liver cancer is present and thus may also be checked to screen for liver cancer. People with chronic hepatitis C are screened similarly, but only if they have cirrhosis.
Treatment
If a drug is the cause, the drug is stopped. If another disorder is the cause, it is treated.
Hepatitis B and C
If chronic hepatitis B or C is worsening or if liver enzyme levels are high, people are usually given antiviral drugs.
For hepatitis B, entecavir or tenofovir is usually used. These drugs are taken by mouth. These drugs are very effective, and the chance that viruses will develop resistance to them is slight. Other drugs that can be used include telbivudine and lamivudine (taken by mouth) and interferon alfa and pegylated interferon alfa (given by injection under the skin).
In some people, hepatitis B tends to recur once drug treatment is stopped and may be even more severe. Thus, these people may need to take an antiviral drug indefinitely.
For hepatitis C, treatment varies based on which type of hepatitis C virus causes it. There are several types of hepatitis C virus (called genotypes). Each type has slightly different genetic material. For some types, the most effective treatment is the following combination of drugs
Cholecystitis
Acute cholecystitis
Acute cholecystitis begins suddenly, resulting in severe, steady pain in the upper abdomen. The pain usually lasts more than 6 hours. At least 95% of people with acute cholecystitis have gallstones. The inflammation almost always begins without infection, although infection may follow later. Inflammation may cause the gallbladder to fill with fluid and its walls to thicken.
Rarely, a form of acute cholecystitis without gallstones (acalculous cholecystitis) occurs. However, the gallbladder may contain sludge (microscopic particles of materials similar to those in gallstones). Acalculous cholecystitis is more serious than other types of cholecystitis.
It tends to occur after the following: Major surgery Critical illnesses such as serious injuries, major burns, or a bloodstream infection (sepsis) Intravenous feedings for a long time Fasting for a long time A deficiency in the immune system
Acute acalculous cholecystitis can occur in young children, perhaps developing from a viral or another infection.
Chronic cholecystitis
Chronic cholecystitis is gallbladder inflammation that has lasted a long time. It almost always results from gallstones and from prior attacks of acute cholecystitis. Chronic cholecystitis is characterized by repeated attacks of pain (biliary colic) that occur when gallstones periodically block the cystic duct.
In chronic cholecystitis, the gallbladder is damaged by repeated attacks of acute inflammation, usually due to gallstones, and may become thick-walled, scarred, and small. The gallstones may block the opening of the gallbladder into the cystic duct or block the cystic duct itself. The gallbladder usually also contains sludge. If scarring is extensive, calcium may be deposited in the walls of the gallbladder, causing them to harden (called porcelain gallbladder).
Symptoms
A gallbladder attack, whether in acute or chronic cholecystitis, begins as pain.
Acute cholecystitis
The pain of acute cholecystitis is similar to biliary colic (pain caused by gallstones) but is more severe and lasts longer—more than 6 hours and often more than 12 hours. The pain peaks after 15 to 60 minutes and remains constant. It usually occurs in the upper right part of the abdomen. The pain may become excruciating. Most people feel a sharp pain when a doctor presses on the upper right part of the abdomen. Breathing deeply may worsen the pain. The pain often extends to the lower part of the right shoulder blade or to the back. Nausea and vomiting are common.
Within a few hours, the abdominal muscles on the right side may become stiff. Fever occurs in about one third of people with acute cholecystitis. The fever tends to rise gradually to above 100.4° F (38° C) and may be accompanied by chills.
In older people, the first or only symptoms of cholecystitis may be vague. For example, older people may lose their appetite, feel tired or weak, or vomit. They may not develop a fever.
Typically, an attack subsides in 2 to 3 days and completely resolves in a week. If the acute episode persists, it may signal a serious complication. Increasingly severe pain, a high fever, and chills suggest pockets of pus (abscesses) in or a tear (perforation) in the gallbladder. Abscesses result from gangrene, which develops when tissue dies. A large stone may tear the gallbladder’s wall and pass into the small intestine and block it. This blockage may cause abdominal pain and bloating.
If people develop jaundice (see page Jaundice in Adults) or pass dark urine and light-colored stools, the common bile duct is probably blocked by a stone, causing a backup of bile in the liver (cholestasis). Inflammation of the pancreas (pancreatitis) can develop. It is caused by a stone blocking the ampulla of Vater (where the common bile duct and the pancreatic duct join together).
Acalculous cholecystitis
Acalculous cholecystitis typically causes sudden, excruciating pain in the upper abdomen in people with no previous symptoms or other evidence of a gallbladder disorder (see page Biliary Pain Without Gallstones). The inflammation is often very severe and can lead to gangrene or rupture of the gallbladder.
People with acalculous cholecystitis tend to be very ill. For example, they may be in the intensive care unit for another reason) and have many other symptoms. Also, because these people are so ill, they may not be able to communicate very clearly. For these reasons, acalculous cholecystitis may be overlooked at first.
The only symptoms may be a swollen (distended), tender abdomen or a fever with no known cause. If untreated, acalculous cholecystitis results in death for 65% of people.
Chronic cholecystitis
People with chronic cholecystitis have recurring attacks of pain. The upper abdomen above the gallbladder is tender to the touch. In contrast to acute cholecystitis, fever rarely occurs in people with chronic cholecystitis. The pain is less severe than the pain of acute cholecystitis and does not last as long.
Diagnosis
Doctors diagnose cholecystitis based mainly on symptoms and results of imaging tests. Ultrasonography is the best way to detect gallstones in the gallbladder. Ultrasonography can also detect fluid around the gallbladder or thickening of its wall, which are typical of acute cholecystitis. Often, when the ultrasound probe is moved across the upper abdomen above the gallbladder, people report tenderness.
Cholescintigraphy, another imaging test, is useful when acute cholecystitis is difficult to diagnose. For this test, a radioactive substance (radionuclide) is injected intravenously. A gamma camera detects the radioactivity given off, and a computer is used to produce an image. Thus, movement of the radionuclide from the liver through the biliary tract can be followed. Images of the liver, bile ducts, gallbladder, and upper part of the small intestine are taken. If the radionuclide does not fill the gallbladder, the cystic duct is probably blocked by a gallstone. Cholescintigraphy is also useful when doctors suspect acute acalculous cholecystitis.
Blood tests to evaluate how well the liver is functioning and whether it is damaged (liver function tests) are done. However, these tests cannot confirm the diagnosis because results are often normal or only slightly high, unless the bile duct is blocked.
Other blood tests are also done. For example, the number (count) of white blood cells is measured. A high white blood cell count suggests inflammation, an abscess, gangrene, or a perforated gallbladder.
Computed tomography (CT) of the abdomen can detect some complications of cholecystitis, such as pancreatitis or a tear in the gallbladder.
Treatment
People with acute or chronic cholecystitis need to be hospitalized. They are not allowed to eat or drink and are given fluids and electrolytes intravenously. A doctor may pass a tube through the nose and into the stomach, so that suctioning can be used to keep the stomach empty and reduce fluid accumulating in the intestine if the intestine is blocked or is not functioning normally. Usually, people are given antibiotics intravenously (because infection is possible) and pain relievers.
The gallbladder is usually removed within 24 to 48 hours after symptoms start if
Acute cholecystitis is confirmed and the risk of surgery is small.
People are older or have diabetes because in such people, cholecystitis is more likely to result in infections.
A complication such as an abscess, gangrene, or perforated gallbladder is suspected.
People have acalculous cholecystitis.
If necessary, surgery can be delayed for 6 weeks or more while the attack subsides. If people have a disorder that makes surgery too risky (such as a heart, lung, or kidney disorder), surgery is delayed until appropriate treatment can control the disorder as well as possible.
In chronic cholecystitis, the gallbladder is usually removed after the current attack subsides.
Surgical removal of the gallbladder (cholecystectomy) is usually done using a flexible viewing tube called a laparoscope. After small incisions are made in the abdomen, the laparoscope and surgical instruments are inserted through the incisions. Doctors then use the instruments to remove the gallbladder.
Cholelithiasis
Gallstones are collections of solid material (predominantly crystals of cholesterol) in the gallbladder.
The liver can secrete too much cholesterol, which is carried with bile, to the gallbladder, where the excess cholesterol forms solid particles and accumulates.
Gallstones sometimes cause upper abdominal pain that can last for hours.
Ultrasonography is quite accurate in detecting gallstones.
If gallstones cause recurrent pain or other problems, the gallbladder is removed.
Most disorders of the gallbladder and bile ducts result from gallstones. The risk factors for gallstones include the following:
Female sex
Older age
American Indian ethnicity
Obesity
Rapid weight loss (as results from a very low calorie diet or weight-loss surgery)
A typical western diet
A family history of gallstones
Stones in the gallbladder (called cholelithiasis) sometimes pass into the bile ducts, or stones may form in the bile ducts. Stones in the bile ducts are called choledocholithiasis. These stones sometimes block a bile duct.
Most gallstones do not cause symptoms. But if symptoms or other problems occur, treatment is necessary. Each year, more than half a million people in the United States have their gallbladder surgically removed.
In the Western world, the major component of most gallstones is cholesterol, a fat (lipid) that normally is dissolved in bile (but not in water). When the liver secretes excess cholesterol, bile becomes oversaturated with cholesterol. The excess forms solid particles (cholesterol crystals). These microscopic crystals accumulate in the gallbladder, where they clump and grow into gallstones.
Other types of gallstones form in the same way, but the solid particles are calcium compounds or bilirubin (the main pigment in bile). Stones composed of bilirubin, called pigment stones, are either black (forming in the gallbladder) or brown (forming in the bile ducts). Black pigment stones are more likely to develop in people who have alcoholic liver disease, who are older, or who have hemolytic anemia (which occurs when the body destroys red blood cells prematurely). Brown pigment stones can form when the gallbladder or bile ducts are inflamed or infected or when the bile ducts are narrowed.
The stones may stay in the gallbladder or pass into bile ducts. Stones can block the cystic duct, common bile duct, or ampulla of Vater (where the common bile duct and pancreatic duct join). Most cholesterol stones in the bile ducts came from the gallbladder.
Any narrowing (stricture) of the bile ducts can lead to a blockage or slow bile flow. Bacterial infections can develop when bile flow is slowed or blocked.
Sometimes microscopic particles of cholesterol, calcium compounds, bilirubin, and other materials accumulate but do not form stones. This material is called biliary sludge. Sludge develops when bile remains in the gallbladder too long, as it does during pregnancy. Gallbladder sludge usually disappears when its cause resolves, for example, when pregnancy ends. However, sludge can evolve into gallstones or pass into the biliary tract and block the ducts.
Symptoms
About 80% of people with gallstones do not have any symptoms for many years, if ever, particularly if the gallstones remain in the gallbladder.
Gallstones may cause pain. Pain develops when the stones pass from the gallbladder into the cystic duct, common bile duct, or ampulla of Vater and block the duct. Then the gallbladder swells, causing pain called biliary colic. The pain is felt in the upper abdomen, usually on the right side under the ribs. Sometimes the location is hard to pinpoint, particularly for people with diabetes and older people. The pain typically increases in intensity over 15 minutes to an hour and remains steady for up to 12 hours. The pain is usually severe enough to send people to the emergency department for relief. Then the pain resolves over 30 to 90 minutes, leaving a dull ache. People often feel nauseated and vomit.
Eating a heavy meal can trigger biliary colic whether people eat fatty foods or not. Gallstones do not cause belching or bloating. Nausea occurs only when biliary colic occurs.
Although most episodes of biliary colic resolve spontaneously, pain returns in 20 to 40% of people each year, and complications may develop. Between episodes, people feel well.
If the blockage persists, the gallbladder becomes inflamed (a condition called acute cholecystitis—see page Cholecystitis). When the gallbladder is inflamed, bacteria flourish, and infection may develop. The inflammation usually causes fever.
Blockage of the common bile duct or the ampulla of Vater is more serious than blockage of the cystic duct. Blockage of a bile duct can cause the ducts to widen (dilate). It can also cause fever, chills, and jaundice (a yellowish discoloration of the skin and the whites of the eyes). This combination of symptoms indicates that a serious infection called acute cholangitis has developed. Bacteria can spread to the bloodstream and cause serious infections elsewhere in the body. Also, pockets of pus (abscesses) can develop in the liver.
Stones that block the ampulla of Vater also can block the pancreatic duct, causing inflammation of the pancreas (pancreatitis), as well as pain.
Inflammation of the gallbladder caused by gallstones can erode the gallbladder wall, sometimes resulting in a hole (perforation). Perforation results in leakage of the gallbladder contents throughout the abdominal cavity, causing severe inflammation (peritonitis). A large gallstone that enters the small intestine can cause intestinal blockage, called a gallstone ileus. This rare complication is more likely to occur in older people.
Treatment
Gallstones that do not cause symptoms (silent gallstones) do not require treatment. If gallstones cause pain, changing the diet (for example, to a low-fat diet) does not help.
Gallstones in the gallbladder
If gallstones cause disruptive, recurring episodes of pain, a doctor may recommend surgical removal of the gallbladder (cholecystectomy). Removal of the gallbladder prevents episodes of biliary colic yet does not affect digestion. No special dietary restrictions are required after surgery. During cholecystectomy, the doctor may also check for stones in the bile ducts.
About 90% of cholecystectomies are done using a flexible viewing tube called a laparoscope. After small incisions are made in the abdomen, the laparoscope is inserted. Surgical tools are passed through the incisions and used to remove the gallbladder. Laparoscopic cholecystectomy has lessened the discomfort after surgery, shortened the length of hospital stays, provided better cosmetic results, and reduced the time needed to recover.
The rest of cholecystectomies are done by open abdominal surgery, which requires a larger incision in the abdomen. Although invasive, this procedure is safe and effective.
Alternatively, gallstones can sometimes be dissolved with drugs, such as bile acids (ursodeoxycholic acid), taken by mouth. Such a drug, taken two or three times daily, can dissolve tiny stones in 6 months. Larger stones may take up to 1 to 2 years. Many never dissolve. Dissolving gallstones with drugs is most likely to work when stones are made of cholesterol and the opening of the gallbladder is not blocked. Even if the stones are successfully dissolved, half of these people develop gallstones again within 5 years. This treatment has limited use, and doctors use it only when surgery is too risky.
Ursodeoxycholic acid can help prevent stones from forming in obese people who are losing weight rapidly after weight-loss surgery or who are on a very low calorie diet.
Gallstones in the bile ducts
Most stones in the bile ducts can be removed during ERCP. During this procedure, doctors pass an instrument through the endoscope and use it to cut the sphincter of Oddi (which opens into the small intestine)—a procedure called endoscopic sphincterotomy. Sometimes the end of the bile duct is also cut and widened. If the stones do not spill out into the small intestine on their own after the cut is made, a catheter with a small basket at its tip is inserted through the endoscope. It can be used to trap and then pull the stone out of the duct. Cutting the end of the bile duct leaves the opening wide enough to let any future stones pass more easily into the small intestine. Gallstones located in the gallbladder cannot be removed using this technique.
ERCP with endoscopic sphincterotomy is successful in 90% of people. It is far safer than open abdominal surgery. Fewer than 1% of people die from this procedure, and up to 7% experience complications soon after surgery. Such complications include bleeding, inflammation of the pancreas (pancreatitis), and perforation or infection of the bile ducts. Later on, in some people, the inflamed bile ducts narrow (called strictures). When the ducts narrow, stones are more likely to form in the ducts, causing more blockages in the ducts.
Most people who have had ERCP and endoscopic sphincterotomy later have their gallbladder removed, typically using a laparoscope. If the gallbladder remains, stones in the gallbladder may pass into the ducts, causing repeated blockages.
Tumours of the Pancreas
The pancreas is an organ located in the upper part of the abdomen. It produces digestive juices that are secreted into the digestive tract. The pancreas also produces insulin, which helps control blood sugar. About 95% of cancerous (malignant) tumors of the pancreas are adenocarcinomas. Adenocarcinomas usually originate in the glandular cells lining the pancreatic duct. Most adenocarcinomas occur in the head of the pancreas, the part nearest the first segment of the small intestine (duodenum).
Risk factors for pancreatic cancer include
Male sex
Smoking
Chronic pancreatitis
These tumors are nearly twice as common among men. Adenocarcinoma of the pancreas is 2 to 3 times more common among smokers than nonsmokers. People with chronic pancreatitis are at greater risk as well. People who have relatives with the disease may be at increased risk. Alcohol and caffeine consumption do not seem to be risk factors.
Rare types of pancreatic cancer
Cystadenocarcinoma of the pancreas is a rare type of pancreatic cancer that develops from a fluid-filled noncancerous (benign) tumor called a cystadenoma. It often causes upper abdominal pain and may grow large enough for a doctor to feel it through the abdominal wall. The diagnosis is usually made by a computed tomography (CT) scan of the abdomen or magnetic resonance imaging (MRI—see page Computed Tomography and Magnetic Resonance Imaging). Only 20% of people with this cancer have tumors that have metastasized (spread) by the time surgery is performed. Therefore, cystadenocarcinoma has a much better prognosis than adenocarcinoma. If the cancer has not spread and the whole pancreas is removed surgically, the person has a 65% chance of surviving for at least 5 years.
Intraductal papillary-mucinous tumor is a rare type of pancreatic tumor characterized by enlargement (dilation) of the main pancreatic duct, mucus overproduction, and occasional pain. The diagnosis is made by CT and sometimes other imaging tests. More than 30% of these tumors are cancerous (malignant), but because diagnostic tests cannot distinguish between noncancerous and cancerous forms of this tumor, surgery is the best diagnostic and treatment option for all people suspected of having this type of tumor. With surgery, people with the noncancerous tumors have a greater than 95% chance of surviving for 5 years. People with cancerous tumors have a 50 to 75% chance of surviving 5 years.
Symptoms
Adenocarcinoma of the body or tail of the pancreas (the middle part of the pancreas and the part farthest from the duodenum) typically causes no symptoms until the tumor has grown large. Thus, at the time of diagnosis, the tumor has already spread (metastasized) beyond the pancreas in 90% of cases. Eventually, most people develop severe upper abdominal pain, which may also be felt in the middle of the back. The pain may be relieved by bending forward or assuming the fetal position. Weight loss is common.
Complications of pancreatic cancer
Tumors in the head of the pancreas can interfere with the drainage of bile (the digestive fluid produced by the liver) into the small intestine (see page Gallbladder and Biliary Tract). Therefore, jaundice (a yellowish discoloration of the skin and the whites of the eyes) caused by obstruction of bile flow is typically an early symptom. The jaundice is accompanied by itchiness all over the body resulting from the deposit of bile salt crystals under the skin. Vomiting may result from instances when cancer in the head of the pancreas obstructs the flow of stomach contents into the small intestine (gastric outlet obstruction) or obstructs the small intestine itself.
Adenocarcinoma of the body or tail of the pancreas may obstruct the vein draining the spleen (the organ that produces, monitors, stores, and destroys blood cells), resulting in enlargement of the spleen (splenomegaly). Obstruction can also cause the veins to become swollen and twisted (varicose) around the esophagus (esophageal varices) and stomach. Severe bleeding may result, particularly from the esophagus, if these varicose veins rupture.
Certain cells in the pancreas produce insulin, a hormone that is essential to control blood sugar levels. Lack of insulin causes diabetes. Thus, because pancreatic cancer cells replace normal pancreatic cells, diabetes develops in 25 to 50% of people, which leads to symptoms of high blood sugar, such as frequently urinating large volumes and excessive thirst.
Pancreatic cancer can also interfere with production of digestive enzymes by the pancreas, resulting in problems breaking down food and absorbing nutrients ( malabsorption). This malabsorption causes bloating and gas and a watery, greasy, and/or foul-smelling diarrhea, leading to weight loss and vitamin deficiencies.
Diagnosis Computed tomography (CT) or magnetic resonance cholangiopancreatography (MRCP)
Early diagnosis of tumors in the body or tail of the pancreas is difficult because symptoms occur late and physical examination and blood test results are often normal. When adenocarcinoma of the pancreas is suspected, the preferred tests are CT (see page Computed Tomography and Magnetic Resonance Imaging) or MRCP (see Magnetic Resonance Imaging).
Other commonly used tests are ultrasonography, endoscopic retrograde cholangiopancreatography (see Figure: Understanding Endoscopic Retrograde Cholangiopancreatography), and magnetic resonance imaging (MRI). Blood tests are also done.
To confirm the diagnosis, a doctor may obtain a sample of the pancreas for examination under a microscope (biopsy) by inserting a needle through the skin using a CT or ultrasound scan as a guide. However, this approach often misses the tumor and may spread cancer cells out of the local area along the track of the needle. The same approach may be used to obtain a biopsy sample from the liver to look for cancer that has spread to the pancreas. If the results of these tests are normal but the doctor still strongly suspects adenocarcinoma, the pancreas may be evaluated surgically.
Prognosis
Because adenocarcinoma of the pancreas has usually spread to other parts of the body before it is discovered, the prognosis is very poor. Fewer than 2% of people with adenocarcinoma of the pancreas survive for 5 years after the diagnosis.
Treatment
Surgery
Pain relievers
The only hope of a cure is surgery, which is performed on the 10 to 20% of people in whom it is believed that the cancer has not spread. Either the pancreas alone or the pancreas and the duodenum are removed. After such surgery, only 15 to 20% of people live for 5 years. Chemotherapy and radiation therapy are usually also given to prolong life but do not cure the cancer.
Pancreatitis
Symptoms of Acute Pancreatitis
Almost everyone with acute pancreatitis has severe abdominal pain in the upper abdomen, below the breastbone (sternum). The pain penetrates to the back in about 50% of people. Rarely, the pain is first felt in the lower abdomen. When acute pancreatitis is caused by gallstones, the pain usually starts suddenly and reaches its maximum intensity in minutes. When pancreatitis is caused by alcoholism, pain develops over a few days. The pain then remains steady and severe, has a penetrating quality, and persists for days.
Coughing, vigorous movement, and deep breathing may worsen the pain. Sitting upright and leaning forward may provide some relief. Most people feel nauseated and have to vomit, sometimes to the point of dry heaves (retching without producing any vomit). Often, even large doses of an injected opioid analgesic do not relieve pain completely.
Some people, especially those who develop acute pancreatitis because of alcohol abuse, may never develop any symptoms other than moderate pain. Other people feel terrible. They look sick and are sweaty and have a fast pulse (100 to 140 beats a minute) and shallow, rapid breathing. Rapid breathing may occur if people have inflammation of the lungs, areas of collapsed lung tissue ( atelectasis), or accumulation of fluid in the chest cavity ( pleural effusion). These conditions decrease the amount of lung tissue available to transfer oxygen from the air to the blood.
At first, body temperature may be normal, but it increases in a few hours to between 100° F and 101° F (37.7° C and 38.3° C). Blood pressure may be high or low, but it tends to fall when the person stands, causing faintness. As acute pancreatitis progresses, people tend to be less and less aware of their surroundings—some are nearly unconscious. Occasionally, the whites of the eyes (sclera) become yellowish.
Complications of Acute Pancreatitis
Damage to the pancreas may permit activated enzymes and toxins such as cytokines to enter the bloodstream and cause low blood pressure and damage to organs outside of the abdominal cavity, such as the lungs and kidneys. The part of the pancreas that produces hormones, especially insulin , tends not to be damaged or affected.
About 20% of people with acute pancreatitis develop some swelling in the upper abdomen. This swelling may occur because the stomach is distended or has been moved out of place by a mass in the pancreas that causes swelling or because the movement of stomach and intestinal contents has stopped (a condition called ileus).
In severe acute pancreatitis, parts of the pancreas die (necrotizing pancreatitis), and blood and pancreatic fluid may escape into the abdominal cavity, which decreases blood volume and results in a large drop in blood pressure, possibly causing shock (see page Shock). Severe acute pancreatitis can be life threatening.
Infection of an inflamed pancreas is a risk, particularly after the first week of illness. Sometimes, a doctor suspects an infection because the person’s condition worsens and because a fever develops and the white blood cell count increases after other symptoms had initially started to subside.
Sometimes, collections of pancreatic enzymes, fluid, and tissue debris form in and around the pancreas. The collection is called a pancreatic pseudocyst. In about half of people, the pseudocyst goes away spontaneously. In other people, the pseudocyst can become infected. If a pseudocyst rapidly grows larger and causes pain or other symptoms, a doctor drains it.
Diagnosis of Acute Pancreatitis
Characteristic abdominal pain leads a doctor to suspect acute pancreatitis, especially in a person who has gallbladder disease or who is an alcoholic. During the examination, a doctor often notes that the abdominal wall muscles are rigid. When listening to the abdomen with a stethoscope, a doctor may hear few or no bowel (intestinal) sounds.
No single blood test proves the diagnosis of acute pancreatitis, but certain tests suggest it. Blood levels of two enzymes produced by the pancreas, amylase and lipase, usually increase on the first day of the illness but return to normal in 3 to 7 days. If the person has had other flare-ups (bouts or attacks) of pancreatitis, however, the levels of these enzymes may not increase, because so much of the pancreas may have been destroyed that few cells are left to release the enzymes. The white blood cell count is usually increased.
X-rays of the abdomen may show dilated loops of intestine or, rarely, one or more gallstones. Chest x-rays may reveal areas of collapsed lung tissue or an accumulation of fluid in the chest cavity. An ultrasound may show gallstones in the gallbladder or sometimes in the common bile duct and also may detect swelling of the pancreas.
A computed tomography (CT) scan is particularly useful in detecting inflammation of the pancreas and is used in people with severe acute pancreatitis and in people with complications, such as extremely low blood pressure. Because the images are so clear, a CT scan helps a doctor make a precise diagnosis.
If doctors suspect the pancreas is infected, they may withdraw a sample of infected material from the pancreas by inserting a needle through the skin and into the pancreas. Magnetic resonance cholangiopancreatography (MRCP), a special magnetic resonance imaging (MRI) test, may also be done.
Prognosis of Acute Pancreatitis
In severe acute pancreatitis, a CT scan helps determine the outlook or prognosis. If the scan indicates that the pancreas is only mildly swollen, the prognosis is excellent. If the scan shows large areas of destroyed pancreas, the prognosis is poor.
When acute pancreatitis is mild, the death rate is about 5% or less. However, in pancreatitis with severe damage and bleeding, or when the inflammation is not confined to the pancreas, the death rate can be as high as 10 to 50%. Death during the first several days of acute pancreatitis is usually caused by failure of the heart, lungs, or kidneys. Death after the first week is usually caused by pancreatic infection or by a pseudocyst that bleeds or ruptures.
Treatment of Acute Pancreatitis
Treatment of mild pancreatitis usually involves short-term hospitalization where analgesics are given for pain relief and the person fasts to try to rest the pancreas. Usually, normal eating can resume after 2 to 3 days without further treatment.
People with moderate to severe pancreatitis need to be hospitalized. They must initially avoid food and liquids, because eating and drinking stimulate the pancreas.
Symptoms of chronic pancreatitis may be identical to those of acute pancreatitis (see page Acute Pancreatitis) and generally fall into two patterns. In one pattern, a person has persistent upper abdominal pain that varies in intensity. In this pattern, a complication of chronic pancreatitis, such as an inflammatory mass, a cyst, or even pancreatic cancer, is more likely. In the second pattern, a person has intermittent flare-ups (bouts or attacks) of pancreatitis with symptoms similar to those of mild to moderate acute pancreatitis. The pain sometimes is severe and lasts for many hours or several days. With either pattern, as chronic pancreatitis progresses, cells that secrete the digestive enzymes are slowly destroyed (over about a 6- to 10-year period), so eventually the pain may stop.
As the number of digestive enzymes decreases (a condition called pancreatic insufficiency), food is inadequately broken down. Food that is inadequately broken down is not absorbed properly (malabsorption), and the person may produce bulky, unusually foul-smelling, greasy stools (steatorrhea). The stool is light-colored and may even contain oil droplets. Undigested muscle fibers may also be found in the feces. The inadequate absorption of food also leads to weight loss. Eventually, the insulin -secreting cells of the pancreas may be destroyed, gradually leading to diabetes.
Diagnosis
A doctor suspects chronic pancreatitis because of a person’s symptoms or history of acute pancreatitis flare-ups or alcohol abuse. Blood tests are less useful in diagnosing chronic pancreatitis than in diagnosing acute pancreatitis, but they may indicate elevated levels of amylase and lipase (two enzymes produced by the pancreas). Also, blood tests can be used to check the level of sugar (glucose) in the blood, which may be elevated.
Computed tomography (CT) may be done to show changes of chronic pancreatitis. If the CT scan does not show any abnormalities, doctors may do endoscopic retrograde cholangiopancreatography (ERCP—see page Imaging Tests of the Liver and Gallbladder : Endoscopic Retrograde Cholangiopancreatography and see Figure: Understanding Endoscopic Retrograde Cholangiopancreatography), endoscopic ultrasonography (passage of a flexible viewing tube through the mouth into the stomach and the first segment of the small intestine), and tests of the function of the pancreas. Many doctors now do a special magnetic resonance imaging (MRI) test called magnetic resonance cholangiopancreatography (MRCP) instead of CT. MRCP shows the bile and pancreatic ducts more clearly than does CT.
People with chronic pancreatitis are at increased risk of pancreatic cancer. Worsening of symptoms, especially narrowing of the pancreatic duct, makes doctors suspect cancer. In such cases, a doctor is likely to do blood tests, an MRI scan, a CT scan, or an endoscopic study.
Treatment
Treatment of repeated flare-ups of chronic pancreatitis is similar to that of acute pancreatitis (see page Acute Pancreatitis). Even if alcohol is not the cause, all people with chronic pancreatitis should avoid drinking alcohol. Avoiding all food and receiving only fluids given by vein (intravenously) can rest the pancreas and intestine and may relieve a painful flare-up. In addition, opioid analgesics (see page Opioid Analgesics) are sometimes needed to relieve the pain. Too often, these measures do not relieve the pain, requiring increased amounts of opioids, which may put the person at risk of addiction. Medical treatment of chronic pancreatic pain is often unsatisfactory.
Later, eating four or five meals a day consisting of food low in fat may help reduce the frequency and intensity of the flare-ups. For people who no longer produce adequate digestive enzymes, taking tablets or capsules of pancreatic enzyme extracts with meals can make the stool less greasy and improve food absorption, but these problems are rarely eliminated. If necessary, a histamine-2 (H2) blocker or a proton pump inhibitor (drugs that reduce or prevent the production of stomach acid) may be taken with the pancreatic enzymes. With such treatment, the person usually gains some weight, has fewer daily bowel movements, has no more oil droplets in the stool, and generally feels better. If these measures are ineffective, the person can try decreasing fat intake. Supplements of the fat-soluble vitamins (A, D, E, and K) also may be needed.
If pain continues, a doctor searches for complications, such as an inflammatory mass in the head of the pancreas or a pseudocyst (a collection of pancreatic enzymes, fluid, and tissue debris resembling a cyst). An inflammatory mass may require surgical treatment. A pancreatic pseudocyst that causes pain as it expands may have to be drained (decompressed).
