Ch.11 The Liver and Biliary System Flashcards

Question

Hepatitis A (type of virus, transmission, source, location, symptoms, prognosis)

Answer 1

- Nonencapsulated RNA virus - Transmitted fecal-oral route - Sources of virus are sewage, contaminated food/drinks - Most prevalent in children of underdeveloped countries - Symptoms start after a short incubation period of 15-50 days - Mild enteric fever, vomiting, loss of appetite, jaundice - Recovery within days - Good prognosis, does not advance to cirrhosis or chronic hepatitis

Answer 2

- Encapsulated DNA virus - HBsAG is circulated in blood early, and can be detected within 1 week after onset of infection - HBsAG dissapears after convalescent period, which is marked by the appearance of antibody to HBsAG - HBsAG persists in circulation only when patients develop chronic hepatitis. These patients can not produce anti-HB's, and can not clear the virus from the body

Answer 3

- HBeAG appeats in acute infection, but dissapears before HBsAG - Found it patients with chronic hepatitis

Answer 4

Appear 40-180 days after infection - in preicteric phase, there is weakness, nausea and vomiting. Mild enlargement and tenderness of the liver. - Some patients develop measles like skin rash - darkening of urine (bilirubin) - Jaundice is found in less than 30%, found 2-3 months after exposure and associated with worsening symptoms and lab finding - HBV produces clinically recognisable symptoms in 1/3 of people

Answer 5

- Found in less than 30% of infected patients - Found 2 months after exposure - Associated with worsening symptoms and lab findings (AST, ALT) - Jaundice persists for several weeks and in most patients resolves spontaneously - More profound the jaundice, more likely the disease will enter an uneventful period of recovery - Mild jaundice may herald a protracted course of disease and transition to chronic hepatitis

Answer 6

Symptomatic: Produces symptomatic in 1/3. Chronic hepatitis develops in less than 10% of those with clinically evident infection Asymptomatic: Remaining 2/3 of people have sublinical disease, which is recognised only as the appearance of antibodies to HBs and HBc - 90% of patients recover completely - Chronic hepatitis in less than 10%

Answer 7

-Subclinical: in 25% of cases - HBsAG seen in serum - Mild portal tract inflammation on liver biopsy is only sign, and these people are chronic asymptomatic carriers.

Answer 8

Develops in 25% of those with serologic evidence of chronic hepatitis, more serious, and may lead to cirrhosis or hepatocellular carcinoma

Answer 9

- RNA virus - Antibodies used for dx. - Infection aquired through IVDU (50%), multiple sex partners (35%), surgery (15%), or needle sticks (10%) - 30% of people do not know how they were infected

Answer 10

- indistinguishable from HBV, but less severe - mild abormalities in lab results - 80% will progress to chronic hepatitis - 20% cirrhosis

Answer 11

hepatic artery, portal vein, bile duct

Answer 12

Total: All forms Direct: Conjugated Indirect: Unconjugated

Answer 13

Albumin: Decrease with injury (liver is only source) * Albumin is critical to oncotic pressure. Half life for albumin is 20 days. Helpful in chronic, not acute liver disease. Prothrombin time: Increase with injury (lack of vit k). * Liver is major source of clotting factors, activation depends on vitamin K (all but factor 5) * In acute, is a sign of significant liver injury, marker of severity

Answer 14

AST (can be associated with other organ damange) ALT (more specific to liver) AST/ALT ratio: alcohol, malnutrition, cirrhosis Lactate Dehydrogenase (LDH)- not used often

Answer 15

- Bilirubin: conjugated, unconjucated - Alkaline Phosphatase: injury to hepatocyte canalicular membrane induces synthesis and release - Gama-glutamyl transferase (GGT): Injury to hepatocyte canilcular membrane or stimulation of microsomal enzymes induce synthesis and release \*GGT and Alk Phosphatase can be elevated in other organs

Answer 16

- then the substances persist and may have adverse effects on other tissues ex. ammonia and hepatic encephalopathy

Answer 17

Yes, liver cells are faculative mitotic - meaning they can regenerate

Answer 18

prehepatic Hepatic Post-Hepatic

Answer 19

-unconjugated bilirubin is bound to albumin does not cross blood brain barrier, and does not enter cerebrospinal fluid -does not filter into urine

Answer 20

-in urine, makes brown and foamy

Answer 21

- conjugated or unconjugated bilirubin - signs of liver injury - is there obstruction of bile ducts?

Answer 22

- clinical syndrome of varying severity - caused by hepatotropic viruses: hepatitis A, B, C, D, E - Is most prevalent liver disease in the world - often no symptoms - Hep C most common in usa

Answer 23

- RNA virus - spread through fecal-oral route (sewage, contaminated food, shellfish) - symptoms: short incubation period 15-50 days - short lived fever, loss of appetite, and jaundice - recovery occurs within days, without complications - transition to chronic hepatits or cirrosis never occurs - favorable prognosis

Answer 24

- DNA virus - symptoms occur 40-180 days after - exposure to blood, blood products, or sexual contact - Pre-icteric features: weakness, n&v, enlargement of liver, some have measles like rash - dianostic: darkening of urine d/t bilirubin - Jaudince is found in 30% of patients - usually associated with worsening clinical and labs (bilirunin, AST, ALT) - HBV produces clinical symptoms in 1/3, rest of 2/3 have subclinical disease, and recognisible due to antibodies to HBs and HBc - 90% of patients recover completely

Answer 25

RNA virus - transmitted by infected needles during IVDU (50%) - sexual partners (35%) - surgery (15%) - accidental needlestick (10%) - 30% of people dont know where they got it Clinical presentation: simliar to HBV, but less severe - progress to chronic hepatitis in 80% - 20% will develop cirrhosis

Answer 26

RNA virus that requires HBV for replication may occur concurrently with HBV or as superinfection following HBV

Answer 27

RNA virus fecal-oral route waterborn epidemics resembles HAV

Answer 28

hepatotropic and invade liver cells, damaging and disrupting normal functions while promoting cell death by apoptosis morphologic changes - reversible hepatocellular changes - irreversible hepatocellular changes - inflammatory infiltrates - regeneration of hepatocytes

Answer 29

mild: mild inflammation limited to portal tracts, limited intralobular infiltration moderate: portal tract inflammation is accompanied by spilling of inflammatory cells across limiting plate, and all the way into the lobule severe: disruption of lobular architecture, secondary to aggresive inflammation and fibrosis that accompanies liver cell death. Bridging fibrosis can lead to cirrhosis

Answer 30

Chronic liver disease characterized by loss of structure and function synonym for end-stage liver disease. -irreversible and incurable - except for transplatiation characterised by fibrosis and regenerative liver cell nodules that replace normal parenchyma

Answer 31

- Alcohol, hepatitis virus most common (65%) - estimated that steatohepatitis will become more prominent - etiology in 20% can not be established

Answer 32

Exact is unknown, however main include 1. Necrosis of liver cells 2. Repair by fibrosis 3. Regeneration of liver cells with formation of nodules

Answer 33

portal cirrhosis and billiary cirrhosis

Answer 34

ascites splenomegaly anastomoses between portal and systemic circulation

Answer 35

Fluid accumilation in the abdominal cavity results from portal HTN and hypoproteinemia - backpressures in the portal vein result in transudation of fluid from the serosal surfaces of the intestines, peritoneal surfaces lining the abdominal cavity - reduced oncotic pressure in the plasma from hypoalbinemia, causes fluids into abdominal cavity - results in hypovolemia which triggers aldosterone from renal cortex- NA and H20 retention = affects kidneys- they stop producing urine and thus hepatorenal syndrome Ascites is resistant to tx., and draining will have no effect

Answer 36

- enlarges 3-6x its size - enalged spleen destroys RBC=anemia, leukopenia, thrombocytopenia

Answer 37

caused by shunting between portal and systemic circulation most important are the lower esophagus - which undergo dilation and develop varicies metabolic consequences: encephalopathy (neurotoxins and ammonia- not processed in liver)

Answer 38

dilated veins in lower esophagus. prone to bleeding may result in hematoemesis or melena

Answer 39

hemmorhage

Answer 40

marked by clouded mentation and neuro symptoms "Cerebral dysfunction is thought to be caused by ammonia and putative neurotoxins absorbed from the intestine. Because the shunts allow the enteric venous blood to bypass the liver, neurotoxic substances are not detoxified and therefore act directly on susceptible cells in the brain. The diseased brain shows edema and altered astrocytes but no other morphologic changes that would explain the patho-genesis of neurologic symptoms. Hepatic coma is associated with a high mortality rate, and the patient’s life can be saved only by emergency liver transplantation"

Answer 41

**Liver cell injury and death:** - ALT and AST levels are the best markers of liver cell injury. Acute liver injury is characterized by an elevation of these liver enzymes in serum, but as the acute injury ceases, the levels of ALT and AST may revert to normal. - In end-stage liver disease, often there is no ongoing liver cell death. ALT and AST concentration in the blood may be only mildly elevated. * **Loss of liver cell function.** Decreased production of albumin leads to hypoalbuminemia, which contributes to the formation of ascites and edema. Do not forget that albumin is the most abundant plasma protein and the most important oncotic component of the blood, keeping the fluid in circulation and preventing edema formation. Decreased synthesis of coagulation proteins results in a bleeding tendency. Defective excretion of bilirubin may result in jaundice, which is usually mild. * **Portal hypertension.** The principal consequences of portal hypertension are ascites, splenomegaly, and anastomosesbetween the portal and systemic circulation. Spleno-megaly results in the pooling of platelets, leading to thrombocytopenia and bleeding tendency. The bleed-ing from ruptured esophageal varices leads to an accumulation of blood in the stomach and the intestines, where it serves as a major source of ammonia. Ammonia is degraded from blood protein and absorbed in the intestines, and thus contributes to hepatic encephalopathy.

Answer 42

Fatty liver alcoholic steatohepatitis cirrhosis

Answer 43

Alcohol is an important source of calories (7 calories per gram) and has complex metabolic and poten-tially toxic effects on many cells in the body. Alcohol affects the liver, inhibiting some enzymes and stimulating others It also alters the fluidity and function of cell membranes, as well as the intracellular transport of organelles and metabolites. Because of increased fatty acid synthesis, decreased fatty acid oxidation, and decreased export of fats in the form of lipoproteins, alcohol invariably produces fatty changes in liver cells in a dose-dependent manner. The liver becomes enlarged but without any metabolic consequences or symptoms. These changes are completely reversible, disappearing after the patient stops drinking.A small number of patients with alcoholic fatty liver (10% to 15%) develop signs of alcoholic hepatitis. These signs usually include fever, leukocytosis, abdominal pain, and jaundice. Histologic examination of the liver shows fatty change of hepatocytes and focal necrosis of liver cells associated with leukocytic infiltrates and bile stasis. The cytoplasm of hepatocytes often contains eosinophilic aggre-gates of intermediate cytoskeletal filaments, which form so-called Mallory-Denk bodies (Figure 11-13). Special stains show pericellular fibrosis, especially around the central venule"

Answer 44

Gilberts disease: benign recurrent jaundice with unconjugated bilirubin Hemochromatosis: excessive accumliation of iron in many organs, cirrhosis Wilsons Disease: excessive accumilation of copper (liver, eye, CNS), cirrhosis Alpha1-antitrypsin deficiency: accumulation of AAT, cirrhosis

Answer 45

"α1-antitrypsin deficiency (α1-AT) is an autosomal reces-sive disorder that is related to the presence of the PiZ allele of the gene that encodes for α1-AT. this mutation in the Pi gene is found in about 5% of the population, and in homozygous PiZ mutants it may cause emphysema and cirrhosis of the liver. α1-AT is synthesized in the liver; in PiZ homozygotes it accumulates in the form of cytoplasmic globules inside the liver cells The exact mechanism of liver cell injury is unknown.A significant number of affected persons develop child-hood cholestasis and chronic hepatitis, which progress to cirrhosis in about 20% of affected individuals. α1-AT defi-ciency is one of the most common causes of childhood cirrhosis. The disease may be latent until puberty or adult-hood, when it usually presents with clinical signs of cirrhosis that may give rise to liver cancer"

Answer 46

Autoimmune hepatitis: occurs in young women;associated with other immune diseases (antibodies in serum, ANA, ASM) Primary biliary cirrhosis: occurs in middle-aged women; chronic jaundice, hypercholesterolemia, (antibodies: AMA) Primary sclerosing cholangitis: occurs in men less than 40 years old, associated with ulcerative cholitis (no specific antibodies)

Answer 47

disease of uknown etiology characterized by the destruction of intrahepatic bile ducts and progression to cirrhosis "non-supurulative destructive cholangitis"resembles t-cell mediated destruction of bile ducts associated with liver teansplant -females more than males

Answer 48

concretions composed of chemicals normally formed in bile. They are extremely common, and in the United States more than half a million people undergo biliary surgery for gallstones each year. An estimated 20% of people older than 65 years have gall-stones. Women are especially at risk; the incidence of gallstones is three times higher in women than in men. Because of a metabolic deficiency, Native Americans, such as Pima Indians, are at an extremely high risk for develop-ing gallstones. Indeed, 75% of the women in this population develop gallstones by the age of 25 years. The incidence of gallstones is higher in whites than in blacks, which further underscores the genetic predisposition for this disease"

Answer 49

There are two types of gallstones: cholesterol stones and pigmentary stones. More than 75% of the gallstones that develop in patients in the United States are cholesterol stones; the remainder are either brown or black pigmentary stones. Each of these stones is formed as a result of a distinct mechanism, although it is not uncommon to have mixed stones, which shows that these pathogenetic mechanisms may be interrelated"

Answer 50

Cholesterol stones are formed in bile that is supersaturated with cholesterol and contain decreased amounts of bile acids and lecithin. Bile acids and lecithin are secreted together by the liver cells, but independently of cholesterol. In the gallbladder these substances form water-soluble micelles with cholesterol. These micelles form only if the three substances are present in appropriate concentrations. If the normal ratio of bile components is altered, the bile becomes lithogenic (i.e., capable of stone formation). This occurs typically in obese persons who excrete large amounts of cholesterol in the bile but also may occur in patients with certain metabolic disorders, such as diabetes. Pregnancy, estrogen therapy, use of oral con-traceptives, and certain drugs used in the treatment of hypercholesterolemia (e.g., clofibrate) also promote choles-terol excretion in the bile. Such bile is prone to accelerated nucleation of cholesterol crystals, which is most apparent during the concentration of bile in the gallbladder. The slower bile flow that occurs with age also predisposes such individuals to gallstone formation. It is thus understandable that most cholesterol gallstones are located in the gallblad-der and that the typical risk factors include the so-called four Fs: female, older than forty, fertile, and fat"

Answer 51

Pigmentary stones are composed of calcium bilirubinate and are either black or brown. The black stones, which are most common in Western countries, form in the gallbladders of patients with chronic hemolytic anemia (e.g., sickle cell anemia) and those with cirrhosis. In such patients the stones form presumably because of supersaturation of bile with bilirubin. Brown stones are often laminated and consist of alternating layers of calcium bilirubinate and cholesterol admixed with calcium. These stones occur more commonly in individuals living in the Far East than in those from the West and are often associated with biliary infections or infestations with liver flukes, such as Clonorchis sinensis. Brown stones are most often located in the extrahepatic bile ducts and tend to recur after removal"

Answer 52

hemangiomas

Answer 53

-highly malignant tumor composed of liver cells Male to female 4:1 originate in cirrhotic livers they produce a-fetoprotein in 50%, level can be used for dx. symptoms are non-specific: weight loss, loss of appetite may block hepatic vein and cause thrombosis and impede outflow of venous blood from liver poor prognosis less than 5%