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40 Cards in this Set

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an increased concentration of bilirubin in the blood = >1.0mg/dL
Jaundice or icterus
describes yellow skin and sclerae; becomes apparent when the bilirubin concentration attains a level of greater than 2.0 to 2.5 ml/dL
the presence of plugs of inspissated bile in dilated bile canaliculi and visible bile pigment in hepatocytes.
Cholestatic jaundice
characterized by histologic cholestasis and hyperbilirubinemia.
Define hepatic failure
• Is a clinical syndrome characterized by jaundice, encephalopathy, and other metabolic derangements that occur when the mass of liver cells is insufficiently diminished or their function is impaired.
Consequences of hepatic failure
o Hepatic encephalopathy
o Jaundice
o Coagulopathy
o Pulmonary vascular shunts (decreased O2 saturation)
o Renal failure (hepatorenal syndrome): acute hepatic failure is commonly marked by an associated renal failure, which is characterized by asotemia and oliguria or anuria.
o Endocrine
Endocrine consequences of hepatic failure
 Gynecomastia
 Vascular spiders, from vascular manifestations of hyperestrogenism; in the territory drained by the superior vena cava; palmar erythema.
 Female escutcheon = female distribution of pubic hair
 Testicular atrophy
Define hepatic encephalopathy.
• Refers to a variety of neurologic signs and symptoms in patients who suffer chronic liver failure or in whom the portal circulation is diverted.
o Progresses from lethargy to deep somnolence, and eventually to coma.
• Probably caused by toxic compounds absorbed from the intestine that have escaped hepatic detoxification because of hepatocyte dysfunction or the existence of structural or functional vascular shunts --> synonym: portasystemic encephalopathy.
Substances that can account for hepatic encephalopathy
o Ammonia: most is of dietary origin
o γ-Amnibutyric acid
o Mercapatans: result from breakdown of sulfur-containing amino acids in the colon.
o False Neurotransmitters: such as OCTAPAMINE.
Cirrhosis, which is the end stage of chronic liver disease, is the destruction of the normal hepatic architecture by fibrous septa that encompass regenerative nodules of hepatocytes.
Micronodular Cirrhosis
• Previously called Laennec, portal, or septal cirrhosis.
• Exhibits nodules that are scarcely larger than a lobule, measuring <3 mm in diameter.
• The connective tissue septa separating the nodules are usually THIN, but irregular focal collapse of parenchyma may lead to wider septa.
• Prototype: ACLOHOLIC cirrhosis
o May also be observed in primary and secondary biliary cirrhosis, hemochromatosis, Wilson disease, and certain inherited metabolic disorders.
Macronodular Cirrhosis
• Formerly called POSTNECROTIC, posthepatic, or multilobular cirrhosis
• Large, irregular nodules mimicking lobules; often contain portal tracts and efferent venous channels  provides evidence that the original process was characterized by multilobular necrosis that healed with the formation of large scars surrounding more than a single lobule.
• It is now recognized that the micronodular pattern can be converted into a macronodular one by continued regeneration and expansion of existing nodules.
• Classically associated with chronic active hepatitis.
o Also occasionally a result of submassive hepatic necrosis.
Describe Alcoholic Liver Disease
• 7% of total U.S. population is alcoholic
• 15% of alcoholics will develop cirrhosis, and many of these people die in hepatic failure or from extrahepatic complications of cirrhosis.
• >10 years of alcoholism are required to produce cirrhosis
• The daily amount of alcohol in patients with established cirrhosis usually ranges from 160-220g.
• A pint of whiskey/day (or its equivalent in other beverages) for 15 years is the threshold for development of cirrhosis.
Spectrum of alcoholic liver disease spans 3 major morphologic and clinical entities:
1. Fatty liver
2. Alcoholic hepatitis
3. Cirrhosis
Fatty Liver
• All patients accumulate fat in hepatocytes = steatosis.
• Ethanol increases lipolysis, and the delivery of free fatty acids to the liver.
• Ethanol:
o Increases fatty acid synthesis
o Decreases mitochondrial oxidation of fatty acids
o Increases production of triglycerides
o Impaired release of lipoproteins.
• Liver becomes yellow and enlarged, sometimes massively.
• Visible fat accumulation varies from minute droplets scattered in the cytoplasm of a few hepatocytes to distention of the entire cytoplasm by coalesced droplets.
Alcoholic Hepatitis is an acute, necrotizing lesion chracterized by (4)
1. Necrosis of hepatocytes, predominantly in the central zone
2. Cytoplasmic hyaline inclusions within hepatocytes
3. A neutrophilic inflammatory response
4. Perivenular fibrosis.
Mallory bodies
(alcoholic hepatitis)
• Scattered hepatocytes contain MALLORY BODIES (alcoholic hyaline). These cytoplasmic inclusions, which are more common in visibly damaged, swollen hepatocytes, are visualized as irregular skeins of eosinophlic material or as solid eosinophlic masses, often in a perinuclear location. They are composed of aggregates of intermediate filaments.
o The damaged hepatocytes, particularly those containing Mallory bodies, are surrounded by neutrophils.
Alcoholic Cirrhosis
• In 15% of alcoholics, hepatocellular necrosis, fibrosis, and regeneration eventually lead to formation of fibrous septa surrounding the hepatocellular nodules, which are the 2 features that define cirrhosis.
• Patients often die from bleeding esophageal varices (portal hypertension), hepatic failure, or both.
Portal Hypertension
• Normal portal pressure = 5-10 mmHg
• Portal hypertension is defined as pressure > 12 mmHg
• Is a sustained increase in portal venous pressure and is almost always the result of obstruction to flow of blood somewhere in the portal circuit.
• Complications arise from the increased pressure and dilatation of the venous bed behind the obstruction.
Etiology of prehepatic portal hypertension
Portal vein thrombosis
Splenic vein thrombosis
Tropical splenomegaly
Arterio-venous fistula
Presinusoidal etiology of intrahepatic portal hypertension
Primary biliary cirrhosis
Chronic active hepatitis
Sinusoidal etiology of intrahepatic portal hypertension
Cirrhosis - post hepatitic, alcohol, metabolic (e.g. Wilson's, hemochromotosis)

Non-cirrhotic - cytotoxic drugs, Vitamin A intoxication
Postsinusoidal etiology of intrahepatic portal hypertension
Budd-Chiari syndrome (occlusion of hepatic veins in venous tributaries)
Veno-occlusive disease
Etiology of posthepatic portal hypertension
Caval abnormality
Constrictive pericarditis
Pathophysiology of portal hypertension
Increased portal pressure reduces portal venous flow
Encourages development of porto-systemic anastomoses
Develop at site of connections between portal and systemic circulation
Gastro-esophageal junction
Lower rectum
Peri-umbilical veins (Caput Medusa)
Retroperitoneal veins of Retzius
Peri-hepatic veins of Sappey
Consequences of portal hypertension
• Esophageal varices (90% of patients develop this)
• Fibrocongestive Splenomegaly  often gives rise to the syndrome of hypersplenism: a decrease in the life span of all of the formed elements of the blood and a reduction in their circulating numbers.
o Attributed to an increased rate of removal or erythrocytes, leukocytes, and platelets.
• Ascites: the accumulation of fluid in the peritoneal cavity. The amount of fluid may be so great that it not only distends the abdomen but also interferes with breathing.
• Spontaneous Bacterial Peritonitis: extremely dangerous and carries a very high mortality rate even when treated with antibiotics.
• Portasystemic encephalopathy (disease of brain)
• Bleeding will occur in 30% of these patients.
• In women, oligomenorrhea, amenorrhea, and sterility are frequent, owing to hypogonadism.
Hepatic Adenoma
• Are benign tumors of hepatocytes that almost always occur in women during the reproductive years.
• Many have been reported since the introduction of oral contraceptives.
• Usually occur as solitary, sharply demarcated masses of as much as 40cm in diameter and 3 kg in weight.
• 1/3 of patients: tumors bleed into the peritoneal cavity and require treatment as a surgical emergency.
Focal Nodular Hyperplasia
• Is a liver mass composed of fibrous septa and hepatocytic nodules, varying in size from 5-15 cm in diameter and weighing as much as 700 g.
• Cut surface shows a characteristic central scar, form which fibrous septa radiate.
• Does not progress to cancer.
• Most common benign tumor of the liver.
• Small and asymptomatic.
• Usually solitary and <5 cm in diameter.
hepatocellular carcinoma
80%-90% in HBV and HCV associated.
Painful enlarging mass.
Ascites, portal vein thrombosis, occlusion of hepatic veins, esophageal varices.
Malignant cachexia; Rupture with bleeding; hepatic failure.
• Is the presence of stone within the gallbladder lumen or the extrahepatic biliary tree.
• ¾ of gallstones consists primarily of cholesterol, and the remainder consist of calcium bilirubinate and other calcium salts (pigment gallstones).
Cholesterol stones
• Are round or faceted, yellow to tan, and single or multiple, varying from 1-4 cm in greatest dimension.
• >50% of the stone is composed of cholesterol, the rest is calcium salts and mucin.
• During their reproductive period, women are 3-fold more likely than men to develop cholesterol gallstones.
Risk factors of cholesterol stones
o Estrogens increase the hepatic secretion of cholesterol.
o Increasing age
o Obesity
o Membership in some ethnic groups (Chilean women, some northern European groups, Pima Indians)
o Familial predisposition
o Diets high in calories and cholesterol.
o Certain metabolic abnormalities associated with high blood levels of cholesterol.
Black pigment stones
o Contain calcium bilirubinate, bilirubin polymers, calcium salts, and mucin.
o Irregular and measure <1 cm across.
o Surface appears glassy.
o Incidence increased in old and undernourished people—no correlation with gender, ethnicity, or obesity.

However, in most instances, no predisposing cause for the formation of black pigment stones is evident.
Brown pigment stones
o Spongy and laminated, and contain principally calcium bilirubinate mixed with cholesterol and calcium soaps of fatty acids.
o Found more frequently in the intrahepatic and extrahepatic bile ducts than in the gallbladder.
o Almost always associated with bacterial cholangitis, in which Escherichia coli is the predominant organism.
Acute pancreatitis results from the inappropriate activation of pancreatic digestive enzymes and the consequent autodigestion of pancrteatic tissue.
Causes of acute pancreatitis
• Secretion against obstruction
• Bile reflux
• Reflux of duodenal contents
• Intracellular activation of proteases
• Activated pancreatic enzymes
• Protease inhibitors
• Ethanol
• Gallstones
• Drugs, toxins, trauma and viruses.
Chronic pancreatitis
• Longstanding alcohol abuse >90% of cases. This results in progressive destruction of the pancreas, with accompanying irregular fibrosis and chronic inflammation.
Carcinoma of the pancreas
• Smoking
• Chemical carcinogens
• Diabetes Mellitus
• Chronic pancreatitis
• Moleculatr genetics (activation of K-ras,. Over expression of erb B2, loss of tumor surppressor gene DPC-4.
• Courvosier sign: Acute, painless dilatation of the gallblader, jaundice due to obstruction of the common bile duct.
• Migratory Throbophlebitis –10% of patients.
• 50% die in a few months.
• year survival is 8%-10%
• 5-year survival is 2%
Medusa means "sovereign female wisdom," in Sanskrit it's Medha, Greek Metis, Egyptian Met or Maat.
Medusa was originally an aspect of the goddess Athene from Libya where she was the Serpent-Goddess of the Libyan Amazons.
In her images, her hair sometimes resembles dread locks, showing her origins in Africa.