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89 Cards in this Set
- Front
- Back
The liver and the gallbladder develop from what embryological structure?
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Ventral foregut
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Most of the blood that enters the liver comes from which vessel--the portal V or the Hepatic A?
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Portal V (75%)
Hepatic A (25%) |
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What are the 4 areas of anastomeses between the portal and systemic venous circulations?1
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1. Gastric and esophageal VV
2. Para-umbilical VV 3. Hemorrhoidal VV 4. Retroperitoneal VV |
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The hepatocytes surrounding the portal tracts are termed the...
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Limiting plate
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What is the least well perfused area of the liver?
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Centrilobar region (zone 3 of acinus)
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What is the best perfused area of the liver?
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Periportal region (zone 1)
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Describe the flow of bile.
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(opposite direction to blood flow)
Centrilobar region --> portal tracts --> small bile canaliculi--> intermediate ductules of Hering --> interlobular bile ducts |
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Where is the majority of bilirubin derived from?
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75% derived from breakdown of RBCs (heme pigment converted to biliverdin, which is then converted to bilirubin)
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How is bilirubin that is formed outside the liver transported?
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It is tightly bound to albumin for transport to the liver
(*Cannot be excreted in urine and cannot pass the blood-brain barrier in this form) |
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If the amount of bilirum exceeds capacity of albumin to bind it, what can be the result?
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Unconjugated (indirect) bilirubin may cross the blood-brain barrer where it tends to localize in the cerebral cortex and basal ganglia causing KERNICTERUS.
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What is kernicterus and what can be the result?
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Accumulation of bilirubin in the cerebral cortex and basal ganglia. This occurs when the amount of bilirubin exceeds the carrying capacity of albumin.
*Can result in brain damage, and if severe enough, DEATH. |
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How and where is bilirubin converted from its insoluble form to its soluble form?
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Bilirubin dissociates from albumin, enters hepatocytes, and is made soluble in the endoplasmic reticulum.
This is accomplished by the enzyme glucuronyl transferase, which conjugates bilirubin to glucoronic acid. |
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How is bilirubin diglucoronide converted to urobilinogen?
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The diglucoronide is split and the bilirubin is converted by small bowel bacteria to urobilinogen.
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What form of bilirubin is reabsorbed into portal circulation to return to the liver or reabsorbed into the general circulation to be excreted by the kidneys?
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Urobilinogen
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What is partially responsible for the normal brown color of stool?
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Urobilin.
Urobilinogen left in the stool is converted to Urobilin. |
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How is jaundice produced?
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Accumulation of bilirubin in the tissues and body fluids
(turns skin and sclera yellow-green color) |
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What are the most frequent causes of jaundice?
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1. Viral hepatitis
2. Cirrhosis 3. Extra-hepatic biliary obstruction 4. Drug-induced cholestasis |
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List 4 mechanisms of bilirubin accumulation.
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1. Excess production of bilirubin
2. Reduced hepatic cell uptake 3. Impaired conjugation 4. Impaired excretion of conjugated bilirubin |
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What will be the result of hemolytic anemia (in reference to its effect on bilirubin)?
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1. Increased levels of unconjugated bilirubin (due to breakdown of RBCs)
2. Mild jaundice |
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What is the major source of intereference in the uptake of unconjugated bilirubin in hepatocytes?
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Drugs
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What is the cause of physiologic jaundice of the newborn?
What is the treatment? |
Immaturity of the hepatic conjugating system
Phototherapy is used to decrease serum bilirubin by breaking down bilirubin into smaller, more polar derivatives that can be excreted in the bile or urine. |
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What might be the cause of breast milk jaundice?
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The presence of glucoronidases in breast milk. May also be presence of glucoronyl transferase inhibition.
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What causes Gilbert syndrome?
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(autosomal dominant disease)
Decreased activity of glucoronyl transferase activity--> impaired conjugation of bilirubin. |
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What syndrome is due a severe defect glucoronyl transferase, resulting in kernicterus?
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Type I Crigler-Najjar syndrome
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What is the difference between Type 1 and Type 2 Crigler-Najjar syndrome?
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Type 1 is far more severe. Bilirubin is NOT conjugated, and results in kernicterus (which is fatal). Autosomal recessive
Type 2 is much less severe. Normal levels of conjugated bilirubin. Not fatal. Similar to Gilbert Syndrome |
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What is cholestasis?
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Any condition in which the flow of bile is obstructed-->results in interference in the excretion of conjugated bilirubin
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What type of lab results are consistent with intrahepatic jaundice?
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1. Increased transaminases
2. Increased LDH 3. Increased prothrombin time |
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Which hereditary disorder results in chronic or recurrent jaundice, mild conjugated bilirubemia, and accumulation of a peculiar dark pigment?
What syndrome is similar to this one, but lacks the hepatic pigmentation? |
Dubin-Johnson syndrome
Rotor syndrome |
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What is the general cause of extrahepatic jaundice?
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Narrowing or obstruction of the biliary tract or ampulla of Vater
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What are the most common causes of extrahepatic jaundice?
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1. Gallstones lodged in common bile duct
2. Bile duct carcinoma 3. Carcinoma of head of pancreas (Acute pancreatitis with swelling of head of pancreas can also be a cause) |
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What causes the formation of "bile lakes" in the liver?
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Rupture of canaliculi produce bile lakes, consisting of dead or dying bile-stained hepatocytes.
(Occurs in obstructive jaundice) |
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What causes pruritis in jaundice?
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Accumulation of bile acids in the blood
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What causes xanthelasma in chronic cholestasis?
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Hypercholesterolemia can result in sharply demarcated, yellowish collections of cholesterol under the skin
(usually begins near inner corner of eye and spreads laterally) *Later tuberous xanthomas may develop on extensor surfaces, pressure areas, and scars. |
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What are some clinical signs and symptoms of obstructive jaundice?
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1. Increased conjugated bilirubin in serum
2. Acholic stools 3. Bilirubinuria 4. Decreased absorption of fats 5. Pruritis Chronic symptoms: 1. Hypercholesterolemia 2. Xanthelasma/ tuberous xanthomas 3. Discoloration of nails 4. Clubbing of digits |
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What sort of lab findings would you expect to find in obstructive jaundice?
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1. Increased ALP (represent damage to biliary epithelium)
2. Increased transaminases 3. Increased LDH |
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What sort of condition results from drugs that interfere with the excretion of conjugated bilirubin from the hepatocytes?
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Cholestasis
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In general, what does the elevation of transaminases indicate?
What does the elevation of alkaline phosphate indicate? |
transaminases --> hepatocellular damage
ALP --> damage to biliary epithelium |
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In individuals with only cholestasis, what levels of ALP or transaminases would you expect?
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Elevated ALP
Norman transaminases |
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What is acute congestion of the liver characterized by?
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Enlarged swollen liver engorged with blood
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What is the cause of "nutmeg liver"?
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Chronic congestion
(Congested central portions of the liver lobules become depressed, but stand out against the paler liver tissue) |
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What is the cause of cardiac sclerosis?
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Chronic congestion
(Long-standing pressure may cause atrophy or necrosis of the liver cells, resulting in fibrosis of the necrotic areas) |
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Occlusion of the hepatic artery is most serious when it occurs where?
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Distal to its last major extrahepatic branch (gastroduodenal A).
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What causes a "Zahn's infarct?"
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Occlusion of a portal vein branch.
(Doesn't lead to a true infarct--demarcated purplish discoloration of the parenchyma, resulting from congestion of sinusoids). |
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What could be some causes of a venous infarction?
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1. Regional infection
2. Thrombus from portal V 3. Hypercoaguable state 4. External compression |
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How is systemic hypotension reflected in the liver?
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Necrosis occurs in the poorly oxygenated centrilobar (zone 3) region.
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Budd-Chiari syndrome results from thrombosis of which veins?
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Major hepatic veins or IVC
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List 2 possible causes of Budd-Chiari syndrome.
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1. Hypercoagulable state
2. Primary carcinoma that extends into hepatic veins |
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What are some symptoms associated with Budd-Chiari syndrome.
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1. Pain and enlargement of liver (acute occlusion)
2. Ascites 3. Hepatic failure--> DEATH |
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Veno-occlusive disease is occurs most frequently in what patients?
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Bone marrow transplant patients who have received high doses of radiation and/or chemotherapy
*Toxic damage to small branches of hepatic veins. |
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What could be some clinical signs of portal vein thrombosis?
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1. Portal hypertension
2. Congestion splenomegaly 3. Ascites |
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In general, what causes portal hypertension?
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Impaired venous flow through portal system.
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List some specific conditions that can lead to portal hypertension.
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1. **Laennec's cirrhosis
2. Budd-Chiari syndrom 3. Veno-occlusive disease 4. Portal vein compression/thrombosis |
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How do the intrahepatic shunts between the hepatic artery and portal vein contribute to increased portal pressure?
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In cirrhosis, these intrahepatic shunts are enlarged, resulting in increased portal pressure
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What are the major symptomatic consequences of portal hypertension?
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1. Ascites
2. Splenomegaly 3. Collateral venous channels |
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Which damaged anastomoses results in esophageal varices?
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Gastroesophageal plexus
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Which collateral venous plexus connects the superior mesenteric V of the portal system with the inferior mesenteric system?
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Hemorrhoidal plexus
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What is the principal cause of death in about half of patients with cirrhosis?
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Bleeding from ruptured esophageal varices
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What condition may develop in patients whose fetal umbilical vein has not become totally obliterated?
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Caput medusa
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Does engorgement of retroperitoneal collateral channels generally produce signs or symptoms or hemorrhages?
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No.
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What are some clinical signs of congestive splenomegaly?
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Hypersplenism may develop which can cause:
1. Anemia 2. Leukopenia 3. Thrombocytopenia *Can lead to Hemorrhagic diathesis (unusual susceptibility to bleeding) |
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Intraperitoneal accumulation of watery fluid.
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Ascites
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Describe the role of renin activity in ascites.
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Decreased blood flow to kidney results in increased renin activity, which results in an increased retention of Na+ and H2O.
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What type of cells might be present in ascitic fluid?
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Mesothelial cells and a few lymphocytes = normal
(RBCs and neutrophils should NOT be present) |
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If RBCs are found in ascitic fluid, what could this indicate?
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Possible involvement of peritoneal surfaces by malignancies
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What does the presence of large numbers of neutrophils in ascitic fluid indicate?
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Peritoneal irritation, most likely peritonitis
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What condition is characterized by purulent bacteria in intrahepatic bile ducts?
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Cholangitis
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How does cholangitis generally begin?
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Extrahepatic biliary obstruction--usually common bile duct obstructed by gallstones
(or carcinoma of head of pancreas) |
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What are some clinical symptoms of cholangitis?
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1. High fever
2. Enlarged liver |
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What is the incubation period for HAV?
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2-6 weeks
*Period of peak infectivity since the virus is shed in the feces during this time. |
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By the time symptoms appear in Hepatitis A, is the virus still being shed?
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No
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Which hepatitis virus consists of a "Dane particle?"
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Hepatitis B
(double shelled particle) |
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What portion of the hepatitis B virus is probably the infections agent?
How is this virus primarily transmitted? |
Dane particle
Parental transmission--blood products or needle-contamination |
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What is the incubation period for Hepatitis B?
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6 weeks - 6 months
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What are the 3 major antigens associated with HBV?
Which ones are associated with the core? |
HBsAg
HBcAg <---core HBeAg <---core |
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Today, most HCV infections are associated with what type of transmission?
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Risky behavior:
1. IV drug use 2. Multiple sex partners 3. Needlestick injury |
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Is a patient more likely to develop a chronic disease with HBV or HCV?
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HCV
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In what circumstance is an HDV infection likely to induce chronic progressive hepatic damage-- in patients with active HBV infection or in HBV carriers?
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HDV infection of HBV carriers is likely to induce chronic progressive hepatic damage
HDV coinfection in patients with an active HBV infection will rarely progress to chronic disease. |
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What is the incubation period of HEV?
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2-9 weeks
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What type of individuals are at a greater risk of developing fulminant hepatitis from an HEV infection?
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Pregnant women
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Which hepatitis virus appears to be non-pathogenic, and may be seen as a co-infection of Hepatitis C?
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Hepatitis G
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What is anicteric hepatitis?
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Hepatitis without the development of increased bilirubin levels, therefore no jaundice appears.
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How is Chronic hepatitis defined?
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Any hepatitis which persists for more than six months
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What is the most common form of cirrhosis?
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Laennec's (alcoholic) cirrhosis
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What type of cirrhosis is frequently associated with hepatocellular carcinoma?
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Postnecrotic cirrhosis
(following episode of viral infection or drug/chemical toxicity) |
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How is copper normally transported in the body after absorption?
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It normally complexes with ceruloplasmin
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How is copper transported in patients with Wilson's disease?
Where is the copper deposited? |
Since there are low levels of ceruloplasmin, the copper in transported by complexing to albumin.
Copper deposits in the liver, brain, kidneys, and cornea |
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Which condition is most common in young children, and consists of fatty liver development associated with encephalopathy? Also associated with the ingestion of Aspirin.
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Reye's syndrome
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What are 2 frequent causes of hepatic failure?
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1. Viral hepatitis
2. Cirrhosis |
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What symptom is not indicative of liver failure, but is almost always present when failure occurs?
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Jaundice
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