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67 Cards in this Set
- Front
- Back
What are the characteristics of Hepatic Steatosis? |
- First stage in alcoholic liver disease |
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What are the characteristics of Alcoholic Hepatitis?
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- Second stage in alcoholic liver disease
- Requires sustained, long-term consumption of alcohol - Swollen and necrotic hepatocytes with neutrophilic infiltration - Mallory bodies (intracytoplasmic eosinophilic inclusions) are present - AST > ALT (ratio usually >1.5) |
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What are the characteristics of Alcoholic Cirrhosis?
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- Final stage of alcoholic liver disease
- Irreversible changes - Micronodular, irregularly shrunken liver with "hobnail" appearance - Sclerosis around central vein (zone III) - Has manifestations of chronic liver disease (eg, jaundice, hypoalbuminemia) |
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When might you see macrovesicular fatty change in the liver?
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Macrovesicular fatty change is a sign of hepatic steatosis (stage 1 of alcoholic liver disease); reversible with alcohol cessation
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When might you see swollen and necrotic hepatocytes with neutrophilic infiltration and Mallory bodies? |
Alcoholic Heptitis (stage 2 of alcoholic liver disease)
- Mallory Bodies: intracytoplasmic eosinophilic inclusions |
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When might you see a micronodular with a "hobnail" appearance? |
Alcoholic cirrhosis (stage 3 of alcoholic liver disease); irreversible and final form
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Where is there sclerosis in the liver with alcoholic cirrhosis?
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Around the central vein (zone III)
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What causes non-alcoholic fatty liver disease? What changes happen?
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Metabolic syndrome (insulin resistance) → fatty infiltration of hepatocytes → cellular "ballooning" and eventual necrosis
ALT > AST (lipids) (independent of alcohol use) |
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What can non-alcoholic fatty liver disease lead to?
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May cause cirrhosis and hepatocellular carcinoma
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What causes hepatic encephalopathy?
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Cirrhosis → portosystemic shunts → ↓ NH3 metabolism → neuropsychiatric dysfunction
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How severe is hepatic encephalopathy?
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Spectrum from disorientation / asterixis (mild) to difficult arousal or coma (severe)
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What an trigger hepatic encephalopathy?
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- ↑ NH3 production: dietary protein, GI bleed, constipation, infection
- ↓ NH3 removal: renal failure, diuretics, post-TIPS |
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What can lead to ↑ NH3 production? Implications?
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- Dietary protein
- GI bleed - Constipation - Infection - Can be a trigger for hepatic encephalopathy |
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What can lead to ↓ NH3 removal? Implications?
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- Renal failure
- Diuretics - Post-TIPS (Transjugular Intrahepatic Portosystemic Shunt) |
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How do you treat patients with hepatic encephalopathy?
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- Lactulose (removes NH3 by converting to NH4+)
- Low protein diet - Rifaximin (kills intestinal bacteria) |
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What is the most common 1° malignant tumor of the liver in adults?
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Hepatocellular Carcinoma (HCC)
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What is Hepatocellular Carcinoma (HCC) associated with?
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- Hepatitis B & C
- Wilson disease - Hemochromatosis - α1-antitrypsin deficiency - Alcoholic cirrhosis - Aflatoxin from Aspergillus (carcinogen) |
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What can Hepatocellular Carcinoma (HCC) lead to?
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Budd-Chiari Syndrome
- Caused by occlusion of the hepatic veins that drain the liver - Presents with the classical triad of abdominal pain, ascites and hepatomegaly |
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What are the findings in patients with Hepatocellular Carcinoma?
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- Jaundice
- Tender hepatomegaly - Ascites - Anorexia - May lead to Budd-Chiari Syndrome |
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How do you diagnose Hepatocellular Carcinoma (HCC)?
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- ↑ α-Fetoprotein
- Ultrasound - Contrast CT (enhancing heterogenous mass) |
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How does Hepatocellular Carcinoma (HCC) spread?
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Hematogenously
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What are the liver tumors?
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- Hepatocellular Carcinoma (most common)
- Cavernous Hemangioma - Hepatic Adenoma - Angiosarcoma |
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What is the common, benign liver tumor that typically occurs at age 30-50 years?
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Cavernous Hemangioma
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What is the rare, benign liver tumor, often related to oral contraceptive or anabolic steroid use?
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Hepatic Adenoma
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What is the malignant liver tumor of endothelial origin associated with exposure to arsenic and vinyl chloride?
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Angiosarcoma
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What are the characteristics of Cavernous Hemangioma?
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- Common, benign liver tumor
- Typically occurs at age 30-50 years - Biopsy contraindicated because of a risk of hemorrhage |
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What are the characteristics of Hepatic Adenoma?
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- Rare, benign liver tumor
- Often related to oral contraceptive or anabolic steroid use - May regress spontaneously or rupture (abdominal pain and shock) |
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What are the characteristics of Angiosarcoma?
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- Malignant tumor of endothelial organ
- Associated with exposure to arsenic and vinyl chloride |
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What causes the liver to have a "nutmeg" appearance?
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- Backup of blood into liver
- Commonly caused by R-sided heart failure and Budd-Chiari Syndrome - Appears mottled by a nutmeg |
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What can nutmeg liver progress to?
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If the condition persists, centrilobular congestion and necrosis can result in cardiac cirrhosis
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What causes Budd-Chiari Syndrome?
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Occlusion of IVC or hepatic vein with centrilobular congestion and necrosis
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What does Budd-Chiari Syndrome lead to?
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- Congestive liver disease → hepatomegaly, ascites, abdominal pain, and eventual live failure
- May develop varices - May have visible abdominal and back veins |
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What is Budd-Chiari Syndrome associated with?
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- Hypercoagulable states
- Polycythemia vera - Pregnancy - Hepatocellular Carcinoma (HCC) - Absence of JVD |
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How does α1-antitrypsin deficiency cause liver damage?
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Misfolded gene product protein aggregates in hepatocellular ER → cirrhosis
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What is the histologic finding of α1-antitrypsin deficiency in the liver?
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Cirrhosis with PAS (+) globules (made of aggregations of misfolded gene product)
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How do you inherit α1-antitrypsin deficiency?
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Codominant trait
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How does α1-antitrypsin deficiency affect other organs besides the liver?
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In lungs, ↓ α1-antitrypsin → uninhibited elastase in alveoli → ↓ elastic tissue → panacinar emphysema
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What causes jaundice?
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- Bilirubin deposition in the skin and/or sclera causing yellowing
- Occurs at high bilirubin levels (>2.5 mg/dL) in the blood 2° to ↑ production or defective metabolism |
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How high does bilirubin need to be to cause jaundice?
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>2.5 mg/dL in blood
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What are the types of hyperbilirubinemia?
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- Unconjugated (indirect) hyperbilirubinemia
- Conjugated (direct) hyperbilirubinemia - Mixed (direct and indirect) hyperbilirubinemia |
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What is the level of urine urobilinogen in unconjugated (indirect) hyperbilirubinemia? What diseases have this finding? |
- Increased urine urobilinogen
- Diseases: hemolytic, physiologic (newborns), Crigler-Najjar, Gilbert syndrome |
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What is the level of urine urobilinogen in conjugated (direct) hyperbilirubinemia? What diseases have this finding? |
- Decreased urine urobilinogen
Diseases: - Biliary tract obstruction: gallstones, pancreatic liver cancer, liver fluke - Biliary tract disease: 1° sclerosing cholangitis and 1° biliary cirrhosis - Excretion defect: Dubin-Johnson syndrome, Rotor syndrome |
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What is the level of urine urobilinogen in mixed (direct and indirect) hyperbilirubinemia? What diseases have this finding?
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- Normal or ↑
- Diseases: hepatitis or cirrhosis |
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What type of hyperbilirubinemia is seen in patients with hemolysis?
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Unconjugated (indirect) hyperbilirubinemia
- ↑ urine urobilinogen |
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What type of hyperbilirubinemia is seen in newborns?
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Physiologic (don't have enzymes to convert to conjugated form)
- Unconjugated (indirect) hyperbilirubinemia - ↑ urine urobilinogen |
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What type of hyperbilirubinemia is seen in patients with Crigler-Najjar syndrome?
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Unconjugated (indirect) hyperbilirubinemia
- ↑ urine urobilinogen |
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What type of hyperbilirubinemia is seen in patients with Gilbert syndrome?
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Unconjugated (indirect) hyperbilirubinemia
- ↑ urine urobilinogen |
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What type of hyperbilirubinemia is seen in patients with a biliary tract obstruction? What can cause this?
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Causes of biliary tract obstruction:
- Gallstones - Pancreatic liver cancer - Liver fluke Conjugated (direct) hyperbilirubinemia - ↓ urine urobilinogen |
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What type of hyperbilirubinemia is seen in patients with a biliary tract disease? What can cause this?
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Causes of biliary tract disease:
- 1° sclerosing cholangitis - 1° biliary cirrhosis Conjugated (direct) hyperbilirubinemia - ↓ urine urobilinogen |
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What type of hyperbilirubinemia is seen in patients with an excretion defect? What can cause this?
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- Dubin-Johnson Syndrome
- Rotor Syndrome Conjugated (direct) hyperbilirubinemia - ↓ urine urobilinogen |
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What type of hyperbilirubinemia is seen in patients with hepatitis and cirrhosis?
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Mixed (direct and indirect) hyperbilirubinemia
- Normal or ↑ urine urobilinogen |
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What is the most common cause of jaundice in a neonate?
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Physiologic Neonatal Jaundice
- At birth, immature UDP-glucuronosyltrasnferase --> unconjugated hyperbilirubinemia --> jaundice / kernicterus |
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How do you treat a neonate with physiologic jaundice?
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Phototherapy (converts unconjugated bilirubin to water-soluble form
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Which hereditary hyperbilirubinemia is associated with mildly DECREASED UDP-glucuronosyltransferase conjugation activity? What does this lead to?
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Gilbert Syndrome
- Decreased bilirubin uptake by hepatocytes - Asymptomatic or mild jaundice (no clinical consequences) - Elevated unconjugated bilirubin without overt hemolysis - Bilirubin increases with fasting and stress |
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Which hereditary hyperbilirubinemia is associated with ABSENT UDP-glucuronosyltransferase conjugation activity? What does this lead to?
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Crigler-Najjar Syndrome (type I)
- Presents early in life, patients die within a few years - Causes jaundice, kernicterus (bilirubin depostion in brain), and ↑ unconjugated bilirubin |
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Which hereditary hyperbilirubinemia is associated with a black liver? Why?
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Dubin-Johnson Syndrome
- Conjugated hyperbilirubinemia is due to defective liver excretion - Benign |
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Which hereditary hyperbilirubinemia causes a mild conjugated hyperbilirubinemia but without turning th eliver black?
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Rotor Syndrome
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Which syndrome causes bilirubin to increase with fasting or stress? Consequences?
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Gilbert Syndrome
- Mildly ↓ UDP-glucuronosyltransferase conjugation activity - Leads to ↓ bilirubin uptake by hepatocytes - Can be asymptomatic or cause mild jaundice - Elevated unconjugated bilirubin without overt hemolysis |
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What is wrong in Gilbert Syndrome? Symptoms? Other characteristics?
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- Very common, no clinical consequences
- Mildly ↓ UDP-glucuronosyltransferase conjugation activity - Leads to ↓ bilirubin uptake by hepatocytes - Can be asymptomatic or cause mild jaundice - Elevated unconjugated bilirubin without overt hemolysis - Bilirubin ↑ with fasting and stress |
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What is wrong in Crigler-Najjar Syndrome, type 1? Symptoms? Other characteristics?
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- Absent UDP-glucuronosyltransferase
- Presents early in life, patients die within a few years - Findings: jaundice, kernicterus (bilirubin deposition in brain), ↑ unconjugated bilirubin - Treat with plasmapheresis and phototherapy |
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What is wrong in Crigler-Najjar Syndrome, type 2? Symptoms? Other characteristics?
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- Type 2 is less severe
- Responds to phenobarbital which ↑ liver enzyme synthesis |
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What is wrong in Dubin-Johnson Syndrome? Symptoms? Other characteristics?
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- Conjugated hyperbilirubinemia
- Due to defective liver excretion - Grossly black liver - Benign |
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What is wrong in Rotor Syndrome? Symptoms? Other characteristics?
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- Similar to Dubin-Johnson Syndrome (problem with liver excretion of bilirubin)
- Mild conjugated hyperbilirubinemia - Even milder, and doesn't cause black liver |
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What does hemoglobin get converted to during its destruction? Where?
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Bilirubin - takes place in hepatic sinussoid
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Which hereditary syndromes cause a problem with bilirubin uptake and conjugation (1)? Leads to?
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Gilbert Syndrome
- Leads to unconjugated bilirubinemia |
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Which hereditary syndromes cause a problem with bilirubin conjugation (2)? Leads to?
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Crigler-Najjar Syndrome
- Leads to unconjugated bilirubinemia |
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Which hereditary syndromes cause a problem with conjugated bilirubin excretion (3) and (4)? Leads to?
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Dubin-Johnson Syndrome
- Leads to conjugated hyperbilirubinemia Rotor Syndrome - Leads to MILD conjugated hyperbilirubinemia |