COMPREHENSIVE REVIEW QUESTIONS

Comprehensive Review Questions

❓ Q1: What merges with the common hepatic duct?
💡 A1: The cystic duct merges with the common hepatic duct to form the CBD.

❓ Q2: What do the hepatic arteries exit the liver to form?
💡 A2: They exit the liver to form the proper hepatic artery.

❓ Q3: What does the Portal Triad contain?
💡 A3: It contains the MPV (main portal vein), proper hepatic artery, and CBD.

❓ Q4: What is the Portal Triad within the hilum composed of?
💡 A4: Within the hilum, it includes the MPV, proper hepatic artery, and the CHD (common hepatic duct).

❓ Q5: What forms the right boundary of the caudate lobe?
💡 A5: The gallbladder fossa forms the right boundary of the caudate lobe.

❓ Q6: What are the normal liver measurements?
💡 A6: Typically 13.5–15.5 cm. More than 16 cm is considered enlarged.

❓ Q7: For pediatric patients, how far can the normal liver extend?
💡 A7: It should not extend more than 1 cm below the costal margin.

❓ Q8: Between which ribs does the right lobe of the liver lie?
💡 A8: Between the 6th and 10th ribs.

❓ Q9: Where is the right lobe of the liver located?
💡 A9: It lies inferior to the diaphragm, superior to the right kidney, and anterior to the hepatic flexure.

❓ Q10: What is the main lobar fissure, and what does it separate?
💡 A10: The main lobar fissure separates the right and left lobes of the liver.

❓ Q11: Which vessel courses within the right segmental fissure, dividing the anterior and posterior segments?
💡 A11: The right hepatic vein.

❓ Q12: Which region does the lateral left lobe occupy?
💡 A12: It occupies the epigastric region.

❓ Q13: Which vessel courses within the left segmental fissure, dividing the lobes into medial and lateral segments?
💡 A13: The left hepatic vein.

❓ Q14: Where is the caudate lobe located (between which structures)?
💡 A14: It is located between the IVC and the medial left lobe.

❓ Q15: Where does the caudate lobe occupy specifically?
💡 A15: The posterior superior surface of the liver.

❓ Q16: By what structure is the caudate lobe bordered anteriorly?
💡 A16: The ligamentum venosum.

❓ Q17: By what structure is the caudate lobe bordered posteriorly?
💡 A17: The IVC.

❓ Q18: By what structure is the caudate lobe bordered inferiorly?
💡 A18: The main portal vein (MPV).

❓ Q19: What attaches the superior liver to the diaphragm?
💡 A19: The triangular ligament.

❓ Q20: Where is the triangular ligament located?
💡 A20: At the medial and lateral edges of the bare area.

❓ Q21: What does the coronary ligament suspend?
💡 A21: It suspends the posterior superior surface of the liver from the diaphragm.

❓ Q22: To what does the coronary ligament connect anteriorly?
💡 A22: It connects to the falciform ligament.

❓ Q23: What margins does the coronary ligament form?
💡 A23: It forms the anterior and posterior margins of the bare area of the liver.

❓ Q24: Where does the falciform ligament attach?
💡 A24: It attaches the anterior surface of the liver to the abdominal wall, extending from the diaphragm to the umbilicus.

❓ Q25: Through which fissure does the falciform ligament course?
💡 A25: Through the left intersegmental fissure, from the umbilicus to the left portal vein.

❓ Q26: What separates the medial and lateral left lobes?
💡 A26: The ligamentum teres (round ligament).

❓ Q27: What is the ligamentum teres a remnant of?
💡 A27: It is a remnant of the umbilical vein.

❓ Q28: What is another name (AKA) for the ligamentum teres?
💡 A28: The round ligament.

❓ Q29: From where to where does the ligamentum teres run?
💡 A29: From the umbilicus to the inferior surface of the left lobe of the liver.

❓ Q30: How does the ligamentum teres appear sonographically?
💡 A30: As a circular echogenic structure in the left lobe.

❓ Q31: Which vessel has the potential to recanalize with portal hypertension?
💡 A31: The umbilical vein can recanalize within the ligamentum teres.

❓ Q32: What is the ligamentum venosum a remnant of?
💡 A32: It is a remnant of the ductus venosus from fetal circulation.

❓ Q33: What does the ductus venosus allow in fetal circulation?
💡 A33: It allows oxygenated maternal blood to bypass the fetal liver and enter the IVC.

❓ Q34: Describe the umbilical vein’s pathway in fetal circulation.
💡 A34: The umbilical vein → left portal vein → ductus venosus → IVC → right atrium.

❓ Q35: How does the ligamentum venosum appear sonographically?
💡 A35: As a thin echogenic line anterior to the caudate lobe.

❓ Q36: What does the ligamentum venosum separate?
💡 A36: It separates the caudate lobe from the left lobe’s medial segment.

❓ Q37: From where to where does the ligamentum venosum travel?
💡 A37: From the left portal vein to the IVC.

❓ Q38: What is the hepatoduodenal ligament?
💡 A38: Peritoneal folds at the porta hepatis that surround the portal vein, bile duct, and hepatic artery.

❓ Q39: What does the hepatoduodenal ligament contain?
💡 A39: The MPV, the proper hepatic artery, and the common bile duct.

❓ Q40: How does the main lobar fissure divide the liver?
💡 A40: It divides the right and left lobes; more specifically, the right anterior lobe and the medial left lobe.

❓ Q41: What does the main lobar fissure contain?
💡 A41: The middle hepatic vein.

❓ Q42: Anatomically, what does the main lobar fissure connect?
💡 A42: It connects the gallbladder (GB) to the IVC fossa.

❓ Q43: How does the main lobar fissure appear sonographically?
💡 A43: As an echogenic line between the gallbladder and right portal vein.

❓ Q44: Which fissure divides the right lobe into anterior and posterior segments (coronal plane)?
💡 A44: The right intersegmental fissure.

❓ Q45: What does the right intersegmental fissure contain?
💡 A45: The right hepatic vein.

❓ Q46: How does the left intersegmental fissure divide the liver?
💡 A46: It divides the left lobe into medial and lateral segments (sagittal division).

❓ Q47: What does the left intersegmental fissure contain?
💡 A47: The left hepatic vein, falciform ligament, and ligamentum teres.

❓ Q48: Each of the eight segments in the Couinaud system has its own segment of which structures?
💡 A48: Each segment has its own branch of the portal vein, hepatic vein, hepatic artery, and bile duct.

❓ Q49: What are the three main lobes of the Couinaud system?
💡 A49: The right lobe, left lobe, and the caudate lobe.

❓ Q50: How is the liver divided into four segments according to hepatic veins?
💡 A50: By the longitudinal course of the hepatic veins.

❓ Q51: In the transverse plane, how is the liver divided?
💡 A51: By the branching of the portal vessels.

❓ Q52: By which imaginary line are the right and left lobes separated?
💡 A52: From the gallbladder fossa to the IVC (Rex–Cantlie line).

❓ Q53: What is this imaginary line called?
💡 A53: The Rex–Cantlie line.

❓ Q54: By what are the right and left lobes divided?
💡 A54: By the branches of the main portal vein.

❓ Q55: Into which segments is the right lobe segmented?
💡 A55: Two anterior and two posterior lobes.

❓ Q56: Into which segments is the left lobe segmented?
💡 A56: Two medial and two lateral segments.

❓ Q57: How do hepatic veins divide the liver?
💡 A57: Longitudinally into segments 2, 4, 7, 8.

❓ Q58: Which ligament separates segment 1 from segment 2?
💡 A58: The ligamentum venosum.

❓ Q59: Which structures separate segment 1 from segment 4?
💡 A59: The left portal vein and the middle hepatic vein.

❓ Q60: Where are segments 2 and 3 located?
💡 A60: To the left of the ligamentum venosum.

❓ Q61: Which ligament separates segment 3 from segment 4?
💡 A61: The falciform ligament.

❓ Q62: Which fissure separates segment 4 from segments 5 and 8?
💡 A62: The main lobar fissure.

❓ Q63: Which vein separates segments 5 and 8 from segments 6 and 7?
💡 A63: The right hepatic vein.

❓ Q64: What is the right branch of the celiac axis?
💡 A64: The common hepatic artery.

❓ Q65: From where does the common hepatic artery originate?
💡 A65: From the superior mesenteric artery (SMA).

❓ Q66: What does the common hepatic artery supply?
💡 A66: The liver, gallbladder, and stomach.

❓ Q67: How much blood does the hepatic artery carry, and what is its oxygen content?
💡 A67: It carries about 20% of the blood to the liver but has a high oxygen content of ~95%.

❓ Q68: How much blood does the portal vein carry, and what is its oxygen content?
💡 A68: It carries about 80% of the blood to the liver but has a lower oxygen content (~85%).

❓ Q69: Which vessel delivers more blood volume to the liver?
💡 A69: The main portal vein delivers more total blood volume, despite lower oxygen concentration.

❓ Q70: What are the branches of the common hepatic artery?
💡 A70: The gastroduodenal artery branches off, after which it becomes the proper hepatic artery.

❓ Q71: What does the proper hepatic artery supply?
💡 A71: The liver and gallbladder.

❓ Q72: How can the proper hepatic artery be identified sonographically?
💡 A72: It lies anterior and to the left of the portal vein as it enters the liver.

❓ Q73: From which artery does the cystic artery usually branch?
💡 A73: From the right hepatic artery.

❓ Q74: What are some indications to scan the common hepatic artery?
💡 A74: Chronic liver disease, liver transplant (pre- and post-op), trauma.

❓ Q75: How is the common hepatic artery best visualized on ultrasound?
💡 A75: In the transverse plane using the “right wing of the bird” sign.

❓ Q76: How does the common hepatic artery travel relative to the pancreas?
💡 A76: It travels along the superior border of the head of the pancreas.

❓ Q77: What does the gastroduodenal artery supply?
💡 A77: The head of the pancreas, the pylorus of the stomach, and the proximal duodenum.

❓ Q78: What is the normal resistance of the hepatic artery?
💡 A78: It shows low resistance with an RI of approximately 0.55–0.8.

❓ Q79: The hepatic artery is considered what type of vessel?
💡 A79: A tortuous vessel, which can invalidate peak velocity measurements if not carefully assessed.

❓ Q80: With which diseases does hepatic artery flow resistance increase?
💡 A80: Cirrhosis, metastasis, and lymphoma.

❓ Q81: What does it imply if the RI in the hepatic artery is >0.8?
💡 A81: It can imply portal hypertension, hepatic congestion, transplant rejection, or chronic hepatocellular disease.

❓ Q82: How does the hepatic artery appear postprandially (after eating)?
💡 A82: Normally, it shows an increased resistive index (RI) due to increased portal inflow.

❓ Q83: How does the hepatic artery appear postprandially in a cirrhotic patient?
💡 A83: There may be diminished changes in the RI after eating because of compromised flow.

❓ Q84: What does the portal venous system do?
💡 A84: It drains blood from the digestive tract and delivers it to the liver for filtration.

❓ Q85: How is the portal venous system formed?
💡 A85: The inferior mesenteric vein (IMV) joins the splenic vein near the tail of the pancreas; then the splenic vein joins the superior mesenteric vein (SMV) to form the portal vein.

❓ Q86: Where is the confluence of the superior mesenteric vein (SMV) and splenic vein (SV)?
💡 A86: Posterior to the head of the pancreas.

❓ Q87: What is the confluence of the SMV and SV called?
💡 A87: The portal confluence.

❓ Q88: Where is the main portal vein (MPV) located?
💡 A88: Slightly right of midline, anterior to the IVC. It enters the porta hepatis and bifurcates inside the liver into the right and left portal veins.

❓ Q89: What does the MPV drain?
💡 A89: It drains blood from the GI tract and sends it to the liver for filtration.

❓ Q90: The MPV enters the liver carrying blood drained from where?
💡 A90: From the digestive system.

❓ Q91: What is the portal vein’s oxygen content?
💡 A91: Around 85%.

❓ Q92: What is the hepatic artery’s oxygen content?
💡 A92: About 95%.

❓ Q93: What does a normal hepatic artery waveform look like?
💡 A93: Low-resistance, monophasic flow.

❓ Q94: What characterizes an abnormal hepatic artery waveform?
💡 A94: High-resistance or biphasic flow is considered abnormal.

❓ Q95: Where do the main portal branches enter?
💡 A95: They enter the center of the liver lobes supplied (intrasegmental vessels).

❓ Q96: What are the main portal branches considered?
💡 A96: Intrasegmental vessels.

❓ Q97: Into what do hepatic veins divide the liver?
💡 A97: They divide it into lobes (intersegmental veins).

❓ Q98: How are hepatic veins described?
💡 A98: They are intersegmental.

❓ Q99: What do portal vessels do in size as they course through the liver?
💡 A99: They decrease in size.

❓ Q100: What do hepatic veins do in size when near the diaphragm (exiting the liver)?
💡 A100: They increase in size near the diaphragm.

❓ Q101: What is the normal pressure of the portal vein?
💡 A101: About 5–10 mmHg.

❓ Q102: How do portal flow rates and diameter change after exercise or when patients are upright?
💡 A102: They tend to decrease.

❓ Q103: How do portal flow rate and diameter change with inspiration and after eating?
💡 A103: They tend to increase.

❓ Q104: A normal portal vein will increase its diameter by more than 20% with what maneuver?
💡 A104: Deep inspiration.

❓ Q105: How is the MPV identified on ultrasound (US)?
💡 A105: Using an oblique subcostal approach and rotating slightly; the portal vein appears tubular from the head of the pancreas to the liver.

❓ Q106: How else is the MPV identified on US?
💡 A106: It has thicker, more echogenic walls than the hepatic veins and enters the liver at the porta hepatis.

❓ Q107: Where should the measurement of the portal vein be obtained?
💡 A107: At the point where the portal vein crosses the IVC.

❓ Q108: How should the MPV be measured?
💡 A108: From inner to inner wall.

❓ Q109: What does deep inspiration do to the portal vein diameter in normal patients?
💡 A109: It can increase the diameter up to 50%.

❓ Q110: If there is no diameter change with respiration, what might be suspected?
💡 A110: Portal hypertension.

❓ Q111: What is the normal diameter of the MPV?
💡 A111: Less than 13 mm.

❓ Q112: How is the MPV typically evaluated with Doppler?
💡 A112: In a transverse/oblique plane from the subcostal position.

❓ Q113: Which direction does normal MPV flow go?
💡 A113: Toward the liver (hepatopetal).

❓ Q114: What does Doppler evaluation of the MPV show?
💡 A114: Continuous flow with mild respiratory/cardiac variation.

❓ Q115: What is the normal velocity of the MPV?
💡 A115: A low velocity ~15–20 cm/s; it can increase after eating.

❓ Q116: What might happen in MPV Doppler with liver disease?
💡 A116: There can be increased resistance to flow or even flow reversal.

❓ Q117: How do hepatic veins course through the liver?
💡 A117: From inferior to superior.

❓ Q118: How do portal veins course through the liver?
💡 A118: Transversely.

❓ Q119: On color Doppler, how will the anterior branch of the right portal vein appear?
💡 A119: It will appear red.

❓ Q120: On color Doppler, how will the posterior right portal vein appear?
💡 A120: It will appear blue.

❓ Q121: Where does the splenic vein originate?
💡 A121: At the splenic hilum.

❓ Q122: How does the splenic vein course?
💡 A122: It courses posterior to the pancreas, meeting the inferior mesenteric vein, then joining the SMV to form the MPV.

❓ Q123: What does the splenic vein drain?
💡 A123: The stomach, spleen, and pancreas.

❓ Q124: How does the splenic vein appear on ultrasound (US)?
💡 A124: In transverse view, it is a tubular structure posterior to the body and tail of the pancreas.

❓ Q125: What is the normal flow of the splenic vein?
💡 A125: Toward the liver and away from the spleen.

❓ Q126: Where does the superior mesenteric vein (SMV) originate?
💡 A126: At the mesentery.

❓ Q127: What does the SMV drain?
💡 A127: The small intestine and the proximal colon.

❓ Q128: How is the SMV best seen on ultrasound?
💡 A128: In the longitudinal view as a tubular structure to the right of the SMA.

❓ Q129: How is the SMV identified in transverse view?
💡 A129: As a circular structure to the right of the SMA.

❓ Q130: What does the inferior mesenteric vein drain?
💡 A130: The distal colon.

❓ Q131: Which are the largest abdominal IVC tributaries?
💡 A131: The hepatic veins.

❓ Q132: Where do the hepatic veins enter?
💡 A132: Just below the IVC.

❓ Q133: What does the hepatic venous system do?
💡 A133: It drains blood from the liver and returns it to the heart.

❓ Q134: Between which structures do the hepatic veins course?
💡 A134: Between the liver segments (intersegmental).

❓ Q135: In which direction do the hepatic veins course?
💡 A135: From inferior to superior (vertically) through the liver to join the IVC.

❓ Q136: Which three branches come together to join the IVC superior to the liver?
💡 A136: The right, middle, and left hepatic veins.

❓ Q137: What does the right hepatic vein drain, and how does it divide the right lobe?
💡 A137: It drains the right lobe, dividing it into anterior and posterior segments.

❓ Q138: What does the left hepatic vein drain, and what does it divide?
💡 A138: It drains the left lobe, dividing it into medial and lateral segments.

❓ Q139: What does the middle hepatic vein (MHV) drain, and what does it divide?
💡 A139: It drains the left medial and right anterior lobes, dividing the liver into right and left lobes.

❓ Q140: What is the most common variation in hepatic vein anatomy?
💡 A140: An accessory right hepatic vein.

❓ Q141: What are some indications to scan the hepatic veins?
💡 A141: CHF (increased liver outflow resistance), thrombosis, tumor mass effect, hepatic congestion, Budd–Chiari, cirrhosis, chronic hepatitis.

❓ Q142: How do we Doppler the middle and left hepatic veins?
💡 A142: Usually in a transverse plane.

❓ Q143: How do we Doppler the right hepatic vein?
💡 A143: Longitudinal approach.

❓ Q144: What is the direction of hepatic vein flow?
💡 A144: Away from the liver (hepatofugal).

❓ Q145: What type of pulsatility do hepatic veins exhibit?
💡 A145: They show more cardiac pulsatility and respiratory phasicity than portal veins.

❓ Q146: How is the flow considered in the hepatic veins?
💡 A146: Triphasic, due to right atrial contraction, relaxation, and filling.

❓ Q147: What does normal hepatic vein flow demonstrate?
💡 A147: Two large antegrade diastolic and systolic waves followed by a small retrograde component (atrial contraction).

❓ Q148: What is the functional unit of the liver?
💡 A148: Lobules.

❓ Q149: Of what are lobules composed?
💡 A149: Hepatocytes.

❓ Q150: Where do hepatocytes surround?
💡 A150: The periphery of the veins in each lobule.

❓ Q151: What do these hepatocytes do?
💡 A151: They synthesize, metabolize, and excrete compounds.

❓ Q152: What are venous sinusoids?
💡 A152: Tiny blood reservoirs within the liver tissues.

❓ Q153: What do the walls of the sinusoids contain?
💡 A153: Endothelial and Kupffer cells that phagocytize bacteria and foreign materials.

❓ Q154: What is included under hepatic function?
💡 A154:

• Metabolism of digestive products
• Storage of vitamins, iron, glycogen, fat, amino acids
• Detoxification
• Bile production/excretion
• Albumin/globulin formation
• Lymph production

❓ Q155: What is included under metabolism of digestive products?
💡 A155: Carbohydrates (blood sugar maintenance), fats (energy), proteins (amino acids).

❓ Q156: What does hepatic detoxification entail?
💡 A156: Removing poisonous substances, bacteria, and alcohol.

❓ Q157: What does bile production and excretion mean for hepatic function?
💡 A157: It’s the exocrine function; liver cells conjugate bilirubin and the bile canaliculi secrete bile into the ductal system.

❓ Q158: Which liver function tests (LFTs) and tumor markers are commonly used?
💡 A158:

• AST (Aspartate Aminotransferase)
• ALT (Alanine Aminotransferase)
• ALP (Alkaline Phosphatase)
• GGTP (Gamma-Glutamyl Transpeptidase)
• LDH (Lactic Dehydrogenase)
• PT (Prothrombin Time)
• Tumor Markers: AFP, CA 125, CA 72-4, CA 19-9, CEA, HCG, Direct/Indirect Bilirubin, Hematocrit, Albumin

❓ Q159: What is Aspartate Aminotransferase (AST), and when does it increase?
💡 A159: Found in the liver, kidneys, skeletal/heart muscle, and brain. It increases with acute hepatitis, cirrhosis, metastases, and Reye syndrome. Mild increase with fatty liver. Not elevated with isolated biliary obstruction.

❓ Q160: What is Alanine Aminotransferase (ALT)?
💡 A160: Needed for energy; released when liver cells are damaged. Used to evaluate jaundice, monitor hepatitis/cirrhosis. Elevated in liver tumors, biliary obstruction, etc.

❓ Q161: When do we see a higher ratio of AST than ALT?
💡 A161: With alcoholic liver disease, cirrhosis, and liver metastasis (indicates liver damage, necrosis).

❓ Q162: When do we see a higher ratio of ALT than AST?
💡 A162: With acute hepatitis and nonmalignant hepatic obstruction.

❓ Q163: What is Alkaline Phosphatase (ALP)?
💡 A163: An enzyme from liver, bone, placenta. It increases with biliary obstruction or liver disease if other LFTs are elevated. If ALP alone is high, bone disease, pregnancy, or hyperparathyroidism may be a cause.

❓ Q164: What is Gamma-Glutamyl Transpeptidase (GGTP)?
💡 A164: Found in liver cells/biliary epithelium. Most sensitive for alcoholism. Marked increase in liver disease or post-hepatic biliary obstruction. Moderate increase with drug/alcohol-induced damage.

❓ Q165: What is Lactic Dehydrogenase (LDH)?
💡 A165: Increases with liver damage (cancer, cirrhosis, chronic viral hepatitis), but is nonspecific because many organs have LDH.

❓ Q166: What does Prothrombin Time (PT) measure?
💡 A166: It checks levels of clotting factors. The liver produces one of these factors, so liver disease can prolong PT (risk of hemorrhage). Increasing vitamin K intake can lower PT unless there’s parenchymal liver disease.

❓ Q167: What are tumor markers?
💡 A167: Substances associated with specific cancers, such as AFP, CA 125, CA 19-9, CEA, etc.

❓ Q168: When is PT increased or prolonged?
💡 A168: With metastasis, liver disease, anticoagulant therapy (e.g., Coumadin), or prolonged biliary obstruction.

❓ Q169: If PT is increased and vitamin K administration does not improve it, what does that indicate?
💡 A169: Parenchymal liver disease rather than obstructive disease.

❓ Q170: What is INR (International Normalized Ratio)?
💡 A170: A standardized measure of PT.

❓ Q171: What is a normal INR?
💡 A171: 0.9–1.3 is considered normal.

❓ Q172: For a patient on coagulotherapy, what is a normal INR range?
💡 A172: About 2.0–3.0.

❓ Q173: What is Alpha-Fetoprotein (AFP)?
💡 A173: A protein produced by fetal liver/yolk sac, minimal in normal adults. Elevated in primary liver cancers, metastases, hepatitis, nonseminomatous testicular cancer, and pregnancy. Greatly increased with HCC.

❓ Q174: When is CA-125 elevated?
💡 A174: Ovarian cancer, endometriosis, lung cancer.

❓ Q175: When is CA 72-4 elevated?
💡 A175: Ovarian cancer, gastrointestinal cancers.

❓ Q176: When is CA 19-9 elevated?
💡 A176: Pancreatic cancer, can also be elevated with colorectal/bile duct cancers.

❓ Q177: What is Human Chorionic Gonadotropin (HCG)?
💡 A177: A tumor marker for testicular cancers.

❓ Q178: What is Direct Bilirubin?
💡 A178: Conjugated bilirubin used by the liver for digestion. Elevated in biliary tract obstruction, hepatitis, cirrhosis.

❓ Q179: What is Indirect Bilirubin?
💡 A179: Unconjugated bilirubin. Elevated with liver cell disease/damage or anemia. Usually total bilirubin minus direct = indirect.

❓ Q180: What is Hematocrit?
💡 A180: The percentage of RBCs in blood; decreases with internal bleeding.

❓ Q181: What is Albumin?
💡 A181: A protein controlling water distribution/osmotic pressure. Elevated with dehydration/hemolysis. Decreased with chronic liver disease, CHF, inflammation. Low albumin → ascites/ fluid issues.

❓ Q182: What is Jaundice?
💡 A182: Elevated serum bilirubin causing yellow skin/eyes, pale stools, dark urine.

❓ Q183: How do we differentiate hepatic jaundice from obstructive jaundice?
💡 A183: By measuring CBD. If ducts are normal in size, it’s likely hepatic jaundice (liver disease). If dilated, it’s obstructive.

❓ Q184: What causes hepatic jaundice?
💡 A184: Liver disease (hepatocellular problems).

❓ Q185: What causes obstructive jaundice?
💡 A185: Biliary obstruction.

❓ Q186: What is pre-hepatic jaundice caused by?
💡 A186: Hepatocellular disease (destruction of hepatocytes).

❓ Q187: What is hepatic jaundice typically caused by?
💡 A187: Hemolytic disease; the liver cells can’t properly conjugate bilirubin.

❓ Q188: What causes post-hepatic jaundice?
💡 A188: Mechanical obstruction of the biliary tree.

❓ Q189: What is agenesis?
💡 A189: Absence of liver formation.

❓ Q190: What is an accessory fissure?
💡 A190: Caused by infoldings of the peritoneum; it’s rare.

❓ Q191: What is partial situs inversus?
💡 A191: Abdominal contents reversed, e.g., liver in the left upper quadrant.

❓ Q192: What is complete situs inversus?
💡 A192: Thoracic and abdominal contents reversed (liver in left upper quadrant, heart in right chest).

❓ Q193: What is a diaphragmatic hernia?
💡 A193: A hole in the diaphragm (the muscle separating chest from abdomen).

❓ Q194: What is a Riedel lobe?
💡 A194: An extension of the right lobe below the lower pole of the right kidney, more common in women.

❓ Q195: What is Caroli Disease?
💡 A195: A cystic dilation of intrahepatic bile ducts communicating with a normal bile duct (“communicating cavernous ectasia”), a congenital defect with numerous biliary cysts.

❓ Q196: What does ectasia mean?
💡 A196: Dilation or distension.

❓ Q197: What does stasis mean?
💡 A197: No movement or activity (e.g., no flow).

❓ Q198: If simple cysts are identified in the liver before age 50, what are they usually related to?
💡 A198: Polycystic disease (and also cysts in kidneys, pancreas, ovaries).

❓ Q199: What are simple cysts?
💡 A199: Fluid-filled spaces with endothelial lining, normal LFTs, usually appear after age 50.

❓ Q200: What are the sonographic criteria for a cyst?
💡 A200: Smooth borders, regular walls, anechoic, through transmission, posterior enhancement.

❓ Q201: What is a hemorrhagic cyst?
💡 A201: Occurs when blood leaks into an existing cyst, forming a thrombus inside.

❓ Q202: What is Polycystic Liver Disease (PCLD)?
💡 A202: An autosomal dominant disorder, usually presenting at 30–40 years, with multiple noncommunicating cysts in the liver; normal LFTs; also cysts in kidneys, pancreas, ovaries.

❓ Q203: What are biliary hamartomas?
💡 A203: Focal developmental lesions of dilated intrahepatic ducts in dense stroma (Von Meyenburg Complex).

❓ Q204: What is another name for biliary hamartomas?
💡 A204: Von Meyenburg Complex.

❓ Q205: What is the sonographic appearance of biliary hamartomas?
💡 A205: Small echogenic or hypoechoic nodules causing a heterogeneous liver. They can be multiple, well-defined, <1 cm. Associated with congenital hepatic fibrosis, ADPKD, cholangiocarcinoma.

❓ Q206: What does anechoic mean?
💡 A206: Without echoes (“black” on ultrasound).

❓ Q207: What does hyperechoic mean?
💡 A207: Brighter echoes compared to the reference structure.

❓ Q208: What does hypoechoic mean?
💡 A208: Fewer echoes, appearing darker than the reference structure.

❓ Q209: What does isoechoic mean?
💡 A209: Same level of echoes as the compared structure.

❓ Q210: Which organs are typically the most hyperechoic?
💡 A210: (From greatest to lesser) 1) Renal sinus, 2) Pancreas, 3) Liver, 4) Spleen.
Renal parenchyma is more hypoechoic.

❓ Q211: What is fatty infiltration (steatosis)?
💡 A211: Excess fat (triglycerides) in hepatocytes, a reversible condition (e.g., from diabetes, alcohol, obesity, etc.); elevated AST/ALT.

❓ Q212: What does steatosis mean?
💡 A212: Too much fat in the liver.

❓ Q213: What is diffuse replacement?
💡 A213: Entire liver is involved with fatty infiltration.

❓ Q214: How is focal fatty sparing defined?
💡 A214: Most of the liver is fatty, except one or more localized areas remain normal (hypoechoic).

❓ Q215: What is focal fatty replacement?
💡 A215: Only a small portion of the liver has fatty infiltration, while the rest is normal.

❓ Q216: How can contrast ultrasound examination help differentiate focal sparing/infiltration from mass formation?
💡 A216: A truly malignant mass will show contrast washout, but fatty changes remain consistent on contrast imaging.

❓ Q217: What measurement indicates hepatomegaly?
💡 A217: >15.5 cm (superior–inferior) in the midclavicular line.

❓ Q218: What is focal infiltration?
💡 A218: A localized hyperechoic area, possibly adjacent to portal structures, not displacing them.

❓ Q219: What is focal sparing?
💡 A219: A hypoechoic region in a diffusely fatty liver, often near the GB fossa, not displacing structures.

❓ Q220: What is amyloid disease, and how does it involve the liver?
💡 A220: Deposition of amyloid protein in vessel walls leading to organ failure; it can involve the liver.

❓ Q221: What is glycogen storage disease?
💡 A221: Autosomal recessive disorder (a.k.a. von Gierke disease) with excess glycogen in hepatocytes, often forming adenomas.

❓ Q222: What happens when glycogen storage is reduced in the hepatocytes?
💡 A222: Prominent portal walls, possibly mimicking acute hepatitis (“starry sky”).

❓ Q223: What is hemochromatosis?
💡 A223: Abnormal iron deposition in multiple organs.

❓ Q224: What is Wilson disease?
💡 A224: Autosomal recessive copper metabolism disorder. Presents with jaundice, hematemesis, portal hypertension, Kayser–Fleischer rings, increased AST/ALT, decreased albumin, echogenic fatty liver, fibrotic periportal thickening.

❓ Q225: What is cirrhosis, and its common features?
💡 A225: Diffuse irreversible liver damage (fibrosis, nodules). Presents with ascites, jaundice, atrophy, splenomegaly, weight loss. Elevated AST, ALT, ALP, indirect bilirubin, etc. Commonly from Hep C or alcohol.

❓ Q226: What are the stages of cirrhosis?
💡 A226:

• Early: Hepatomegaly, diffuse echogenicity
• Late: Smaller liver, coarse texture, nodules, ascites, edema.
  • Micronodular (alcoholism) or macronodular (chronic viral hepatitis).

❓ Q227: What is hepatitis, and what causes it?
💡 A227: Inflammation of the liver. Reversible. Causes: viruses (A, B, C, etc.), toxins, autoimmune, or medications.

❓ Q228: What characterizes acute hepatitis?
💡 A228: Organ enlargement, diffuse decreased echogenicity, periportal cuffing (“starry night”), possible ascites, GB wall thickening.

❓ Q229: What characterizes chronic hepatitis?
💡 A229: Smaller liver, increased echogenicity, poor portal visualization, possible granulomas. Elastography can measure fibrosis.

❓ Q230: What is hydatid disease (Echinococcal cysts)?
💡 A230: Caused by parasites from feces of infested animals. Infects liver via portal system. Early: cyst with debris. Late: large “daughter cysts,” honeycomb, “water lily” sign.

❓ Q231: What is schistosomiasis?
💡 A231: A fluke parasite from polluted water. The portal vein carries ova to the liver, causing periportal fibrosis and portal hypertension. It’s the most common parasitic infection globally.

❓ Q232: What is Pneumocystis jirovecci?
💡 A232: Formerly Pneumocystis carinii, a yeast-like fungus in immunosuppressed patients (AIDS). Causes echogenic foci in the liver without shadowing.

❓ Q233: What are granulomatous infections?
💡 A233: Systemic fungal infections (e.g., histoplasmosis, tuberculosis). Histoplasmosis from bird/bat droppings, TB from airborne germs.

❓ Q234: What is a hepatic abscess?
💡 A234: Can be pyogenic, amebic, or fungal, presenting with fever, nausea, diarrhea, RUQ pain, hepatomegaly, high LFTs, leukocytosis.

❓ Q235: How do we evaluate liver neoplasms on ultrasound?
💡 A235: Check if it is intrahepatic (pushing outward) or extrahepatic (pushing inward on capsule). Evaluate vascular flow, echotexture, displacement.

❓ Q236: What is a hemangioma?
💡 A236: The #1 benign liver lesion, usually asymptomatic, can enlarge with estrogen. Typically hyperechoic and homogeneous with posterior enhancement.

❓ Q237: What is Kasabach–Merritt syndrome?
💡 A237: Hemangioma–thrombocytopenia syndrome in infants with large hemangiomas. Platelets are destroyed, leading to thrombocytopenia.

❓ Q238: What is infantile hemangioendothelioma?
💡 A238: The most common benign vascular liver tumor in infancy, presents <6 months of age, can cause heart failure due to AV malformation. Often regresses by age 2.

❓ Q239: What is focal nodular hyperplasia (FNH)?
💡 A239: The second most common benign liver mass. Usually <5 cm, isoechoic with a central scar and radial vessels. Contrast flow differs from adenoma or malignancy.

❓ Q240: What is a hepatic adenoma?
💡 A240: Strongly linked to oral contraceptives and glycogen storage disease. A well-defined, usually hypoechoic solid tumor. Surgery if risk of hemorrhage or malignancy.

❓ Q241: What is hepatocellular carcinoma (HCC)?
💡 A241: The most common primary malignant tumor of the liver. Elevated liver enzymes, moderate AFP. Common in cirrhotic livers. Often multiple nodules. Can invade vessels.

❓ Q242: What is fibrolamellar carcinoma?
💡 A242: A subtype of HCC in adolescents/young adults without liver disease. Normal AFP, large solitary mass, can show calcifications and a central scar.

❓ Q243: What is hepatoblastoma?
💡 A243: The #1 pediatric primary liver malignancy, usually before age 2, associated with Beckwith–Wiedemann. Elevated AFP, abdominal enlargement.

❓ Q244: What is hepatic metastatic disease?
💡 A244: The most common solid mass in the liver. Often from gallbladder, colon, pancreas, breast, or lung cancers. Multiple variable-appearance lesions. Rapid washout on contrast US.

❓ Q245: What is Kaposi sarcoma?
💡 A245: A connective tissue malignancy seen with HIV/AIDS, can involve liver, skin, lungs, GI tract.

❓ Q246: What is lymphoma?
💡 A246: A malignancy of the lymphatic system, including Non-Hodgkin’s lymphoma. Solid tumors, possibly single or multiple, often hypoechoic or complex.

❓ Q247: What is Budd–Chiari syndrome?
💡 A247: Obstruction of hepatic veins by thrombus/tumor. Associated with contraceptives, HCC, renal carcinoma, adrenal carcinoma, polycythemia. Pain, jaundice, ascites, portal HTN.

❓ Q248: What is the sonographic appearance of Budd–Chiari syndrome?
💡 A248: Varies with obstruction degree: missing hepatic veins, echogenic thrombi, hepatomegaly, caudate hypertrophy, IVC compression, ascites, splenomegaly, reversed or slowed portal flow.

❓ Q249: What does air in the hepatic veins indicate?
💡 A249: Can lead to pulmonary embolism, often bacterial infection introducing gas. Shows mobile echogenic foci, ring-down, dirty shadow.

❓ Q250: What is a hepatic infarct?
💡 A250: Loss of arterial supply to part of the liver. A wedge-shaped defect, widest at periphery, appearing hypoechoic with no flow.

❓ Q251: What is hepatic congestion?
💡 A251: Hepatomegaly from poor venous outflow, often CHF. Palpable liver, elevated LFTs.

❓ Q252: How does hepatic congestion appear sonographically?
💡 A252: Enlarged liver, possibly IVC dilation, signs of heart failure. Palpable liver, increased LFTs.

❓ Q253: When is the IVC considered dilated?
💡 A253: When >2.5 cm diameter. It may lose respiratory phasicity with CHF or other circulatory issues. Thrombus can form if stasis.

❓ Q254: What is portal hypertension?
💡 A254: A portal venous system pressure >5–10 mmHg, typically from cirrhosis. Signs include caput medusae, varices, ascites. Evaluate portal vein diameter/flow direction/velocity.

❓ Q255: What are causes of portal vein thrombosis?
💡 A255: Non-tumoral: portal HTN, inflammation, trauma, surgery. Tumoral: HCC, metastasis, compression by masses. Symptoms: pain, fever, rigid abdomen, elevated LFTs.

❓ Q256: What is the sonographic appearance of portal vein thrombosis?
💡 A256:

• Acute: Echogenic debris, >13 mm diameter, no flow
• Chronic: More echogenic, <13 mm, cavernous transformation with collateral vessels

❓ Q257: What is tumor invasion of the portal vein?
💡 A257: Malignant thrombus, typically from HCC. Shows arterial flow in the thrombus. Thrombus can form around tumor, obstructing flow.

❓ Q258: What is a portosystemic or portal–caval shunt?
💡 A258: A procedure (like TIPS) to reduce portal hypertension by bypassing the liver. Commonly between MPV and RHV. Evaluate patency, direction (hepatofugal), velocities, complications.

❓ Q259: What is the sonographic appearance of a portosystemic (portal–caval) shunt?
💡 A259:

• Early post-placement: Air can hamper US
• Shunt walls echogenic
• Watch for stenosis (neointimal hyperplasia)
• Normal flow: portal → hepatic
• Peak velocity 50–200 cm/s

❓ Q260: What are direct signs of portal shunt failure?
💡 A260:

• Absent flow in the shunt
• Hepatopetal flow in intrahepatic branches
• Hepatofugal flow in main portal vein
• Main portal velocity <30 cm/s
• Reverse hepatic vein flow

❓ Q261: What are secondary signs of shunt failure?
💡 A261:

• Recanalization of the umbilical vein
• Ascites reaccumulation
• Reappearance of varices

❓ Q262: What is portal venous gas?
💡 A262: Caused by ulcerative colitis, necrotizing enterocolitis, or other pathology. Shows echogenic bands in portal flow near liver periphery, with dirty shadow/ring-down.

❓ Q263: What is a portal vein aneurysm?
💡 A263: Congenital or from portal HTN, often at the junction of the splenic vein and SMV.

❓ Q264: What is hereditary hemorrhagic telangiectasia?
💡 A264: AKA Osler–Weber–Rendu disease, a genetic disorder with AV malformations, cirrhosis, recurrent bleeding. US shows a dilated hepatic artery (~10 mm), multiple tubular color-flow channels, dilated hepatic veins.

❓ Q265: What is Peliosis Hepatis on ultrasound?
💡 A265: Blood-filled cavities in liver tissue, from chronic wasting, transplants, drugs, HIV. Sonographically, single or multiple heterogeneous masses ± calcifications.

❓ Q266: What is a normal liver transplant, and why is it performed?
💡 A266: Commonly for hepatitis C, biliary atresia in children. Orthotopic is entire-liver replacement. Evaluate IVC/hepatic/portal patency, especially hepatic artery supply to biliary tree.

❓ Q267: What are some normal post–liver transplant fast facts?
💡 A267:

• Slight heterogeneity
• Thin biliary walls
• Patent vessels, monophasic portal flow, triphasic hepatic veins/IVC
• HA peak systolic <200 cm/s, RI 0.5–0.7
• Watch for hepatic artery thrombosis

❓ Q268: What types of liver trauma are recognized?
💡 A268:

• Subcapsular: between capsule and liver
• Extracapsular: outside the capsule
• Intraparenchymal: within the liver tissue

End of Flash Cards