Question 1: Hepatocellular Carcinoma (HCC)
Stem: A 65-year-old man with a known history of hepatitis C-related cirrhosis undergoes a multiphase liver CT scan for screening. The scan reveals a 4 cm, solitary nodule in the right lobe. The nodule demonstrates intense, avid enhancement during the arterial phase and “washes out” (becoming hypodense relative to the liver) on the venous and delayed phases.
Question: This specific enhancement pattern is classic for:
(A) Hepatocellular Carcinoma (HCC) (B) Cavernous Haemangioma (C) Focal Nodular Hyperplasia (FNH) (D) Hepatic Metastasis (E) Hepatic Abscess
Correct Answer: (A) Hepatocellular Carcinoma (HCC).
Explanation:
- Why (A) is correct: The classic hallmark of HCC is its neo-vascularity, supplied by the hepatic artery. This results in arterial phase hyperenhancement (APHE). Because the tumour lacks normal portal venous drainage, the contrast “washes out” during the portal venous and delayed phases, making it appear hypodense. This “APHE and washout” pattern in a cirrhotic liver is diagnostic (LI-RADS 5).
- Why (B) is wrong: A haemangioma shows peripheral nodular enhancement that fills in centripetally and remains bright (isodense) on delayed phases.
- Why (C) is wrong: FNH is also hyperarterial but is typically isodense (stealth) on venous/delayed phases. It also has a characteristic (though not always present) non-enhancing central scar that is T2 bright.
- Why (D) is wrong: Metastases can be hyperarterial (e.g., from renal/neuroendocrine) or hypoarterial (e.g., from colon). Hypovascular metastases (colon) show “rim enhancement” and never wash out. Hypervascular metastases may wash out but are uncommon in a cirrhotic liver.
- Why (E) is wrong: An abscess is a complex fluid collection with a thick, enhancing rim (the “cluster sign” or “double target sign”), not a solid, washing-out mass.
Key Points: Hepatocellular Carcinoma (HCC)
- Risk Factors: Cirrhosis (from any cause – Hepatitis B/C, alcohol, NAFLD), Haemochromatosis.
- Tumour Marker: Alpha-fetoprotein (AFP) – often elevated.
- CT/MRI Hallmarks (LI-RADS 5):
- Arterial Phase Hyperenhancement (APHE).
- Portal Venous or Delayed Phase “Washout”.
- Other features: A “capsule” (enhancing rim on delayed phase) is also a major feature.
Question 2: Cavernous Haemangioma
Stem: A 40-year-old woman has an incidental 3 cm liver lesion found on an ultrasound. A multiphase MRI is performed. The lesion is T2-bright and, after gadolinium administration, demonstrates discontinuous, peripheral, nodular enhancement on the arterial phase. On subsequent portal venous and delayed phases, this enhancement progressively fills in towards the centre of the lesion.
Question: This enhancement pattern is pathognomonic for:
(A) Hepatocellular Carcinoma (HCC) (B) Cavernous Haemangioma (C) Focal Nodular Hyperplasia (FNH) (D) Hepatic Adenoma (E) Metastasis
Correct Answer: (B) Cavernous Haemangioma.
Explanation:
- Why (B) is correct: This is the textbook description of a haemangioma, the most common benign liver tumour. It is a vascular malformation, not a true tumour. The discontinuous peripheral nodular enhancement that fills in centripetally (from outside to inside) and retains contrast on delayed phases (remaining bright) is its pathognomonic sign.
- Why (A) is wrong: HCC has arterial wash-in and venous washout.
- Why (C) is wrong: FNH has intense, homogeneous arterial enhancement (not nodular) and a central scar.
- Why (D) is wrong: An adenoma is also hyperarterial but does not have this specific fill-in pattern.
- Why (E) is wrong: Metastases (hypervascular) show rim enhancement that “washes out,” not this progressive fill-in.
Key Points: Cavernous Haemangioma
- Definition: The most common benign liver tumour.
- CT/MRI Hallmarks:
- T2-bright (very bright, like a lightbulb) on MRI.
- Discontinuous, Peripheral, Nodular Enhancement on arterial phase.
- Centripetal (inward) fill-in on portal venous and delayed phases.
- No washout (remains bright).
- Note: “Flash-filling” haemangiomas (small ones that enhance fully and immediately) are a common variant.
Question 3: Focal Nodular Hyperplasia (FNH)
Stem: A 35-year-old woman, with no other medical history, has an incidental liver mass found on CT. The lesion is 5 cm, demonstrates intense, homogeneous arterial enhancement (making it “disappear” or become isodense on portal venous phase), and contains a stellate, non-enhancing central scar. On MRI, this scar is T2-hyperintense (bright).
Question: What is the most likely diagnosis?
(A) Cavernous Haemangioma (B) Hepatic Adenoma (C) Hepatocellular Carcinoma (HCC) (D) Focal Nodular Hyperplasia (FNH) (E) Fibrolamellar HCC
Correct Answer: (D) Focal Nodular Hyperplasia (FNH).
Explanation:
- Why (D) is correct: This is the classic FNH, the second most common benign liver tumour. It is a “hamartoma-like” lesion of hepatocytes. The key features are: 1) Homogeneous, intense arterial enhancement (a “stealth lesion” as it becomes isodense to the liver on other phases), and 2) A central scar that is T1-dark and T2-bright and does not enhance (or enhances late).
- Why (A) is wrong: A haemangioma has peripheral nodular enhancement, not homogeneous.
- Why (B) is wrong: An adenoma is hyperarterial but typically lacks a T2-bright central scar.
- Why (C) is wrong: HCC has washout and occurs in a cirrhotic liver.
- Why (E) is wrong: Fibrolamellar HCC is a malignant tumour in young patients. It also has a central scar, but its scar is T1-dark, T2-dark (fibrous), and does enhance. The T2-bright scar is the key to FNH.
Key Points: Focal Nodular Hyperplasia (FNH)
- Definition: Second most common benign liver tumour; a hyperplastic response to a vascular anomaly.
- CT/MRI Hallmarks:
- Intense, homogeneous arterial enhancement.
- Isodense (stealth) on portal venous/delayed phases.
- Central Scar: The key differentiator.
- T1-dark, T2-bright.
- No enhancement (or late, faint enhancement).
Question 4: Hepatic Adenoma
Stem: A 30-year-old woman with a 10-year history of oral contraceptive pill (OCP) use presents with sudden, severe right upper quadrant pain and hypotension. A CT scan reveals a 10 cm, heterogeneous liver mass that is actively bleeding, with a large subcapsular and intraperitoneal haematoma. An MRI from 6 months prior had shown that the mass contained areas of signal drop-out on “out-of-phase” T1-weighted images.
Question: What is the most likely underlying diagnosis for this haemorrhagic lesion?
(A) Hepatic Adenoma **(B) ** Focal Nodular Hyperplasia (FNH) (C) Hepatocellular Carcinoma (HCC) (D) Cavernous Haemangioma (E) Metastasis
Correct Answer: (A) Hepatic Adenoma.
Explanation:
- Why (A) is correct: This is the classic presentation. Hepatic adenomas are benign tumours strongly linked to OCP use and anabolic steroids. They are prone to spontaneous haemorrhage and rupture, which can be life-threatening (as in this patient). A key imaging feature of the most common subtype (HNF1-alpha inactivated) is the presence of intralesional fat, which appears as signal drop-out on out-of-phase MRI.
- Why (B) is wrong: FNH is not associated with OCPs and has a very low risk of bleeding.
- Why (C) is wrong: HCC can bleed, but it occurs in cirrhotic livers and is not associated with OCPs.
- Why (D) is wrong: Haemangiomas are vascular but have a very low risk of spontaneous rupture.
- Why (E) is wrong: Metastases can bleed (e.g., from melanoma, RCC), but the OCP history and intralesional fat point strongly to adenoma.
Key Points: Hepatic Adenoma
- Risk Factors: Oral Contraceptive Pill (OCP) use, anabolic steroids, glycogen storage disease.
- Clinical Significance: High risk of spontaneous haemorrhage and rupture. Small risk of malignant transformation to HCC.
- Imaging:
- Hypervascular (arterial enhancement).
- Intralesional Fat (signal drop on out-of-phase MRI) is common in the most frequent subtype.
- Lacks a T2-bright scar (unlike FNH).
Question 5: Acute Cholecystitis
Stem: A 50-year-old woman presents with 12 hours of constant right upper quadrant (RUQ) pain, fever, and nausea. On ultrasound, the gallbladder is distended, and a 2 cm gallstone is seen impacted in the gallbladder neck. The ultrasound also demonstrates a gallbladder wall thickness of 5 mm, pericholecystic fluid, and the “sonographic Murphy’s sign” is positive.
Question: This constellation of findings is diagnostic of:
(A) Acute Cholecystitis (B) Chronic Cholecystitis (C) Gallbladder Carcinoma (D) Adenomyomatosis (E) Biliary Colic
Correct Answer: (A) Acute Cholecystitis.
Explanation:
- Why (A) is correct: This is the classic ultrasound triad for acute cholecystitis (inflammation from an impacted stone). The findings are: 1) Gallstones (usually impacted in the neck), 2) Gallbladder wall thickening (> 3-4 mm), 3) Pericholecystic fluid, and 4) A positive sonographic Murphy’s sign (maximal tenderness when the probe presses on the gallbladder).
- Why (B) is wrong: Chronic cholecystitis would show a contracted, thick-walled gallbladder, but without the acute inflammatory signs (oedema, pericholecystic fluid, Murphy’s sign).
- Why (C) is wrong: Carcinoma is a focal, infiltrative mass, not diffuse inflammatory thickening.
- Why (D) is wrong: Adenomyomatosis is a benign condition with “comet-tail” artefacts (Rokitansky-Aschoff sinuses).
- Why (E) is wrong: Biliary colic is symptomatic pain from a stone, but the ultrasound would not show inflammatory wall changes. It is a diagnosis of pain, not inflammation.
Key Points: Acute Cholecystitis (Ultrasound)
- Definition: Acute inflammation of the gallbladder, almost always from an impacted stone in the cystic duct.
- Ultrasound Findings:
- Gallstone (cholelithiasis), especially if impacted in the neck.
- Gallbladder wall thickening (> 3 mm).
- Pericholecystic fluid.
- Sonographic Murphy’s Sign (focal tenderness).
- Gallbladder distension (> 4 cm).
Question 6: Gallbladder Carcinoma
Stem: A 78-year-old woman has an incidental finding on a CT scan. The entire gallbladder wall is circumferentially and densely calcified.
Question: This finding, known as a “porcelain gallbladder,” is significant because it is a strong risk factor for:
(A) Gallbladder Carcinoma (B) Emphysematous Cholecystitis (C) Gallstone Ileus (D) Mirizzi Syndrome (E) Acute Pancreatitis
Correct Answer: (A) Gallbladder Carcinoma.
Explanation:
- Why (A) is correct: A porcelain gallbladder (diffuse intramural calcification) is a rare finding, but it is strongly associated with gallbladder adenocarcinoma. The chronic inflammation that leads to the calcification is thought to be the carcinogenic driver.
- Why (B) is wrong: Emphysematous cholecystitis is an acute, gas-forming infection, which would show air in the wall, not calcium.
- Why (C) is wrong: Gallstone ileus is a complication of a cholecysto-enteric fistula, not wall calcification.
- Why (D) is wrong: Mirizzi syndrome is extrinsic compression from a stone in the cystic duct.
- Why (E) is wrong: This is caused by gallstones passing into the bile duct, not by wall calcification.
Key Points: Gallbladder Carcinoma
- Definition: A highly aggressive adenocarcinoma.
- Presentation: Usually late, mimics cholecystitis or presents with jaundice.
- Risk Factors: Gallstones (most common), Porcelain Gallbladder, primary sclerosing cholangitis.
- Imaging Patterns:
- Infiltrating mass (most common): Diffuse, asymmetric wall thickening.
- Polypoid mass (> 1 cm).
- Mass replacing the gallbladder.
- Prognosis: Very poor; often invades the liver directly.
Question 7: Cirrhosis
Stem: A 55-year-old man with a history of chronic alcohol abuse presents with haematemesis. A CT scan of the abdomen shows a shrunken, nodular liver surface, splenomegaly, ascites, and large oesophageal varices.
Question: These findings are most consistent with:
(A) Cirrhosis and Portal Hypertension (B) Budd-Chiari Syndrome (C) Disseminated Liver Metastases (D) Acute Viral Hepatitis (E) Pyogenic Liver Abscesses
Correct Answer: (A) Cirrhosis and Portal Hypertension.
Explanation:
- Why (A) is correct: This is the classic constellation of end-stage liver disease. Cirrhosis is the morphological end-point, seen as a shrunken, nodular liver. This leads to portal hypertension (high pressure in the portal system), which in turn causes the secondary findings: splenomegaly (from “back-pressure”), ascites (fluid leaking from the high-pressure system), and varices (porto-systemic collaterals).
- Why (B) is wrong: Budd-Chiari (hepatic vein thrombosis) is a cause of portal hypertension, but it has a specific imaging pattern: a “nutmeg” liver with a massively enhancing, hypertrophied caudate lobe (which has separate drainage).
- Why (C) is wrong: Metastases would appear as multiple focal lesions, not a shrunken, nodular liver.
- Why (D) is wrong: Acute hepatitis causes a swollen, hypodense liver (hepatomegaly), not a shrunken, nodular one.
- Why (E) is wrong: Abscesses are focal, rim-enhancing collections.
Key Points: Cirrhosis & Portal Hypertension
- Cirrhosis (Morphology):
- Shrunken, nodular liver surface.
- Hypertrophy of the caudate lobe and lateral segments.
- Atrophy of the right lobe and medial segment.
- Steatosis (fatty liver) is often seen.
- Portal Hypertension (Haemodynamics):
- Ascites.
- Splenomegaly.
- Porto-systemic Varices (oesophageal, gastric, umbilical “caput medusae”).
- Portal vein diameter > 13 mm.
Question 8: Pyogenic Liver Abscess
Stem: A 60-year-old man with a recent history of diverticulitis presents with high fever, rigors, and RUQ pain. An ultrasound shows multiple, complex, hypoechoic lesions in the liver. A CT scan confirms these are multiple, low-density, rim-enhancing lesions that seem to be coalescing, forming a “cluster” in the right lobe.
Question: This “cluster sign” is highly suggestive of:
(A) Pyogenic Liver Abscess (B) Amoebic Liver Abscess (C) Hydatid Cysts (D) Necrotic Metastases (E) Cavernous Haemangiomas
Correct Answer: (A) Pyogenic Liver Abscess.
Explanation:
- Why (A) is correct: The clinical picture (high fever, rigors) and recent history (diverticulitis, a source for portal pylephlebitis) strongly suggest infection. The “cluster sign” (multiple small abscesses coalescing into one large cavity) is a specific finding for pyogenic (bacterial) abscesses.
- Why (B) is wrong: An amoebic abscess is also possible but is classically a solitary, large, non-rim-enhancing abscess in a patient with a travel history.
- Why (C) is wrong: Hydatid cysts are non-inflammatory (no fever) and have “daughter cysts” and “water lily” signs; they do not “cluster.”
- Why (D) is wrong: Necrotic metastases (e.g., from colon cancer, which is also linked to diverticulitis) can mimic this, but the high fever and rigors make abscess the primary diagnosis.
- Why (E) is wrong: Haemangiomas are benign vascular lesions with a specific enhancement pattern.
Key Points: Pyogenic Liver Abscess
- Definition: A bacterial (e.g., E. coli, Klebsiella) abscess in the liver.
- Cause: Often from portal vein spread (e.g., diverticulitis, appendicitis) or biliary obstruction (cholangitis).
- Clinical: High fever, rigors, RUQ pain, leukocytosis.
- CT/MRI Findings:
- Thick, irregular, enhancing rim.
- “Cluster Sign”: Coalescing smaller abscesses.
- “Double Target Sign”: (Inner rim, outer low-density oedema).
- Often contain gas bubbles.
Question 9: Hydatid Cyst
Stem: A 40-year-old immigrant from a sheep-farming region in the Mediterranean is found to have an incidental 10 cm, well-defined, cystic mass in his liver. A CT scan shows the mass is composed of a large “mother” cyst containing multiple smaller “daughter” cysts. The wall of the main cyst is calcified.
Question: This appearance is pathognomonic for:
(A) Hydatid (Echinococcal) Cyst (B) Pyogenic Abscess (C) Amoebic Abscess (D) Biliary Cystadenoma (E) Simple Hepatic Cyst
Correct Answer: (A) Hydatid (Echinococcal) Cyst.
Explanation:
- Why (A) is correct: The combination of the epidemiology (sheep-farming region) and the imaging is classic. A large cyst containing multiple “daughter cysts” (multivesicular appearance) is pathognomonic for a hydatid cyst (caused by the parasite Echinococcus granulosus). Wall calcification is also very common.
- Why (B) & (C) are wrong: Abscesses are inflammatory collections of pus, often with a thick rim, and do not contain daughter cysts.
- Why (D) is wrong: A biliary cystadenoma is a rare, complex, septated cystic tumour, but it does not have the “cyst-within-a-cyst” appearance.
- Why (E) is wrong: A simple cyst is a thin-walled, unilocular, water-density structure with no internal components.
Key Points: Hydatid Cyst (Echinococcus)
- Pathogen: Echinococcus granulosus (parasitic tapeworm).
- Epidemiology: Associated with sheep and dogs. Endemic in the Mediterranean, Middle East, South America.
- Imaging (WHO Classification):
- CE1/2: Simple cyst, may have “water lily sign” (detached endocyst).
- CE3: “Daughter Cysts” (pathognomonic) within a “mother” cyst.
- CE4/5: Solid, heavily calcified inactive cyst.
- Risk: Anaphylactic shock if the cyst is ruptured.
Question 10: Hepatic Steatosis (Fatty Liver)
Stem: A 50-year-old obese man with type 2 diabetes has a non-contrast CT of the abdomen. The scan demonstrates that the liver parenchyma is diffusely dark (hypodense) compared to the spleen, which appears relatively bright. The intrahepatic vessels appear bright against the dark liver.
Question: This finding is diagnostic of:
(A) Hepatic Steatosis (Fatty Liver) (B) Cirrhosis (C) Acute Hepatitis (D) Haemochromatosis (E) Budd-Chiari Syndrome
Correct Answer: (A) Hepatic Steatosis (Fatty Liver).
Explanation:
- Why (A) is correct: On a non-contrast CT, a normal liver has a density equal to or slightly greater than the spleen. Fat is dark (hypodense) on CT. When fat infiltrates the liver (steatosis), the liver’s overall density decreases. A liver that is hypodense to the spleen is the key sign of hepatic steatosis.
- Why (B) is wrong: Cirrhosis is a morphological diagnosis (nodular surface); the density can be fatty, normal, or even high (if from haemochromatosis).
- Why (C) is wrong: Acute hepatitis causes the liver to swell, but it doesn’t typically alter the density this way.
- Why (D) is wrong: Haemochromatosis is iron deposition. Iron is dense on CT, so the liver would appear bright white (hyperdense) compared to the spleen.
- Why (E) is wrong: Budd-Chiari has a specific “nutmeg” enhancement pattern and does not cause diffuse low density.
Key Points: Hepatic Steatosis
- Definition: Fat infiltration of the liver (NAFLD/NASH).
- Causes: Obesity, diabetes, alcohol, chemotherapy.
- CT (Non-contrast):
- Liver is hypodense (darker) than the spleen.
- Intrahepatic vessels appear hyperdense (“pseudo-enhancement”).
- MRI (Best):
- Signal drop-out on out-of-phase T1-weighted imaging (this is the most sensitive and specific method).
Question 11: Budd-Chiari Syndrome
Stem: A 30-year-old woman with a history of polycythaemia vera presents with acute, painful hepatomegaly and ascites. A multiphase CT scan demonstrates thrombosis of all three hepatic veins. The central liver (including the caudate lobe) enhances avidly, while the periphery of the liver appears mottled and hypoenhancing.
Question: This specific enhancement pattern is characteristic of:
(A) Budd-Chiari Syndrome (B) Cirrhosis with Portal Hypertension (C) Acute Viral Hepatitis (D) Disseminated Metastases (E) Veno-occlusive Disease
Correct Answer: (A) Budd-Chiari Syndrome.
Explanation:
- Why (A) is correct: This is the classic, pathognomonic appearance. Budd-Chiari is hepatic vein thrombosis. This causes massive congestion of the liver except for the caudate lobe, which has its own separate, direct drainage to the IVC. This leads to the “nutmeg” liver appearance: a congested, non-enhancing periphery and an intensely enhancing, hypertrophied central liver and caudate lobe.
- Why (B) is wrong: Cirrhosis has a nodular surface and signs of portal (inflow) hypertension, not hepatic vein (outflow) thrombosis.
- Why (C) is wrong: Acute hepatitis is a diffuse process.
- Why (D) is wrong: Metastases are focal lesions.
- Why (E) is wrong: Veno-occlusive disease is a microscopic occlusion of post-sinusoidal venules (e.g., in bone marrow transplant patients). It causes hepatomegaly and ascites but without large-vessel (hepatic vein) thrombosis.
Key Points: Budd-Chiari Syndrome
- Definition: Obstruction of hepatic venous outflow.
- Cause: Thrombosis (e.g., hypercoagulable states, polycythaemia vera, OCP use) or a web (IVC).
- CT/MRI Hallmarks (Pathognomonic):
- Thrombosis of the hepatic veins / IVC.
- Hypertrophy and intense enhancement of the caudate lobe.
- Peripheral, “nutmeg” liver (mottled, congested, poor enhancement).
- Massive ascites.
Question 12: Mirizzi Syndrome
Stem: A 60-year-old woman presents with RUQ pain and new-onset jaundice. An MRCP is performed. It shows a large gallstone impacted in the cystic duct or gallbladder neck, which is externally compressing the common hepatic duct, causing a stricture and proximal biliary dilatation.
Question: This specific clinical and radiological syndrome is known as:
(A) Mirizzi Syndrome (B) Bouveret’s Syndrome (C) Gallstone Ileus (D) Klatskin Tumour (E) Primary Sclerosing Cholangitis
Correct Answer: (A) Mirizzi Syndrome.
Explanation:
- Why (A) is correct: This is the definition of Mirizzi syndrome. An impacted stone in the cystic duct (which runs parallel to the common hepatic duct, CHD) causes extrinsic compression and inflammation of the CHD, leading to obstructive jaundice.
- Why (B) is wrong: Bouveret’s syndrome is a stone in the duodenum causing gastric outlet obstruction.
- Why (C) is wrong: Gallstone ileus is a stone in the small bowel causing SBO.
- Why (D) is wrong: A Klatskin tumour is a cholangiocarcinoma (a primary tumour) at the biliary confluence, not extrinsic compression from a stone.
- Why (E) is wrong: PSC is a diffuse, inflammatory, fibrosing disease of the bile ducts, not a focal compression.
Key Points: Mirizzi Syndrome
- Definition: Extrinsic compression of the common hepatic duct (CHD) by a stone impacted in the cystic duct or gallbladder neck.
- Clinical: Presents like cholangitis or a biliary tumour (RUQ pain, jaundice).
- Imaging (US/MRCP):
- Stone impacted in the cystic duct.
- Extrinsic narrowing of the CHD at the point of impaction.
- Dilatation of the biliary tree above the compression.
- Complication: Can erode into the CHD, forming a cholecysto-choledochal fistula.
Question 13: Cholangiocarcinoma (Klatskin)
Stem: A 70-year-old man presents with painless jaundice and a raised CA 19-9. An MRCP shows dilatation of the intrahepatic bile ducts in both the right and left lobes, but the common hepatic duct and common bile duct are collapsed. A small, infiltrative, enhancing mass is seen at the bifurcation of the right and left hepatic ducts.
Question: This specific location for a cholangiocarcinoma is known as a:
(A) Klatskin Tumour (B) Pancreatic Head Adenocarcinoma (C) Ampullary Carcinoma (D) Gallbladder Carcinoma (E) Mirizzi Syndrome
Correct Answer: (A) Klatskin Tumour.
Explanation:
- Why (A) is correct: A Klatskin tumour is the eponym for a perihilar cholangiocarcinoma, which is a primary adenocarcinoma of the bile ducts located at the bifurcation of the main right and left hepatic ducts. This location causes obstruction of both lobes, leading to intrahepatic dilatation, but the distal ducts (CHD, CBD) are collapsed.
- Why (B) is wrong: A pancreatic head tumour would obstruct the distal CBD, causing both intra- and extrahepatic dilatation.
- Why (C) is wrong: An ampullary carcinoma would also obstruct the distal CBD.
- Why (D) is wrong: Gallbladder carcinoma is a mass in the gallbladder, which may invade the ducts, but “Klatskin” is the specific term for the hilar location.
- Why (E) is wrong: Mirizzi syndrome is compression from a stone, not a primary tumour.
Key Points: Cholangiocarcinoma (Bile Duct Cancer)
- Risk Factors: Primary Sclerosing Cholangitis (PSC), liver flukes, choledochal cysts.
- Classification by Location:
- Intrahepatic: Mass within the liver.
- Perihilar (Klatskin Tumour): At the hepatic duct bifurcation. (Most common type).
- Distal: In the distal CBD (mimics pancreatic cancer).
- Imaging: An infiltrative, enhancing, desmoplastic (fibrotic) tumour causing an abrupt stricture and proximal duct dilatation.
Question 14: Adenomyomatosis
Stem: A 45-year-old woman has an incidental finding on a RUQ ultrasound for non-specific pain. The ultrasound shows focal thickening of the gallbladder fundus. Within this thickened wall, there are multiple, small, anechoic (cystic) spaces containing bright, echogenic foci that produce “V-shaped” or “comet-tail” reverberation artefacts.
Question: This specific artefact is pathognomonic for:
(A) Adenomyomatosis (B) Acute Cholecystitis (C) Gallbladder Carcinoma (D) Emphysematous Cholecystitis (E) Gallstones
Correct Answer: (A) Adenomyomatosis.
Explanation:
- Why (A) is correct: This is the classic US appearance. Adenomyomatosis is a benign, hyperplastic condition of the gallbladder wall, characterized by mucosal out-pouchings into the muscle layer called Rokitansky-Aschoff sinuses. These sinuses become filled with bile or cholesterol crystals. On US, the tiny, bright cholesterol crystals within these anechoic sinuses produce the characteristic “comet-tail” reverberation artefact.
- Why (B) is wrong: Acute cholecystitis has wall oedema and fluid, not these artefacts.
- Why (C) is wrong: Carcinoma is an irregular, solid, vascular mass.
- Why (D) is wrong: Emphysematous cholecystitis has “dirty” shadowing from air, not clean comet-tail artefacts.
- Why (E) is wrong: Gallstones are large, mobile, and produce a clean posterior acoustic shadow, not a reverberation artefact.
Key Points: Adenomyomatosis
- Definition: A benign, hyperplastic condition of the gallbladder wall.
- Pathology: Mucosal invaginations into the thickened muscularis propria, called Rokitansky-Aschoff sinuses.
- Ultrasound (Pathognomonic):
- Focal or diffuse wall thickening.
- “Comet-tail artefacts”: V-shaped reverberations from cholesterol crystals trapped within the sinuses.
- Note: It is a benign “do-not-touch” lesion and is not pre-malignant.
Question 15: Amoebic Liver Abscess
Stem: A 38-year-old man returns from a trip to Southeast Asia and presents with a 1-week history of fever and RUQ pain. A CT scan reveals a large, 8 cm, solitary, well-defined, low-density lesion in the right lobe of the liver, adjacent to the capsule. The lesion has a thin, enhancing rim. Aspiration of the lesion yields thick, reddish-brown, odourless fluid.
Question: This presentation, including the “anchovy paste” aspirate, is most characteristic of:
(A) Amoebic Liver Abscess (B) Pyogenic Liver Abscess (C) Hydatid Cyst (D) Hepatocellular Carcinoma (E) Metastasis
Correct Answer: (A) Amoebic Liver Abscess.
Explanation:
- Why (A) is correct: The key features are the travel history (endemic area for Entamoeba histolytica), the solitary, subcapsular nature of the abscess, and the classic “anchovy paste” aspirate (which is necrotic liver tissue, not true pus). Unlike pyogenic abscesses, patients are often less systemically toxic.
- Why (B) is wrong: Pyogenic abscesses are often multiple, associated with a “cluster sign,” and are filled with frank pus. The patient is usually more septic (e.g., rigors).
- Why (C) is wrong: A hydatid cyst is non-inflammatory (no fever) and contains “daughter cysts.”
- Why (D) & (E) are wrong: These are tumours, not acute, febrile, cystic lesions.
Key Points: Amoebic Liver Abscess
- Pathogen: Entamoeba histolytica (a protozoan).
- Epidemiology: Travel history to an endemic area (e.g., Mexico, India, Southeast Asia, Africa).
- Clinical: Fever, RUQ pain (but often less toxic than a pyogenic abscess).
- Imaging:
- Classically a solitary, round, subcapsular abscess in the right lobe.
- Has a thin rim (unlike the thick, shaggy rim of a pyogenic abscess).
- Aspiration: “Anchovy paste” (thick, reddish-brown fluid) is characteristic.
