Imaging of Liver — MCQs
What is the next best step for a 22-year-old with a hepatic hemangioma on ultrasound?
A patient with known cirrhosis presents with jaundice and abdominal distention. Ultrasound reveals ascites and splenomegaly. What is the most likely cause of his ascites?
A patient with a history of alcohol dependence syndrome presents with sudden and unintentional weight loss. What is the most likely diagnosis?
Which is the most sensitive imaging modality for detecting liver metastases?
Central stellate scar is typically associated with which of the following conditions?
Which of the following investigations work on the same principle?
How does 'hepatic vein thrombosis' present on Doppler ultrasound?
Which of the following is the MOST common risk factor for hepatocellular carcinoma worldwide?
Which of the following is the site of venous thrombosis in Budd-Chiari syndrome?
Which of the following is a characteristic of Wilson's disease?
Imaging of Liver Indian Medical PG Practice Questions and MCQs
Question 1: What is the next best step for a 22-year-old with a hepatic hemangioma on ultrasound?
- A. Angiography
- B. CT
- C. Biopsy
- D. MRI (Correct Answer)
Explanation: ***MRI*** - **Magnetic Resonance Imaging (MRI)** is the most sensitive and specific imaging modality for confirming the diagnosis of a **hepatic hemangioma** due to its characteristic enhancement patterns. - An MRI with contrast (e.g., gadolinium) can definitively distinguish a hemangioma from other **benign or malignant liver lesions**, especially when the ultrasound findings are equivocal. *Angiography* - **Angiography** is an invasive procedure and is typically reserved for cases where **embolization** or surgical resection of a very large or symptomatic hemangioma is being considered. - It is not the initial diagnostic choice for confirming a suspected hemangioma identified on **ultrasound**. *CT* - A **CT scan** with contrast can also characterize a hemangioma, showing peripheral nodular enhancement followed by progressive centripetal fill-in. - However, **MRI** generally offers superior soft tissue contrast and provides more definitive diagnostic features for hemangiomas, particularly in younger patients where radiation exposure from CT is a concern. *Biopsy* - **Biopsy** of a suspected hepatic hemangioma is generally contraindicated due to the risk of **hemorrhage** and is rarely necessary for diagnosis. - Imaging characteristics (especially on MRI) are usually sufficient to confirm the diagnosis without the need for an invasive procedure.
Question 2: A patient with known cirrhosis presents with jaundice and abdominal distention. Ultrasound reveals ascites and splenomegaly. What is the most likely cause of his ascites?
- A. Portal hypertension (Correct Answer)
- B. Peritoneal carcinomatosis
- C. Nephrotic syndrome
- D. Congestive heart failure
Explanation: ***Portal hypertension*** - In cirrhosis, **fibrosis** and **regenerative nodules** increase resistance to blood flow through the liver, leading to **portal hypertension** [1]. - This increased pressure in the portal venous system, combined with **splanchnic vasodilation** and **renal sodium retention**, drives the transudation of fluid into the peritoneal cavity, forming ascites [1]. *Peritoneal carcinomatosis* - This would typically result in **exudative ascites**, often with a high protein content and positive cytology for malignant cells [1]. - While it can cause abdominal distention, it is not directly linked to the pathology of **cirrhosis** and **splenomegaly** as the primary cause of ascites in this context. *Nephrotic syndrome* - Characterized by **massive proteinuria**, **hypoalbuminemia**, and **generalized edema**, including ascites. - While it causes fluid retention, the clinical picture of **jaundice** and **splenomegaly** strongly points to liver pathology rather than primary renal disease [1]. *Congestive heart failure* - Can cause **dependent edema** and ascites due to elevated systemic venous pressures, but typically presents with other signs like **dyspnea**, orthopnea, and pulmonary edema [1]. - The patient's history of **cirrhosis** and the presence of **splenomegaly** make portal hypertension a significantly more likely cause of ascites [1].
Question 3: A patient with a history of alcohol dependence syndrome presents with sudden and unintentional weight loss. What is the most likely diagnosis?
- A. Hepatic adenoma
- B. Cholangiocarcinoma
- C. Hepatocellular carcinoma (Correct Answer)
- D. Alcoholic hepatitis
Explanation: ***Hepatocellular carcinoma*** - The **alpha-fetoprotein (AFP)** level of **600 ng/mL** is significantly elevated, suggesting a diagnosis of hepatocellular carcinoma, especially in a patient with a history of **alcohol dependence syndrome** [1]. - The **AST/ALT ratio of 0.5** indicates significant liver damage, commonly seen in chronic liver disease leading to **hepatocellular cancer**. *Alcoholic hepatitis* - Typically presents with **elevated AST and ALT**, usually with a ratio >2:1, which is not the case here [2]. - May cause weight loss, as alcoholic patients often lose weight due to self-neglect and poor dietary intake, but the **elevated AFP** is not characteristic of merely alcoholic hepatitis [3]. *Cholangiocarcinoma* - This type of cancer primarily presents with **biliary obstruction** symptoms, such as jaundice, which is not indicated here given **normal bilirubin levels**. - Does not typically lead to such high levels of **AFP**, making it less likely with the provided lab results. *Hepatic adenoma* - More commonly associated with **oral contraceptive use** or anabolic steroid use, not primarily alcohol dependence. - AFP levels are usually normal or only mildly elevated in hepatic adenoma, making this option less viable with an **AFP level of 600 ng/mL**.
Question 4: Which is the most sensitive imaging modality for detecting liver metastases?
- A. Ultrasound
- B. PET scan
- C. MRI with contrast (Correct Answer)
- D. CT with contrast
Explanation: ***MRI with contrast*** - **Magnetic resonance imaging (MRI)** with **gadolinium-based contrast agents** (particularly hepatocyte-specific agents like gadoxetic acid) combined with **diffusion-weighted imaging (DWI)** is considered the most sensitive imaging modality for detecting liver metastases due to its superior soft tissue contrast resolution. - It allows for better characterization of lesions, particularly small ones (<1 cm), and distinguishes them from benign liver lesions. - MRI can detect lesions that are often missed by CT, making it the gold standard for liver metastasis detection. *Ultrasound* - **Ultrasound** is often the initial imaging modality for liver evaluation due to its availability and low cost, but its sensitivity for detecting small metastases is limited and highly operator-dependent. - It may miss small or **isoechoic lesions**, especially in patients with fatty liver disease. *PET scan* - **PET (Positron Emission Tomography)** scans are useful for detecting metabolically active lesions and distant metastases throughout the body, but their spatial resolution for small liver lesions can be lower than MRI. - While good for whole-body staging, it may not be as sensitive as MRI for detecting tiny metastases within the liver parenchyma itself. *CT with contrast* - **Computed tomography (CT)** with intravenous contrast is a widely used and effective modality for detecting liver metastases, but it is generally less sensitive than MRI, especially for lesions under 1 cm. - CT scans can sometimes struggle to differentiate small metastases from benign lesions or areas of perfusion abnormality.
Question 5: Central stellate scar is typically associated with which of the following conditions?
- A. Focal nodular hyperplasia (FNH) (Correct Answer)
- B. Hepatic adenoma
- C. Chronic liver disease
- D. Hepatocellular carcinoma
Explanation: ***Focal nodular hyperplasia (FNH)*** - FNH is a benign liver lesion characterized by a central fibrous scar with radiating septa, giving it the characteristic appearance of a **central stellate scar** on imaging. - This scar contains **malformed blood vessels** and bile ductules, which are key diagnostic features. - On dynamic imaging, FNH typically shows **spoke-wheel arterial enhancement** pattern and the central scar shows **delayed enhancement** on MRI. *Hepatic adenoma* - Hepatic adenomas are typically composed of sheets of **hepatocytes** with absent portal triads and are usually **homogeneous** on imaging without a central scar. - They are associated with **oral contraceptive use** and have a risk of hemorrhage and malignant transformation. *Chronic liver disease* - Chronic liver disease, such as **cirrhosis**, is characterized by widespread **fibrosis** and **nodule formation** throughout the liver, but it does not typically present with a solitary lesion with a central stellate scar. - The scarring in cirrhosis is diffuse and leads to architectural distortion, rather than a focal central scar. *Hepatocellular carcinoma* - Hepatocellular carcinoma (HCC) typically presents as a **vascular mass** that may or may not be solitary, usually arising in the context of chronic liver disease or cirrhosis. - Although the **fibrolamellar variant of HCC** (seen in younger patients without cirrhosis) can show a central scar, this is less common and the scar typically shows **hypointensity on T2-weighted imaging**, unlike FNH where the scar is **hyperintense on T2**. - Typical HCC does not show a distinct central stellate scar as a characteristic feature.
Question 6: Which of the following investigations work on the same principle?
- A. MRI and PET Scan
- B. CT and MRI
- C. CT and X-ray (Correct Answer)
- D. USG and HIDA Scan
Explanation: ***CT and X-ray*** - Both **Computed Tomography (CT)** and **X-ray** imaging utilize **ionizing radiation** to generate images of the body's internal structures. - They work by passing X-ray beams through the patient, with different tissues absorbing the radiation to varying degrees, which is then detected to create an image. *MRI and PET Scan* - **Magnetic Resonance Imaging (MRI)** uses **strong magnetic fields and radio waves** to create detailed images of soft tissues, based on water content. - **Positron Emission Tomography (PET) scans** use **radioactive tracers** to visualize metabolic activity and blood flow, detecting gamma rays emitted from the patient. *CT and MRI* - **CT scans** use **ionizing radiation** (X-rays) to produce cross-sectional images. - **MRI scans** use **magnetic fields and radio waves** and do not involve ionizing radiation. *USG and HIDA Scan* - **Ultrasound (USG)** uses **high-frequency sound waves** to create real-time images of organs and structures. - **Hepatobiliary Iminodiacetic Acid (HIDA) scans** are a type of nuclear medicine study that uses a **radioactive tracer** to evaluate liver and gallbladder function.
Question 7: How does 'hepatic vein thrombosis' present on Doppler ultrasound?
- A. Absent or reversed flow (Correct Answer)
- B. Anechoic appearance
- C. Increased flow
- D. Normal triphasic flow
Explanation: ***Absent or reversed flow*** - **Hepatic vein thrombosis** directly obstructs blood flow, leading to either an absence of detectable flow or, in some cases, reversal of flow due to high downstream pressure and collateral formation. - This finding on **Doppler ultrasound** is a key indicator of **Budd-Chiari syndrome**, caused by the obstruction of hepatic venous outflow. *Anechoic appearance* - An **anechoic appearance** on ultrasound typically refers to a fluid-filled structure, such as a cyst or gallbladder, which allows sound waves to pass through without reflection. - While thrombosis can affect the lumen of a vessel, the thrombus itself often has some echogenicity, and the primary Doppler finding relates to flow dynamics, not simply the anechoic nature of the vessel. *Increased flow* - **Increased flow** in the hepatic veins would suggest a hyperdynamic state or shunting, which is not characteristic of venous thrombosis. - Thrombosis causes obstruction, leading to a reduction or cessation of flow, not an increase. *Normal triphasic flow* - **Normal triphasic flow** in the hepatic veins is characterized by three distinct phases corresponding to cardiac cycles: antegrade flow during systole and diastole, and a brief period of reversed flow during atrial contraction. - The presence of thrombosis would disrupt this normal pattern, making it an unlikely finding in **hepatic vein thrombosis**.
Question 8: Which of the following is the MOST common risk factor for hepatocellular carcinoma worldwide?
- A. HCV
- B. Alcohol
- C. HBV (Correct Answer)
- D. Aflatoxin exposure
Explanation: HBV - **Hepatitis B virus (HBV)** infection is the leading cause of **hepatocellular carcinoma (HCC)** globally, especially in regions with high endemicity like Southeast Asia and sub-Saharan Africa. - Chronic HBV infection leads to persistent **inflammation and fibrosis** in the liver, increasing the risk of malignant transformation. HCV - **Hepatitis C virus (HCV)** is a significant risk factor for HCC, particularly in Western countries. - While a major cause of chronic liver disease, its overall global prevalence as a cause of HCC is slightly lower than HBV. Alcohol - **Chronic alcohol consumption** can lead to alcoholic liver disease, cirrhosis, and subsequently increase the risk of HCC. - However, worldwide, chronic viral hepatitis (HBV and HCV) accounts for a larger proportion of HCC cases compared to alcohol-related liver disease. Aflatoxin exposure - **Aflatoxins**, particularly **aflatoxin B1**, are potent liver carcinogens produced by certain fungi (e.g., *Aspergillus flavus*) that contaminate food crops. - While significant in some regions, especially when combined with HBV infection, its global impact as a sole risk factor for HCC is less widespread compared to viral hepatitis.
Question 9: Which of the following is the site of venous thrombosis in Budd-Chiari syndrome?
- A. Infrahepatic inferior vena cava
- B. Infrarenal inferior vena cava
- C. Hepatic vein (Correct Answer)
- D. Portal vein
Explanation: ***Hepatic vein*** - **Budd-Chiari syndrome** is specifically defined by **thrombosis of the hepatic veins** [3] or the suprahepatic inferior vena cava, obstructing venous outflow from the liver. - This obstruction leads to **hepatic congestion** [2], liver enlargement, abdominal pain, and ascites. *Infrahepatic inferior vena cava* - While thrombosis can occur in the inferior vena cava, if it is located **below the liver**, it would not directly cause the classic features of Budd-Chiari syndrome. - Obstruction at this level would primarily lead to **lower extremity edema** and potentially renal vein thrombosis. *Infrarenal inferior vena cava* - Thrombosis in the **infrarenal portion of the IVC** would cause symptoms in the lower body, such as leg swelling [3], but not the hepatic congestion characteristic of Budd-Chiari syndrome. - This condition is distinct and typically presents with symptoms localized to the **inferior vena cava drainage area below the kidneys**. *Portal vein* - **Portal vein thrombosis** causes **portal hypertension** but does not directly involve the hepatic veins [1]. - While it can lead to ascites, it does not typically cause the acute, severe hepatic necrosis and sinusoidal congestion seen in Budd-Chiari syndrome as liver outflow is not obstructed.
Question 10: Which of the following is a characteristic of Wilson's disease?
- A. Increased copper in liver (Correct Answer)
- B. Autosomal dominant
- C. Increased serum ceruloplasmin
- D. Decreased copper excretion in urine
Explanation: ***Increased copper in liver*** - Wilson's disease is characterized by **accumulation of copper** in liver tissues due to defective copper transport [1]. - This excess leads to **hepatocellular damage**, resulting in liver dysfunction and potential cirrhosis [1]. *Decreased copper excretion in urine* - In Wilson's disease, there is actually **decreased excretion of copper**, which results in accumulation in the liver [1]. - **Urine copper levels** are typically low to normal in early stages because the liver fails to excrete excess copper effectively. *Autosomal dominant* - Wilson's disease is inherited in an **autosomal recessive** pattern, not dominant. - It is caused by mutations in the gene responsible for copper transport (ATP7B) [1]. *Increased serum ceruloplasmin* - Serum ceruloplasmin levels are often **decreased** in Wilson's disease due to impaired copper incorporation into this protein [1]. - Low ceruloplasmin is a key laboratory finding, contrasting the assertion of this option.
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