Liver and Biliary Pathology — MCQs
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Mallory hyaline bodies are present in all of the following conditions, except?
Increased risk of liver adenoma is found in which of the following diseases?
A 36-year-old man from sub-Saharan Africa presents with jaundice and right upper quadrant pain. On examination, the liver is palpably enlarged. Laboratory studies demonstrate an increase in liver enzymes. Computed tomography demonstrates a single large mass in the right lobe of the liver, and serum a-fetoprotein is markedly elevated. Which of the following is likely to have contributed to the patient's condition?
Which one of the following statements is not true regarding fibrolamellar carcinoma?
Chronic alcoholism is associated with the development of all of the following liver diseases, EXCEPT?
A 38-year-old man, a chronic alcoholic, presents with pain in the abdomen. On examination, his liver is enlarged and serum alpha-fetoprotein is elevated. What is the most likely diagnosis?
Which one of the following is not a feature of liver histology in non-cirrhotic portal fibrosis (NCPF)?
Multiple liver secondaries are most common in which of the following cancers?
Primary sinusoidal dilatation of liver is also known as?
Which virus, besides HBV, is implicated in hepatocellular carcinoma?
Liver and Biliary Pathology Indian Medical PG Practice Questions and MCQs
Question 21: Mallory hyaline bodies are present in all of the following conditions, except?
- A. Primary biliary cirrhosis
- B. Secondary biliary cirrhosis (Correct Answer)
- C. Indian childhood cirrhosis
- D. Alcoholic cirrhosis
Explanation: **Explanation:** **Mallory-Denk Bodies (MDBs)**, often referred to as Mallory hyaline, are eosinophilic cytoplasmic inclusions found within hepatocytes. They are composed of tangled intermediate filaments, specifically **Pre-keratin (Cytokeratin 8 and 18)**, ubiquitinated proteins, and heat shock proteins. **Why Secondary Biliary Cirrhosis is the correct answer:** Mallory bodies are characteristic of chronic cholestatic conditions and toxic liver injuries. While they are frequently seen in **Primary Biliary Cirrhosis (PBC)** due to chronic bile stasis and hepatocyte stress [1], they are typically **absent** in **Secondary Biliary Cirrhosis**. Secondary biliary cirrhosis results from extrahepatic biliary obstruction (e.g., gallstones or strictures); the pathology here is dominated by bile lakes and infarcts rather than the specific cytoskeletal derangement required to form MDBs. **Analysis of Incorrect Options:** * **Alcoholic Cirrhosis:** This is the most classic association. MDBs are a hallmark of alcoholic hepatitis and subsequent cirrhosis [1]. * **Indian Childhood Cirrhosis (ICC):** This condition is characterized by excessive copper deposition and is famous for having the **most numerous** and prominent Mallory bodies. * **Primary Biliary Cirrhosis (PBC):** As a chronic intrahepatic cholestatic disease, MDBs are frequently found in the periportal hepatocytes [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Mallory Bodies (W-A-I-P-H-E-R):** **W**ilson’s disease, **A**lcoholic hepatitis, **I**ndian childhood cirrhosis, **P**rimary biliary cirrhosis, **H**epatocellular carcinoma, **E**nd-stage liver disease (NASH), and **R**esection (post-bypass). * **Staining:** They are eosinophilic (pink) on H&E stain and can be highlighted using **Ubiquitin** or **Cytokeratin** immunohistochemical stains. * **Key Fact:** Mallory bodies are **not** specific to any single disease but are a marker of hepatocyte injury and oxidative stress. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 388-390.
Question 22: Increased risk of liver adenoma is found in which of the following diseases?
- A. Lipid storage disorder
- B. Mitochondrial disease
- C. Glycogen storage disorder (Correct Answer)
- D. Lysosomal storage disorder
Explanation: **Explanation:** **Hepatic Adenoma (Hepatocellular Adenoma)** is a benign liver tumor strongly associated with hormonal influences and specific metabolic disturbances [1]. **Why Glycogen Storage Disorder (GSD) is correct:** The strongest association between a metabolic disease and hepatic adenoma is found in **GSD Type I (von Gierke disease)** [2] and occasionally **GSD Type III**. In GSD Type I, the deficiency of glucose-6-phosphatase leads to chronic hypoglycemia and hyperinsulinemia [2]. These metabolic imbalances, combined with the accumulation of glycogen in hepatocytes, trigger hepatocyte proliferation and the formation of multiple adenomas (adenomatosis). Notably, adenomas in GSD patients carry a higher risk of malignant transformation into hepatocellular carcinoma (HCC) compared to those induced by oral contraceptives. **Why other options are incorrect:** * **Lipid storage disorders** (e.g., Gaucher disease) primarily involve the accumulation of lipids in macrophages (Kupffer cells), leading to hepatosplenomegaly but not typically predisposing to adenomas. * **Mitochondrial diseases** usually present with liver failure, steatosis, or cirrhosis (e.g., Alpers syndrome) rather than discrete benign tumors. * **Lysosomal storage disorders** (a broad category including many lipid and mucopolysaccharide disorders) generally cause organomegaly and cellular dysfunction rather than neoplastic transformation into adenomas. **High-Yield Clinical Pearls for NEET-PG:** 1. **Risk Factors:** Oral Contraceptive Pills (OCPs) are the most common cause; others include anabolic steroids and GSD Type I [1]. 2. **Molecular Subtypes:** [1] * *HNF1α-inactivated:* Lowest risk of malignancy. [1] * *β-catenin activated:* **Highest risk** of malignant transformation to HCC. [1] * *Inflammatory:* Associated with obesity and fatty liver. 3. **Complications:** The most feared acute complication is **spontaneous rupture and intraperitoneal hemorrhage**, especially during pregnancy. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 874-875. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 164-165.
Question 23: A 36-year-old man from sub-Saharan Africa presents with jaundice and right upper quadrant pain. On examination, the liver is palpably enlarged. Laboratory studies demonstrate an increase in liver enzymes. Computed tomography demonstrates a single large mass in the right lobe of the liver, and serum a-fetoprotein is markedly elevated. Which of the following is likely to have contributed to the patient's condition?
- A. Aflatoxin B1 (Correct Answer)
- B. Clonorchis sinensis
- C. Hepatitis A
- D. Polyvinyl chloride
Explanation: ### Explanation The clinical presentation of a young patient from sub-Saharan Africa with a large hepatic mass, jaundice, and markedly elevated **alpha-fetoprotein (AFP)** is classic for **Hepatocellular Carcinoma (HCC)** [1]. **1. Why Aflatoxin B1 is Correct:** In sub-Saharan Africa and parts of Southeast Asia, HCC is frequently linked to dietary exposure to **Aflatoxin B1**, a toxin produced by *Aspergillus flavus* (found in contaminated stored grains and peanuts) [1]. Aflatoxin B1 causes a specific **mutation in the p53 tumor suppressor gene** (typically a G:C to T:A transversion at codon 249). When combined with chronic Hepatitis B infection, which is endemic in these regions, the risk of HCC increases synergistically [1]. **2. Analysis of Incorrect Options:** * **B. Clonorchis sinensis:** This Chinese liver fluke is a major risk factor for **Cholangiocarcinoma** (bile duct cancer), not HCC [3]. AFP is typically normal in cholangiocarcinoma. * **C. Hepatitis A:** This virus causes acute self-limiting hepatitis and does not progress to chronic liver disease or cirrhosis; therefore, it is not associated with HCC. * **D. Polyvinyl chloride (PVC):** Exposure to PVC (used in the plastics industry) is a specific risk factor for **Hepatic Angiosarcoma**, a rare malignant vascular tumor, rather than HCC. **Clinical Pearls for NEET-PG:** * **Most common primary site of HCC:** Right lobe of the liver. * **Tumor Marker:** AFP >400–500 ng/mL is highly suggestive of HCC in the presence of a liver mass [2]. * **Fibrolamellar Variant:** A subtype of HCC seen in young adults (20s) without cirrhosis; it has a better prognosis and normal AFP levels. * **Microscopy:** Look for "Mallory bodies" and "Bile plugs" within the malignant hepatocytes. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 876-877. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 399-400. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 879-880.
Question 24: Which one of the following statements is not true regarding fibrolamellar carcinoma?
- A. Seen in young adults
- B. Better prognosis than hepatocellular carcinoma
- C. Associated with Hepatitis B virus infection (Correct Answer)
- D. Elevated alpha-fetoprotein is not seen
Explanation: **Fibrolamellar Carcinoma (FLC)** is a distinct variant of hepatocellular carcinoma (HCC) that differs significantly from the conventional type in terms of demographics, risk factors, and clinical presentation. ### **Explanation of the Correct Option** **Option C is the correct answer (not true)** because Fibrolamellar Carcinoma is **not associated** with Hepatitis B virus (HBV), Hepatitis C virus (HCV), or cirrhosis. Unlike conventional HCC, which typically arises in a background of chronic liver disease or viral infection, FLC occurs in non-cirrhotic, healthy livers [1]. ### **Analysis of Other Options** * **Option A (Seen in young adults):** This is true. FLC typically affects adolescents and young adults (ages 20–40), with no gender predilection, whereas conventional HCC usually affects older patients. * **Option B (Better prognosis):** This is true. Because FLC usually occurs in a non-cirrhotic liver and is often slow-growing, it is more amenable to surgical resection, leading to a better 5-year survival rate compared to conventional HCC [1]. * **Option D (Elevated AFP not seen):** This is true. Serum **Alpha-fetoprotein (AFP) levels are typically normal** in FLC [1]. This is a high-yield diagnostic differentiator from conventional HCC, where AFP is often significantly elevated. ### **High-Yield Clinical Pearls for NEET-PG** * **Morphology:** Characterized by large, polygonal cells with abundant eosinophilic cytoplasm (oncocytic appearance) and prominent nucleoli, separated by **parallel lamellae of collagen bundles**. * **Molecular Marker:** A highly specific genetic translocation, **DNAJB1-PRKACA fusion gene**, is found in nearly all cases of FLC. * **Radiology:** Often presents as a large solitary mass with a **central stellate scar** (similar to Focal Nodular Hyperplasia), but the scar in FLC shows delayed enhancement on CT. * **Neurotensin:** Serum neurotensin or vitamin B12-binding capacity may be elevated in some patients. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 399-400.
Question 25: Chronic alcoholism is associated with the development of all of the following liver diseases, EXCEPT?
- A. Cirrhosis
- B. Fatty degeneration
- C. Cholestatic hepatitis
- D. Granuloma formation (Correct Answer)
Explanation: Alcoholic liver disease (ALD) follows a well-defined spectrum of pathological changes driven by the toxic effects of acetaldehyde and oxidative stress [5]. **Why Granuloma formation is the correct answer:** Granulomas are organized collections of macrophages (epithelioid cells) typically formed in response to persistent irritants that cannot be easily degraded [1]. Common causes of hepatic granulomas include **Sarcoidosis, Tuberculosis, Schistosomiasis, and certain drugs (e.g., Allopurinol)** [1]. Chronic alcoholism does not trigger a granulomatous immune response; instead, it causes direct metabolic injury and neutrophilic inflammation. **Analysis of Incorrect Options:** * **Fatty degeneration (Steatosis):** This is the **earliest** and most common response to alcohol [4]. It occurs due to an increased NADH/NAD+ ratio, which inhibits fatty acid oxidation and promotes lipogenesis [5]. * **Cholestatic hepatitis:** Alcoholic hepatitis often presents with features of cholestasis (jaundice, elevated alkaline phosphatase) [3]. Histologically, it is characterized by hepatocyte swelling (ballooning), **Mallory-Denk bodies**, and neutrophilic infiltration [4]. * **Cirrhosis:** This is the **end-stage** of chronic alcohol consumption [3]. Persistent inflammation and cytokine release (especially TGF-β) activate **Stellate cells**, leading to diffuse fibrosis and regenerating nodules that architecturaly distort the liver [5]. **High-Yield Clinical Pearls for NEET-PG:** * **Mallory-Denk Bodies:** These are eosinophilic cytoplasmic inclusions made of **damaged intermediate filaments (cytokeratin)** [4]. While classic for ALD, they are not pathognomonic (also seen in Wilson’s disease and NASH) [2]. * **AST:ALT Ratio:** In alcoholic liver disease, the ratio is typically **>2:1** (Alcoholic **S**tatistics are **T**errible) [3]. * **First change:** Microvesicular steatosis; **Most common change:** Macrovesicular steatosis. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 401-402. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 388-389. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 850-851. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 389-390. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 848-850.
Question 26: A 38-year-old man, a chronic alcoholic, presents with pain in the abdomen. On examination, his liver is enlarged and serum alpha-fetoprotein is elevated. What is the most likely diagnosis?
- A. Hepatocellular carcinoma (Correct Answer)
- B. Liver cell hyperplasia
- C. Hepatic adenoma
- D. Hepatitis
Explanation: ### Explanation **Correct Option: A. Hepatocellular Carcinoma (HCC)** The diagnosis is based on the classic triad of **chronic alcoholism (cirrhosis), hepatomegaly, and elevated serum Alpha-Fetoprotein (AFP)** [1]. * **Pathophysiology:** Chronic alcohol consumption leads to cirrhosis, which is the strongest predisposing factor for HCC [2]. * **Tumor Marker:** AFP is a highly specific glycoprotein marker for HCC when significantly elevated (typically >400 ng/mL) [1]. In a patient with underlying liver disease and a new liver mass/enlargement, a rise in AFP is pathognomonic for malignant transformation. **Why other options are incorrect:** * **B. Liver cell hyperplasia:** This is a benign compensatory process (e.g., Focal Nodular Hyperplasia). While it causes hepatomegaly, it does **not** cause an elevation in AFP. * **C. Hepatic adenoma:** These are benign epithelial tumors most commonly associated with **oral contraceptive use** in women or anabolic steroid use. They rarely cause significant AFP elevation. * **D. Hepatitis:** While acute or chronic hepatitis can cause liver enlargement and mild AFP elevations during liver regeneration, the combination of chronic alcoholism and a significant rise in AFP in an older male strongly points toward malignancy (HCC) rather than simple inflammation. **NEET-PG High-Yield Pearls:** * **Most common site of metastasis for HCC:** Lungs (via hematogenous spread). * **Fibrolamellar Variant:** A subtype of HCC seen in young adults, **not** associated with cirrhosis, and usually has **normal AFP levels**. It has a better prognosis. * **Microscopic Hallmark:** Presence of **Mallory-Denk bodies** (also seen in alcoholic hepatitis) and "bile plugs" within the tumor cells. * **Screening:** Patients with cirrhosis should be screened every 6 months using Ultrasound and AFP levels [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 399-400. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 876-877.
Question 27: Which one of the following is not a feature of liver histology in non-cirrhotic portal fibrosis (NCPF)?
- A. Fibrosis in and around the portal tracts
- B. Thrombosis of the medium and small portal vein branches
- C. Non-specific inflammatory cell infiltrates in the portal tracts
- D. Bridging fibrosis (Correct Answer)
Explanation: **Explanation:** **Non-Cirrhotic Portal Fibrosis (NCPF)**, also known as Idiopathic Portal Hypertension (IPH), is a clinical syndrome characterized by portal hypertension in the absence of cirrhosis or extrahepatic portal vein obstruction. **Why Bridging Fibrosis is the Correct Answer:** The hallmark of NCPF is that the **liver architecture remains preserved**. Bridging fibrosis (fibrosis connecting portal tracts to each other or to central veins) and regenerative nodules are the defining features of **cirrhosis**, which is explicitly absent in NCPF [1]. Therefore, bridging fibrosis is not a feature of this condition. **Analysis of Incorrect Options:** * **A. Fibrosis in and around the portal tracts:** This is a classic finding. There is dense collagenous thickening of the portal tracts (periportal fibrosis), but it does not progress to bridge between tracts. * **B. Thrombosis of the medium and small portal vein branches:** NCPF is considered an "obliterative portal venopathy." Microscopic examination often reveals "obliterative venopathy," where small portal vein branches are narrowed, thrombosed, or replaced by fibrous tissue. * **C. Non-specific inflammatory cell infiltrates:** Mild, chronic inflammatory cell infiltration (lymphocytes) within the portal tracts is a common, non-specific finding in NCPF biopsies. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Presentation:** Typically presents with massive splenomegaly and recurrent variceal bleeding in a young/middle-aged patient with **normal liver function tests (LFTs)**. * **Gross Appearance:** The liver surface is usually smooth or slightly granular, unlike the nodular surface of cirrhosis [1]. * **Key Histology:** Look for "Aberrant vessels" (herniation of portal vein branches into the parenchyma) and "Portal tract collagenization." * **Schistosomiasis:** This is the most common cause of non-cirrhotic portal fibrosis worldwide (Pipe-stem fibrosis), though NCPF in India is often idiopathic or linked to poor socioeconomic status. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 395-396.
Question 28: Multiple liver secondaries are most common in which of the following cancers?
- A. Pancreatic cancer
- B. Gastric cancer
- C. Gallbladder cancer (Correct Answer)
- D. Periampullary cancer
Explanation: **Explanation:** The liver is the most common site for hematogenous and lymphatic metastases due to its dual blood supply (portal and systemic) and fenestrated endothelium. **Why Gallbladder Cancer is the correct answer:** Gallbladder carcinoma (GBC) has a unique anatomical relationship with the liver. It is located in the gallbladder fossa, directly adjacent to the liver segments IV and V. Unlike the other options, GBC spreads to the liver via **three distinct routes**: 1. **Direct Extension:** Due to the lack of a serosa between the gallbladder and the liver [1]. 2. **Lymphatic Spread:** Through the cholecysto-retropancreatic pathways. 3. **Venous Drainage:** Small veins from the gallbladder drain directly into the portal venous system of the adjacent liver parenchyma. Statistically, liver involvement is seen in **60-90%** of cases at the time of diagnosis, making it the most frequent site for secondaries among the given options. **Analysis of Incorrect Options:** * **Pancreatic and Gastric Cancer:** While these frequently metastasize to the liver via the portal circulation, the incidence of liver secondaries at the time of presentation is lower compared to the direct and aggressive spread seen in GBC [2]. * **Periampullary Cancer:** These often present early with obstructive jaundice, leading to earlier diagnosis before extensive liver secondaries have developed. **High-Yield Pearls for NEET-PG:** * **Most common site of secondaries in the liver:** Colon (overall), followed by Stomach and Pancreas. * **Most common primary tumor of the liver:** Hepatocellular Carcinoma (HCC). * **Most common liver tumor overall:** Metastatic/Secondary carcinoma. * **Imaging Sign:** "Umbilication" of liver nodules is a classic sign of hepatic secondaries due to central necrosis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, p. 886. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 408-409.
Question 29: Primary sinusoidal dilatation of liver is also known as?
- A. Hepar lobatum
- B. Peliosis hepatis (Correct Answer)
- C. Von-Meyerburg complex
- D. Caroli's disease
Explanation: **Explanation:** **Peliosis hepatis** is a rare vascular condition characterized by the **primary dilatation of hepatic sinusoids**, resulting in the formation of irregular, blood-filled cystic spaces within the liver parenchyma. These cysts are typically not lined by endothelium. * **Pathogenesis:** It is most commonly associated with the use of **anabolic steroids**, oral contraceptives, and certain infections (notably **Bartonella henselae** in HIV patients, known as bacillary peliosis). * **Clinical Significance:** While often asymptomatic, it can lead to massive intra-abdominal hemorrhage or liver failure. **Why the other options are incorrect:** * **Hepar lobatum:** This refers to the coarsely scarred, lobulated appearance of the liver seen in **Tertiary Syphilis** due to the healing of multiple gummas. * **Von-Meyenburg Complex:** These are **biliary hamartomas**. They are small, benign clusters of dilated bile ducts embedded in a fibrous stroma, representing a malformation of the ductal plate. * **Caroli’s Disease:** This is a congenital disorder characterized by **segmental dilatation of the intrahepatic bile ducts**. It is part of the spectrum of fibropolycystic liver diseases and is associated with an increased risk of cholangiocarcinoma. **High-Yield Pearls for NEET-PG:** * **Peliosis Hepatis + HIV:** Always think of *Bartonella henselae* (Bacillary Peliosis). * **Drug Association:** Anabolic steroids are the most frequently cited pharmacological cause in exams. * **Gross Appearance:** The liver shows "blood-filled lakes" or a "Swiss cheese" appearance on cross-section.
Question 30: Which virus, besides HBV, is implicated in hepatocellular carcinoma?
- A. Hepatitis C virus (HCV) (Correct Answer)
- B. Herpes simplex virus
- C. Hepatitis A virus (HAV)
- D. Hepatitis E virus (HEV)
Explanation: Hepatocellular Carcinoma (HCC) is most commonly associated with chronic viral hepatitis, specifically **Hepatitis B Virus (HBV)** and **Hepatitis C Virus (HCV)**. [1] **Why HCV is the correct answer:** HCV is a major risk factor for HCC globally. [1] Unlike HBV (a DNA virus), HCV is an RNA virus that does not integrate into the host genome. [2] Instead, it promotes carcinogenesis through **chronic inflammation, repeated cycles of hepatocyte necrosis, and regeneration**, eventually leading to cirrhosis. [3] The HCV core protein and non-structural proteins (like NS5A) also interfere with cell signaling pathways and inhibit tumor suppressor genes (e.g., p53), further driving malignant transformation. [3] **Why the other options are incorrect:** * **Herpes Simplex Virus (HSV):** While it can cause fulminant hepatitis in immunocompromised patients or pregnant women, it does not cause chronic infection or lead to malignancy. * **Hepatitis A (HAV) & Hepatitis E (HEV):** These are primarily transmitted via the fecal-oral route and cause **acute hepatitis**. [2] They do not progress to chronic carrier states or cirrhosis, and therefore are not associated with an increased risk of HCC. (Note: HEV can be chronic in immunocompromised patients, but is not a recognized cause of HCC). [2] **High-Yield NEET-PG Pearls:** * **Most common cause of HCC worldwide:** HBV (due to high prevalence in Asia/Africa). [1] * **Most common cause of HCC in developed nations:** HCV and NAFLD/NASH. * **HBV Mechanism:** Can be direct (DNA integration/HBx protein) or indirect (cirrhosis). [3] * **HCV Mechanism:** Indirect (almost always occurs in the setting of established cirrhosis). [1] * **Tumor Marker:** Alpha-fetoprotein (AFP) is the most common screening marker for HCC. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 876-877. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, p. 842. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 336-337.
Practice by Chapter
Jaundice and Cholestasis
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Viral Hepatitis
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Alcoholic and Non-alcoholic Fatty Liver Disease
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Drug and Toxin Induced Liver Injury
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Cirrhosis and Its Complications
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Metabolic Liver Diseases
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Liver Tumors
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Gallbladder and Biliary Tract Diseases
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Congenital Liver Diseases
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Liver Transplantation Pathology
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