Pancreatic Pathology — MCQs

A 63-year-old woman presents with a 6-month history of recurrent epigastric pain and nausea. Abdominal ultrasound reveals a 13-mm hypoechoic lesion in the tail of the pancreas. Physical examination shows flushing of the face, periorbital edema, and hypotension. Laboratory studies disclose normal serum levels of gastrin, amylase, insulin, and vasoactive intestinal polypeptide. Urinalysis demonstrates elevated levels of metanephrines. Which of the following is the most likely diagnosis?

Q26Easy

Which of the following is a commonly seen pancreatic endocrine tumor?

Q27Medium

All of the following statements are true regarding Intraductal papillary mucinous neoplasms (IPMNs) of the pancreas, except:

Q28Medium

A 1-month-old infant presents with repeated bouts of bilious vomiting over the past month and inadequate feeding. The infant is in the 10th percentile for weight and 50th percentile for length. An upper GI series reveals marked narrowing of the midportion of the duodenum. What is the most likely cause of this infant's gastrointestinal obstruction?

Q29Easy

An important triggering event in acute pancreatitis is activation of?

Q30Easy

Which of the following can be used as a tumor marker in pancreatic carcinoma?

Pancreatic Pathology Indian Medical PG Practice Questions and MCQs

Question 21: What is the most common oncogene involved in pancreatic adenocarcinoma?

A. P53
B. K-RAS (Correct Answer)
C. APC
D. DCC

Explanation: **Explanation:** **K-RAS** is the most frequently mutated gene in pancreatic adenocarcinoma, occurring in approximately **90-95%** of cases [1]. It is an **oncogene** located on chromosome 12p [1]. The mutation typically involves a point mutation (most commonly at codon 12), which impairs the intrinsic GTPase activity of the RAS protein [2]. This locks the protein in a "constitutively active" GTP-bound state, leading to continuous activation of downstream signaling pathways (like MAPK and PI3K) that promote uncontrolled cell proliferation and survival [2]. **Analysis of Incorrect Options:** * **P53 (Option A):** This is a **tumor suppressor gene** (not an oncogene). While it is mutated in about 70-75% of pancreatic cancers, it usually occurs later in the progression from PanIN (Pancreatic Intraepithelial Neoplasia) to invasive carcinoma [1]. * **APC (Option C):** Mutations in the Adenomatous Polyposis Coli (APC) gene are primarily associated with **Familial Adenomatous Polyposis (FAP)** and sporadic colorectal cancer, not pancreatic adenocarcinoma. * **DCC (Option D):** "Deleted in Colorectal Cancer" is a tumor suppressor gene associated with the progression of **colorectal neoplasia**. **High-Yield Clinical Pearls for NEET-PG:** * **Sequence of Mutations:** K-RAS mutations are an **early event** in pancreatic carcinogenesis (seen in low-grade PanINs), whereas CDKN2A (p16), TP53, and SMAD4 (DPC4) mutations occur later [1]. * **SMAD4 (DPC4):** Inactivation of this gene is relatively specific to pancreatic cancer among GI malignancies [1]. * **Risk Factors:** Smoking is the strongest environmental risk factor. * **Tumor Marker:** **CA 19-9** is used for monitoring response to treatment, though it is not specific for screening. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Pancreas, pp. 897-898. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 292-293.

Question 22: Which is the least malignant pancreatic endocrine tumor?

A. Zollinger-Ellison syndrome
B. Insulinoma (Correct Answer)
C. VIPoma
D. Glucagonoma

Explanation: Pancreatic Neuroendocrine Tumors (PanNETs) are classified based on the hormones they secrete. The malignancy potential varies significantly across these subtypes. **Why Insulinoma is the correct answer:** Insulinoma is the most common functional PanNET. It is unique because **over 90% of insulinomas are benign**, solitary, and small (<2 cm). This makes it the "least malignant" of the endocrine pancreatic tumors [1]. Clinically, it presents with the **Whipple Triad**: symptoms of hypoglycemia, low blood glucose levels, and relief of symptoms upon glucose administration [1]. **Why the other options are incorrect:** * **Zollinger-Ellison Syndrome (Gastrinoma):** These are the second most common PanNETs. Unlike insulinomas, over **60-90% of gastrinomas are malignant** and have often metastasized to the liver or lymph nodes at the time of diagnosis [1]. * **VIPoma (Verner-Morrison Syndrome):** These tumors secrete Vasoactive Intestinal Peptide, causing "Pancreatic Cholera" (WDHA syndrome). Approximately **60-80% of VIPomas are malignant**. * **Glucagonoma:** These tumors present with Necrolytic Migratory Erythema (NME). They are typically large at diagnosis, and **60-90% are malignant**. **High-Yield Clinical Pearls for NEET-PG:** * **Rule of 90s for Insulinoma:** 90% are benign, 90% are solitary, and 90% are sporadic (not associated with MEN1). * **MEN1 Association:** While most PanNETs are sporadic, they are the most common cause of death in patients with **MEN1 syndrome** (3Ps: Pituitary, Parathyroid, Pancreas) [1]. * **Localization:** Most insulinomas are found within the pancreas, whereas gastrinomas are often found in the **"Gastrinoma Triangle"** (confluence of cystic/common bile duct, duodenum, and neck of the pancreas) [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, p. 1125. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1124-1125.

Question 23: Which of the following is NOT an etiology of pancreatitis?

A. Abdominal trauma
B. Hyperlipidemia
C. Islet cell hyperplasia (Correct Answer)
D. Germline mutations in the cationic trypsinogen gene

Explanation: **Explanation:** The correct answer is **Islet cell hyperplasia**. Pancreatitis is an inflammatory condition of the exocrine pancreas [4], whereas islet cell hyperplasia involves the endocrine component (Beta cells) and typically leads to hyperinsulinemic hypoglycemia, not inflammation. **Why the other options are causes of pancreatitis:** * **Abdominal Trauma (Option A):** Blunt trauma or medical procedures like ERCP can cause direct mechanical injury to the acinar cells, triggering the premature activation of digestive enzymes [1]. * **Hyperlipidemia (Option B):** Specifically, Hypertriglyceridemia (typically levels >1000 mg/dL) leads to the breakdown of triglycerides by pancreatic lipase into toxic free fatty acids, which damage the capillary endothelium and acinar cells [1]. * **Germline mutations (Option D):** Mutations in the **PRSS1 gene** (encoding cationic trypsinogen) prevent the self-inactivation of trypsin [3]. This leads to "Hereditary Pancreatitis," characterized by recurrent attacks from childhood. **NEET-PG High-Yield Pearls:** 1. **Most Common Causes:** Gallstones (obstructive) and Alcohol (metabolic/toxic) account for 80% of cases [1][4]. 2. **Genetic Factors:** Besides *PRSS1*, mutations in **SPINK1** (trypsin inhibitor) and **CFTR** (Cystic Fibrosis) are high-yield associations [2]. 3. **Drugs:** "I GET SMASHED" mnemonic—Azathioprine, Sulfonamides, and Valproate are classic culprits [1]. 4. **Morphology:** Look for **Proteolysis**, **Fat Necrosis** (saponification with calcium), and **Hemorrhage** (due to elastase destroying vessel walls). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 406-407. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Pancreas, pp. 891-892. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Pancreas, pp. 890-891. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Pancreas, pp. 889-890.

Question 24: Histology for type 2 autoimmune pancreatitis characteristically demonstrates which of the following?

A. IgG4 positive plasma cells > 10/HPF
B. Granulocytic epithelial lesion (Correct Answer)
C. Storiform fibrosis
D. Microvascular thrombosis

Explanation: ### Explanation Autoimmune Pancreatitis (AIP) is a distinct form of chronic pancreatitis categorized into two subtypes based on histological and clinical features. [1] **1. Why "Granulocytic Epithelial Lesion" is correct:** Type 2 AIP (also known as **Idiopathic Duct-Centric Pancreatitis**) is characterized by the presence of **Granulocytic Epithelial Lesions (GELs)**. These are pathognomonic histological findings where neutrophils infiltrate and destroy the epithelium of the small pancreatic ducts. Unlike Type 1, Type 2 AIP is not associated with elevated serum IgG4 levels and is often linked with Inflammatory Bowel Disease (IBD), particularly Ulcerative Colitis. **2. Analysis of Incorrect Options:** * **Option A (IgG4 positive plasma cells > 10/HPF):** This is a hallmark of **Type 1 AIP**, which is the pancreatic manifestation of IgG4-Related Disease (IgG4-RD). [1] * **Option C (Storiform fibrosis):** This "cartwheel" pattern of fibrosis is characteristic of **Type 1 AIP** and other IgG4-related systemic diseases. Type 2 AIP typically lacks prominent storiform fibrosis. * **Option D (Microvascular thrombosis):** This is not a characteristic feature of AIP; it is more commonly associated with acute necrotizing pancreatitis or pancreatic infarction. **3. High-Yield Clinical Pearls for NEET-PG:** | Feature | Type 1 AIP (LPSP) | Type 2 AIP (IDCP) | | :--- | :--- | :--- | | **Full Name** | Lymphoplasmacytic Sclerosing Pancreatitis | Idiopathic Duct-Centric Pancreatitis | | **Histology** | IgG4+ plasma cells, Storiform fibrosis, Obliterative phlebitis | **Granulocytic Epithelial Lesions (GELs)** | | **IgG4 Levels** | Elevated | Normal | | **Associations** | Systemic (Sialadenitis, Retroperitoneal fibrosis) | **Inflammatory Bowel Disease (IBD)** | | **Demographics** | Elderly males | Younger patients, no gender bias | **Key Takeaway:** If the question mentions "GELs" or "Neutrophilic duct injury," think **Type 2 AIP**. If it mentions "IgG4," "Storiform fibrosis," or "Obliterative phlebitis," think **Type 1 AIP**. [1] **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Pancreas, pp. 893-895.

Question 25: A 63-year-old woman presents with a 6-month history of recurrent epigastric pain and nausea. Abdominal ultrasound reveals a 13-mm hypoechoic lesion in the tail of the pancreas. Physical examination shows flushing of the face, periorbital edema, and hypotension. Laboratory studies disclose normal serum levels of gastrin, amylase, insulin, and vasoactive intestinal polypeptide. Urinalysis demonstrates elevated levels of metanephrines. Which of the following is the most likely diagnosis?

A. Adenocarcinoma of pancreas
B. Glucagonoma
C. Insulinoma
D. Pancreatic carcinoid (Correct Answer)

Explanation: **Explanation:** The clinical presentation points toward **Carcinoid Syndrome** secondary to a **Pancreatic Carcinoid tumor** (a type of Pancreatic Neuroendocrine Tumor or PanNET). 1. **Why the correct answer is right:** The patient exhibits the classic triad of carcinoid syndrome: **flushing, periorbital edema, and hypotension** (vasodilation) [1]. While most carcinoids occur in the GI tract (midgut), they can arise in the pancreas [1]. These tumors secrete bioactive amines like serotonin and kallikrein. The key diagnostic clue here is the **elevated urinary metanephrines**, which can sometimes be seen in carcinoid tumors due to cross-reactivity or co-secretion, though more typically, elevated **5-HIAA** is the hallmark [1]. The normal levels of gastrin, insulin, and VIP rule out other common PanNETs [2]. 2. **Why incorrect options are wrong:** * **Adenocarcinoma of the pancreas:** Usually presents with painless obstructive jaundice (head) or weight loss and back pain (tail). It does not cause vasomotor symptoms like flushing or hypotension. * **Glucagonoma:** Characterized by the "4 Ds": Diabetes, Dermatitis (Necrolytic Migratory Erythema), Deep vein thrombosis, and Depression. * **Insulinoma:** Presents with Whipple’s triad (hypoglycemic symptoms, low blood glucose, and relief upon glucose administration) [2]. Serum insulin would be elevated. 3. **High-Yield Clinical Pearls for NEET-PG:** * **Carcinoid Syndrome:** Only occurs when tumor metabolites bypass hepatic metabolism (i.e., hepatic metastasis or primary extra-portal sites like the lungs/ovaries) [1]. * **Diagnosis:** Best initial test is **24-hour urinary 5-HIAA**. * **Localization:** Somatostatin receptor scintigraphy (OctreoScan) is highly sensitive for PanNETs. * **Treatment:** Octreotide (Somatostatin analog) is used to manage symptomatic flushing and diarrhea. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 780-782. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1124-1125.

Question 26: Which of the following is a commonly seen pancreatic endocrine tumor?

A. Insulinoma (Correct Answer)
B. Somatostatinoma
C. Gastrinoma
D. Glucagonoma

Explanation: **Explanation:** Pancreatic Neuroendocrine Tumors (PanNETs) are rare neoplasms arising from the islet cells [1]. Among these, **Insulinoma** is the most common functional pancreatic endocrine tumor. **1. Why Insulinoma is the correct answer:** Insulinomas originate from the beta cells of the islets of Langerhans. They are characterized by the "Rule of 90": approximately 90% are benign, 90% are solitary, and 90% are less than 2 cm in diameter. Clinically, they present with the **Whipple Triad**: symptoms of hypoglycemia (confusion, sweating, palpitations), low blood glucose levels (<50 mg/dL), and immediate relief of symptoms upon glucose administration [1]. **2. Why the other options are incorrect:** * **Gastrinoma (Option C):** This is the second most common functional PanNET. It causes **Zollinger-Ellison Syndrome**, leading to multiple, refractory peptic ulcers [1]. Notably, many gastrinomas are found in the "Gastrinoma Triangle" (duodenum/peripancreatic tissue) rather than the pancreas itself [1]. * **Glucagonoma (Option D):** A rare tumor of alpha cells. It is classically associated with **Necrolytic Migratory Erythema (NME)**, diabetes mellitus, and anemia. * **Somatostatinoma (Option B):** The rarest of the functional PanNETs. It presents with a clinical triad of diabetes, cholelithiasis, and steatorrhea due to the inhibitory effect of somatostatin on insulin, CCK, and pancreatic enzymes. **High-Yield Clinical Pearls for NEET-PG:** * **Most common PanNET overall:** Non-functional tumors (often asymptomatic until large). * **Most common functional PanNET:** Insulinoma. * **Genetic Association:** PanNETs (especially Gastrinomas and Insulinomas) are frequently associated with **MEN1 Syndrome** (Pituitary, Parathyroid, Pancreas) [1]. * **Histology:** Typical "salt and pepper" chromatin and organoid/nesting patterns are characteristic of neuroendocrine tumors. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1123-1125.

Question 27: All of the following statements are true regarding Intraductal papillary mucinous neoplasms (IPMNs) of the pancreas, except:

A. Mainly involve the head of the pancreas
B. Are precursor lesions of pancreatic carcinoma
C. Usually involve the large ducts of the pancreas
D. There is the presence of ovarian stroma on histology (Correct Answer)

Explanation: **Explanation:** Intraductal Papillary Mucinous Neoplasms (IPMNs) are mucin-producing epithelial neoplasms that arise within the pancreatic ductal system [1]. **Why Option D is the correct answer (The Exception):** The presence of **"ovarian-type subepithelial stroma"** is the pathognomonic histological feature of **Mucinous Cystic Neoplasms (MCNs)**, not IPMNs. MCNs occur almost exclusively in females and are typically located in the tail of the pancreas. IPMNs lack this specialized stroma. **Analysis of Incorrect Options:** * **Option A:** IPMNs most frequently involve the **head of the pancreas** (unlike MCNs, which favor the tail). * **Option B:** IPMNs are recognized **precursor lesions** to invasive pancreatic adenocarcinoma [1]. They follow a progression from low-grade dysplasia to high-grade dysplasia and finally invasive carcinoma. * **Option C:** By definition, IPMNs involve the **larger pancreatic ducts** (either the main pancreatic duct or its major side branches). This distinguishes them from Pancreatic Intraepithelial Neoplasia (PanIN), which involves small microscopic ducts (<5mm). **High-Yield Clinical Pearls for NEET-PG:** * **Demographics:** IPMNs are more common in **men** (unlike MCNs). * **Imaging:** Classically described as a "grape-like" cluster of cysts communicating with the pancreatic duct. * **Key Distinction:** If a question mentions a mucinous cyst in a **female** with **ovarian stroma** and **no ductal communication**, think **MCN**. If it mentions a **male**, the **pancreatic head**, and **ductal communication**, think **IPMN**. * **Markers:** Both IPMN and MCN may show elevated CEA levels in the cyst fluid [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Pancreas, p. 897.

Question 28: A 1-month-old infant presents with repeated bouts of bilious vomiting over the past month and inadequate feeding. The infant is in the 10th percentile for weight and 50th percentile for length. An upper GI series reveals marked narrowing of the midportion of the duodenum. What is the most likely cause of this infant's gastrointestinal obstruction?

A. Annular pancreas (Correct Answer)
B. Duodenal polyp
C. Islet cell adenoma
D. Pancreatic pseudocyst

Explanation: ### Explanation **Correct Answer: A. Annular Pancreas** **Mechanism:** Annular pancreas is a congenital anomaly where a ring of pancreatic tissue completely or partially encircles the **second part of the duodenum**. This occurs due to the **failure of the ventral pancreatic bud to rotate properly** behind the duodenum. Instead, the bifid ventral bud migrates in opposite directions, fusing with the dorsal bud and creating a constricting band. This leads to extrinsic duodenal obstruction, typically presenting in infancy with **bilious vomiting** (as the obstruction is usually distal to the ampulla of Vater) and failure to thrive. **Why other options are incorrect:** * **B. Duodenal polyp:** While polyps can cause obstruction, they are extremely rare in neonates and typically present with occult bleeding or intussusception in older children/adults. * **C. Islet cell adenoma:** These are functional neuroendocrine tumors (e.g., insulinomas) that present with metabolic symptoms like hypoglycemia, not mechanical bowel obstruction. * **D. Pancreatic pseudocyst:** These are complications of acute or chronic pancreatitis [1]. They are rare in a 1-month-old and would typically follow a history of trauma or systemic illness. **NEET-PG High-Yield Pearls:** * **Embryology:** Caused by abnormal migration of the **ventral pancreatic bud**. * **Radiology:** Characterized by the **"Double Bubble Sign"** on X-ray (air in the stomach and proximal duodenum), similar to duodenal atresia. * **Associations:** Strongly associated with **Down Syndrome (Trisomy 21)**, duodenal atresia, and malrotation. * **Clinical Presentation:** Can be asymptomatic in adults or present with peptic ulcers due to stasis. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 407-408.

Question 29: An important triggering event in acute pancreatitis is activation of?

A. Pepsinogen
B. Prekallikrein
C. Trypsinogen (Correct Answer)
D. Lipase

Explanation: ### Explanation **Correct Answer: C. Trypsinogen** The fundamental pathophysiology of **Acute Pancreatitis** involves the **inappropriate intrapancreatic activation of digestive enzymes**, leading to autodigestion of the gland [1, 3]. **Trypsinogen** is the critical "trigger" or "master switch." Under normal physiological conditions, trypsinogen is converted to its active form, **Trypsin**, only in the duodenum by the enzyme enteropeptidase [2]. In acute pancreatitis, various insults (e.g., gallstones, alcohol, or trauma) cause the premature activation of trypsinogen within the pancreatic acinar cells [1, 3]. Once activated, Trypsin initiates a **catalytic cascade** by activating other zymogens (proelastase, prophospholipase, and prekallikrein), leading to proteolysis, fat necrosis, and vascular damage [1, 2]. #### Why other options are incorrect: * **A. Pepsinogen:** This is a precursor to pepsin, secreted by the gastric chief cells. It plays a role in protein digestion in the stomach, not the pancreas. * **B. Prekallikrein:** While trypsin does activate the kallikrein-kinin system (leading to vasodilation and increased permeability), this is a **downstream effect**. Prekallikrein activation is a consequence, not the primary triggering event. * **D. Lipase:** Pancreatic lipase is secreted in its active form. While it contributes to fat necrosis (enzymatic fat necrosis), it does not trigger the systemic inflammatory cascade or activate other zymogens. #### High-Yield Clinical Pearls for NEET-PG: * **The "Colocalization Hypothesis":** Intracellular activation of trypsinogen often occurs when digestive enzymes and lysosomal hydrolases (like **Cathepsin B**) are packaged together into the same vacuoles. * **Protective Mechanisms:** The pancreas normally prevents autodigestion via **SPINK1** (Serine Protease Inhibitor Kazal-type 1), which inactivates small amounts of prematurely formed trypsin [4]. * **Genetic Link:** Mutations in the **PRSS1** gene (cationic trypsinogen) lead to hereditary pancreatitis by making trypsin resistant to inactivation [4]. * **Morphological Hallmark:** The most characteristic histological feature of acute pancreatitis is **Enzymatic Fat Necrosis** (chalky white deposits). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Pancreas, pp. 890-891. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Pancreas, pp. 889-890. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 406-407. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Pancreas, pp. 892-893.

Question 30: Which of the following can be used as a tumor marker in pancreatic carcinoma?

A. CA-125
B. CA 27-29
C. CA 19-9 (Correct Answer)
D. CA 15-3

Explanation: **Explanation:** **CA 19-9 (Carbohydrate Antigen 19-9)** is the most widely used and clinically validated tumor marker for **Pancreatic Adenocarcinoma**. It is a sialylated Lewis (a) blood group antigen. While it lacks the sensitivity and specificity required for population screening, it is invaluable for **monitoring treatment response** and **detecting disease recurrence** following surgical resection. **Analysis of Incorrect Options:** * **CA-125:** This is the primary tumor marker for **Ovarian Cancer** (specifically non-mucinous epithelial tumors). It can also be elevated in endometriosis and pelvic inflammatory disease. * **CA 15-3 & CA 27-29:** These are both markers primarily used to monitor **Breast Cancer**. They are used to track the clinical course of patients with metastatic disease rather than for initial diagnosis. **High-Yield Clinical Pearls for NEET-PG:** 1. **Lewis Antigen Status:** Approximately 5–10% of the population is "Lewis antigen-negative" (Le a-/b-). These individuals lack the enzyme to synthesize CA 19-9; therefore, they will not show elevated levels even in the presence of advanced pancreatic cancer. 2. **Obstructive Jaundice:** CA 19-9 can be falsely elevated in benign conditions like biliary obstruction (cholangitis or gallstones). Levels should be re-evaluated after biliary decompression. 3. **Prognosis:** Very high preoperative levels of CA 19-9 (>1000 U/mL) usually correlate with occult metastatic disease and poor resectability [1]. 4. **Other Markers:** While **CEA** (Carcinoembryonic Antigen) can also be elevated in pancreatic cancer, it is less specific than CA 19-9. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Pancreas, p. 901.

Practice by Chapter

Congenital Anomalies of Pancreas

Practice Questions

Acute Pancreatitis

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Chronic Pancreatitis

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Pancreatic Neoplasms

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Cystic Lesions of Pancreas

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Endocrine Tumors of Pancreas

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Pancreatic Manifestations of Systemic Diseases

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Pancreatic Transplantation Pathology

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Pancreatic Pseudocysts

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Laboratory Assessment of Pancreatic Diseases

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