Liver/ pancreas

Splenic vein in relation to the pancreas

·       The splenic vein lies posterior to the body and tail of the pancreas, runs posterior/medial to the head, and joins with the SMV at the pancreatic neck to form the portal–splenic confluence (main portal vein).

Location of the liver — where it lies in the body, relationships to other organs and structures.

• It’s in the right upper quadrant (RUQ) of the abdomen.

• It spans across to the left upper quadrant (LUQ) somewhat (left lobe).

• Inferior to the diaphragm, the stomach, duodenum, right kidney, colon are inferior. the IVC is posterior and medially it is connected to the gallbladder and porta hepatis structure

Covering of the liver — what covers it, what the capsule is, where it is not covered.

• The liver is covered entirely by a fibrous capsule called Glisson’s capsule — that covers its surface and ensheathes vessels, bile ducts, etc.

• Over that, it is partly covered by visceral peritoneum (serous membrane), except in certain areas.

• The bare area of the liver is the area not covered by peritoneum (on the posterior superior surface, in direct contact with the diaphragm). This is the one spot without peritoneal covering, but it is still covered by Glisson’s capsule, since Glisson’s is the connective tissue capsule.

• The bare area is bounded by the coronary ligaments and the right triangular ligament of the liver.

A)   Classical Lobes (Anatomic)

• Right lobe – largest; separated from left lobe by the main lobar fissure and gallbladder fossa/IVC.

• Left lobe – smaller; divided from right lobe by falciform ligament (surface anatomy).

• Caudate lobe – posterior, bounded by IVC (posterior) and ligamentum venosum (anterior).

• Quadrate lobe – inferior, between gallbladder fossa (right) and ligamentum teres (left).

B)   Couinauds liver segments

Instead of just lobes, we use 8 Couinaud segments, each with its own portal triad inflow and hepatic vein outflow.

Segment I = Caudate lobe

Segments II–VIII correspond to left/right lobe subdivisions (left lateral, left medial, right anterior, right posterior; divided into superior/inferior).

Quick segment breakdown:

• Segment I = Caudate lobe

• II & III = Left lateral (superior/inferior)

• IVa & IVb = Left medial

• V–VIII = Right lobe (anterior/posterior, caudal/cephalad).

Ligaments (structure of real tissue) and Fissures (anatomic landmark) of the Liver

On ultrasound, these appear echogenic because of collagen and fat around them. They’re key landmarks:

Glisson’s Capsule

• Definition: Thin fibrous connective tissue capsule that covers the liver.

• Extends inward with vessels and ducts at the porta hepatis.

• US appearance: echogenic outline of the liver.

2. Main Lobar Fissure (MLF)

• Definition: Echogenic line from the neck of the gallbladder → right portal vein → IVC.

• Function: Separates right and left lobes functionally.

• Sonography: Crucial landmark to find gallbladder and right portal vein.

Main lobar fissure = Gallbladder → IVC

Ligamentum teres fissure = Separates left lobe from quadrate

3. Falciform Ligament

• Definition: Peritoneal reflection attaching the liver to the anterior abdominal wall and diaphragm.

• Contains the ligamentum teres (round ligament).

• Sonography: Appears as an echogenic line extending from anterior abdominal wall to liver.

4. Ligamentum Teres (Round Ligament)

• Definition: Remnant of the fetal umbilical vein.

• Runs in the falciform ligament to the left portal vein.

• Sonography: Bright echogenic round structure in the left lobe; helps locate left PV.

5. Ligamentum Venosum

• Definition: Remnant of the fetal ductus venosus.

• Separates the caudate lobe (posterior) from the left lobe (anterior).

• Sonography: Appears as an echogenic line between left PV and IVC.

6. Other Peritoneal Reflections (extras)

• Coronary ligaments: Suspend the liver from the diaphragm; define the bare area.

Right & left triangular ligaments: where the coronary ligaments come together (right and left sides).

• 👉 Exam tip: If they ask “what’s echogenic and helps divide lobes/segments?” — answer: ligaments and fissures.

Why This Matters in Scanning

• Ligamentum teres = bright round structure in left lobe; helps locate left PV.

• Main lobar fissure = pointer line from gallbladder → IVC; helps locate main portal vein.

• Portal vs hepatic veins = differentiate by wall brightness and flow direction.

• Couinaud’s system = surgeons and radiologists use for segmental resections and for reporting lesions.

3. Vascular Anatomy of the Liver

Portal Venous System

• Main portal vein (MPV): formed by splenic vein + SMV; enters porta hepatis.

• Splits into right and left portal veins.

  • Right PV → anterior & posterior branches.

  • Left PV → medial & lateral branches.

• Portal flow is hepatopetal (toward liver). On US: bright echogenic walls (because of collagen sheath).

Hepatic Veins

  Right HV – in right intersegmental fissure → divides right lobe (anterior vs posterior).

  Middle HV – in main lobar fissure → separates right and left lobes.

  Left HV – in left intersegmental fissure → divides medial and lateral segments.

• Flow is hepatofugal (away from liver).

👉 Sonography trick: PVs = echogenic borders, HVs = thin walls.

Hepatic Artery

• Usually branches from celiac trunk → common hepatic → proper hepatic.

• Runs with PV and bile duct in portal triad (“Mickey Mouse sign”).

• Supplies 20–30% of blood to liver (oxygen-rich).

• Sonography: Small anechoic tubular structure anterior to PV, with low-resistance Doppler waveform.

Portal Triad

• Components: Portal vein, Hepatic artery, Common bile duct.

• Seen on transverse scan at porta hepatis = “Mickey Mouse sign”:

  • Portal vein = head (largest, posterior).

  • CBD = right ear (anterior lateral).

  • Hepatic artery = left ear (anterior medial).

Clinical Relevance

• Portal hypertension: PV flow may reverse (hepatofugal).

• Budd–Chiari syndrome: Hepatic vein obstruction.

• TIPS procedure: Stent placed between PV and HV to relieve portal pressure.

Functions of the Liver

1. Metabolic Functions

• Carbohydrate metabolism

  • Converts dietary sugars into glucose.

  • Stores glucose as glycogen.

  • Breaks down glycogen back into glucose when needed.

• Fat metabolism

  • Converts fats into lipoproteins (for transport).

  • Stores and mobilizes fat for energy.

• Protein metabolism

  • Converts amino acids → urea (for excretion).

  • Synthesizes plasma proteins (albumin, clotting factors).

2. Storage Functions

• Stores glycogen, iron, vitamins (A, D, B12, K).

• Acts as a reservoir for nutrients between meals.

3. Digestive Functions

• Produces bile, which emulsifies fats in the small intestine.

• Bile carries away waste products (bilirubin, cholesterol).

4. Detoxification Functions

• Detoxifies drugs, alcohol, poisons.

• Processes by-products of metabolism (like ammonia → urea).

• Breaks down hormones.

5. Immune / Filtering Functions

• Kupffer cells in the liver phagocytize bacteria, old RBCs, and debris.

• Helps regulate blood composition.

🔍 Clinical Connection

• If the liver can’t perform these functions → you see lab abnormalities:

  • Poor protein synthesis → ↓ albumin, ↑ PT/INR.

  • Poor bilirubin metabolism → ↑ bilirubin, jaundice.

  • Poor detox → encephalopathy (ammonia buildup).

2. Liver Diseases (Types)

Hepatocellular disease- disease class

 Definition: The problem is primarily in the liver cells (hepatocytes).

Examples:

·       Viral hepatitis (A, B, C)       *Cirrhosis (from alcohol, viral hepatitis, etc.)

·       Glycogen storage disease              *Hemochromatosis

·        Labs: ↑ AST, ↑ ALT, ↑ bilirubin (conjugated & unconjugated).

Treatment: Usually medical (antivirals, lifestyle, supportive).

Obstructive disease- disease class

 Definition: The hepatocytes are working, but bile can’t get out (block in biliary tree).

Examples:

o   Gallstones in common bile duct (choledocholithiasis)

o   Tumor in pancreas head compressing bile duct

o   Cholangiocarcinoma (bile duct cancer)

o   Porta hepatis mass compressing ducts

•  Labs: ↑ alkaline phosphatase, ↑ direct bilirubin.

•  Treatment: Usually surgical or interventional (ERCP, stents, removal of stones/tumor).

3. Liver Function Tests (Labs)

Common ones you should know:

• AST (asparate Aminotransferase), ALT (Alanine Aminotransferase) – increase with liver cell injury. Increase when hepatocytes are damaged. ALT more specific of hepatocellular injury.

·       Alkaline Phosphatase (ALP)- Enzyme in bile duct epithelium. ↑ when bile flow is obstructed. Pattern: High ALP → Obstructive disease (stones, tumor)

·       Bilirubin- Breakdown product of hemoglobin. Indirect (unconjugated): Before liver conjugation. Direct (conjugated): After conjugation in liver.

Patterns:   ↑ Both → Hepatocellular disease (cells can’t excrete it).                                                                         …………...↑ Direct only → Obstructive disease (can’t drain bile).

Clinical: Jaundice, dark urine, pale stools, pruritus.

• PT (prothrombin time) – Reflects clotting factor by liver. This is going to be low in chronic liver diseases (causing ascites and edema). ↑ PT (slower clotting) → poor synthetic function (cirrhosis, severe hepatitis).

• Albumin & globulins – major plasma protein made by liver. Low in chronic liver disease → ascites, edema.

  Globulins: Can be elevated in cirrhosis and chronic hepatitis.

👉 Exam tip: “Direct bilirubin ↑ = obstruction; both direct & indirect ↑ = hepatocellular disease.”

4. Developmental Anomalies

• Agenesis – Failure of part or all of the liver to develop. very rare, incompatible with life (total).

• Anomalies of position

  • situs inversus organs reversed (liver on the left, spleen on the right).

  •  Congenital diaphragimatic hernia/ omphalacele (portions of liver hernia outside the chest or abdomen)

• Accessory fissures: Extra grooves or folds caused by peritoneal infolding. Can look like scars/ lesions.

• Vascular anomalies:  Hepatic artery variations (very common ~45%):

  • Replaced left hepatic artery from left gastric artery.

  • Replaced right hepatic artery from superior mesenteric artery.

  • Replaced common hepatic artery from SMA.

•  Portal venous anomalies: Rare; can include atresia, strictures, abnormal branching.

•  Hepatic vein anomalies: Accessory veins may drain parts of right lobe into IVC or join middle HV.

Ultrasound: Altered vascular course, can impact Doppler assessment

5. Diffuse Diseases

A) Fatty Liver (Hepatic Steatosis)- Reversable accumulation of triglycerides in hepatocytes.

·       Definition: Reversible buildup of triglycerides in hepatocytes.

·       Causes: Obesity, alcohol, diabetes, steroids, pregnancy, hyperlipidemia.

·       Labs: Mild ↑ AST/ALT; may be normal.

·       Ultrasound: ↑ echogenicity, poor penetration, obscured diaphragm/vessels.

·       Treatment: Reversible with lifestyle change, stop alcohol, treat underlying condition.

B) Hepatitis- inflammation of liver, mostly from viral infection.

• Most common in USA: Hepatitis B.

• Types: A (fecal-oral), B (blood/body fluids, high risk for health workers), C (chronic, blood-borne).

• Acute hepatitis US: “starry sky” (bright PV walls, hypoechoic parenchyma). Hepatomegaly. Texture may look normal. Gallbladder wall thickening may be seen.

·       Chronic hepatitis US: coarse parenchyma, may lead to fibrosis. Coarse echotexture. Normal or small liver size. Fibrosis may be seen, but not as bright as fatty infiltration. May progress to cirrhosis

C) Cirrhosis- scar tissue

• Chronic, irreversible scarring and fibrosis.

• Causes: alcohol (micronodular), hepatitis/infection (macronodular).

• Leads to: Portal hypertention, ascites, hepatocellular carcinoma

• Cirrhosis shows a coarse, heterogeneous liver echotexture, often with nodular contour. Early cirrhosis may show hepatomegaly, while advanced cases show a small shrunken right lobe with caudate and left lobe hypertrophy. Surface nodularity and ascites are common

D) Glycogen Storage Disease- glycogen accumulation

• Inherited, will cause glycogen accumulation in liver and kidneys. (most common Von Gierke disease).

• US: hepatomegaly, increased echogenicity. AST, ALT may be elevated

• Associated with adenomas- which is possible to become malignant. Can cause hypoglycemia.

E) Hemochromatosis- rare disorder of iron metabolism

• body absorbs and stores too much iron, which deposits in organs (especially liver, pancreas, heart, skin).

• Can → cirrhosis, portal hypertension hepatocellular carcinoma.

• US: hepatomegaly, ↑ echogenicity.

F) Budd–Chiari Syndrome- Obstruction of the hepatic veins or IVC, preventing normal venous outflow from the liver

• Cause: hepatic vein or IVC thrombosis.

• Symptoms: abdominal pain, ascites, hepatomegaly, jaundice, nausea.

• Types:

  • Primary (congenital obstruction of hepatic veins/IVC).

  • Secondary (aquired obstruction from thrombus/tumor invasion). Causes: clotting disorders and renal cell carcinoma, hepatocellular carcinoma.

• Prognosis: poor, often fatal.

*Important Anatomy Note:

• Caudate lobe = Segment I.

• It has direct venous drainage to the IVC (separate from hepatic veins).

• Because of this, the caudate lobe often enlarges in Budd–Chiari (while the rest of the liver is congested).

G. Portal Hypertension- abnormally high pressure in portal venous system (Diffuse)

• Causes: cirrhosis (most common), diffuse mets, portal vein thrombosis, Budd–Chiari, right heart failure.

• Flow changes:

  • Normal PV flow = hepatopetal (toward liver).

  • Portal HTN = hepatofugal (away from liver).

• Collateral pathways: Alternate ways for blood to flow= esophageal, gastric, hemorrhoidal, splenorenal, recanalized umbilical vein. They can look tortuous

Portal vein thrombosis is the presence of thrombus in the portal vein, often caused by cirrhosis, malignancy, or hypercoagulable states. It prevents normal hepatopetal flow, leading to portal hypertension. On ultrasound, look for echogenic thrombus, absent PV flow, dilated portal vein, and possible cavernous transformation.

7. Portal Vein Thrombosis & Shunts

• PV thrombosis: blockage by thrombus/tumor → ascites, splenomegaly.

• Shunts-

  • Portacaval (PV at the confluence to IVC).

  • Mesocaval (SMV to IVC). Decompresses portal system but draining intestinal blood direct into IVC.

  • Splenorenal (splenic vein to LRV). Bypass portal system by draining SV into systemic circulation.

·       Tips is both a shunt and stent, stent bc the pathway is kept open using metal stent, but it creates a new pathway.

• TIPS (Transjugular Intrahepatic Portosystemic Shunt):

  • stent between PV and HV. Used to reduce portal pressure and variceal bleeding. This is only one that goes inside the liver

  • The stent connects a branch of the portal vein to a hepatic vein → creating an artificial pathway for blood to bypass the scarred/fibrotic liver.

  • the shunt is the artificial connection between the portal and hepatic veins, and the stent is the device that holds that connection open.

H) Biliary Obstruction (Diffuse)

• Proximal (above cystic duct) causes: gallstones, bile duct carcinoma, porta hepatis tumor.

• Distal (below CD) causes: CBD stones, stricture, pancreatic head mass.

• Symptoms: jaundice, pruritus (itching), RUQ pain, ↑ direct bilirubin & ALP.

10. Focal Liver Lesions (important differentials)

1. Hepatic cysts- Benign, fluid filled

   • benign, anechoic, posterior enhancement. Usually asymptomatic. Simple and uniform in appearance.

2. Hepatic Adenoma- Benign liver tumor made of hepatocytes

   • linked to glycogen storage disease, contraceptives.

   • Most often seen in young women on oral contraceptives or with glycogen storage disease.

   • On ultrasound it appears as a well-defined mass, variable in echogenicity, and carries risk of rupture or malignant transformation.

3. Polycystic liver disease- Inherited disorder where liver develops multiple liver cysts

   • usually associated with polycystic kidney disease. Most patients are asymptomatic, but large cysts can cause pain or obstruction.

   • On ultrasound, cysts are anechoic, thin-walled, with posterior enhancement.

4. Abscess- localize collection of pus and/ or infection in liver.

   • Pyogenic (bacteria) – fever, pain.

   • Amebic (parasite)- RUQ pain, diarrhea, fever, hepatomegaly

   • Echinococcal (Parasite- tapeworm- sheepdog)- RUQ pain, nausea, may rupture. Appearance: Waterlily, daughter cyst

   • Hepatic candidiasis (fungal)- RUQ pain, hepatomegaly, sepsis immunocompromised pts (such as chemo/ transplant/ HIV), multiple small “bull’s eye” lesions.

   • US for all abscesses: complex mass, may have debris.

5. Chronic Granulomatous Disease- Inherited immune system, often diagnosed in infancy

   • defective white blood cells (phagocytes) that cannot kill certain bacteria and fungi.

   • Leads to recurrent infections (lungs, lymph nodes, liver, skin). Often accompanied by splenomegaly.

   • Multiple small, hypoechoic nodules or granulomas scattered in the liver and spleen.

6. Cavernous hemangioma- most common benign liver tumor, tangle of dilated vessels

   • Common in women 20-50. Usually asymptomatic.

   • Hyperechoic, well-defined lesion (usually located in the right lobe). Homogeneous echotexture. If very large: may look heterogeneous.

7. Focal nodular hyperplasia (FNH)- Benign, increased number of normal cells in tissue in response to irritation or stimulus.

   •  young women, central scar forms and FNH develops causing nodular overgrowth

8. HCC (hepatocellular carcinoma)- Highly malignant. Most common primary (originates in the liver) malignant liver tumor

   •  linked to cirrhosis, hepatitis and history of chronic liver disease. More common in men.

   • Weight loss, hepatomegaly, RUQ pain

   • Can invade vessels (especially the portal vein and hepatic vein).

9. Metastatic liver disease (Mets)- Most common secondary (cancer begins elsewhere and goes to the liver) malignant liver tumor

   • Primary sources are colon, breast, lung primaries.

   • Target or “bull’s eye” appearance: hypoechoic rim with echogenic center.

   • Calcifications: seen with mucinous adenocarcinoma (colon, ovary), jaundice, ascites.

   • Diffuse infiltration: “moth-eaten” appearance with multiple lesions.

   • Short survival rate after detection of liver metastases hepatocellular carcinoma, pancreas, stomach, and esophagus.

10.   Lymphoma: can be primary or secondary, often hypoechoic.

Symptoms include hepatomegaly, fever, weight loss, night sweats, and fatigue. On ultrasound, it often appears as multiple hypoechoic lesions or diffuse infiltration.

·        Primary hepatic lymphoma (rare):

o   Cancer originates in the liver itself.

o   Very uncommon; usually associated with immunocompromised patients (HIV, transplant, hepatitis C).

·        Secondary hepatic lymphoma (much more common):

o   Liver involvement from systemic lymphoma (non-Hodgkin’s or Hodgkin’s).

o   The liver is frequently affected in disseminated disease.

11.   Hepatic Trauma- liver is the most commonly injured from blunt or penetrating abdominal trauma

·       Ultrasound is the best evaluated with ultrasound. FAST exam

• Check: Morison’s pouch- liver and RT kidney, subphrenic (liver and diaphragm), subhepatic (below right lobe of liver), Pouch of Douglas (lowest point of peritoneal cavity): Check for free fluid in pelvis

• Also check around the spleen, heart and both kidneys

• Symptoms: RUQ pain, hypotension/ shock

Symptoms of biliary obstruction

·       Symptoms of biliary obstruction include jaundice, pruritus, dark urine, pale stools, RUQ pain, and sometimes nausea/vomiting

·       correlates ↑ direct bilirubin and ↑ ALP.

Symptoms= what pt feels/ sees

Labs= what we measure: ↑ direct bilirubin, ↑ ALP, mild ↑ AST/ALT.

Elevation of bilirubin results in

·       include jaundice, pruritus, dark urine, pale stools, RUQ pain, and sometimes nausea/vomiting

“Most Common” Facts (easy test points)

• Most common benign liver tumor = hemangioma.

• 2nd most common benign = FNH.

• Most common primary malignant = HCC.

• Most common malignant overall = Mets.

• Most common organ injured in blunt trauma = liver.

Pancreas is divided into five regions

-The head lies within the C-loop of the duodenum, with the gastroduodenal artery (GDA) along its anterior border and the IVC, renal veins, and portal-splenic confluence posteriorly.

-Extending from the head is the uncinate process, a hook-like projection that lies posterior to the superior mesenteric vein (SMV).

-The neck is a small portion between the head and body, positioned anterior to the portal-splenic confluence.

-The body is the largest portion of the pancreas, located anterior to the aorta and superior mesenteric artery (SMA), with the splenic vein coursing along its posterior border.

-Finally, the tail is the most lateral portion, situated in the left upper quadrant as it extends to the splenic hilum, also bordered posteriorly by the splenic vein.

Ducts of the pancreas – where they run and what they drain

-          The main pancreatic duct of Wirsung

o   runs the entire length of the pancreas, joins the CBD, and drains into the duodenum at the ampulla of Vater with the sphincter of Oddi.

-          The accessory duct (Santorini)

o   branches in the head and drains separately into the duodenum at the minor papilla.

Vascular landmarks of the pancreas

The Head

• Anterior: Gastroduodenal artery (GDA).

• Posterior: Inferior vena cava (IVC), portal-splenic confluence, and renal veins.

Uncinate Process

• Anterior border: Superior mesenteric vein (SMV).

• Posterior border: Aorta and IVC.

• (Key: the uncinate hooks behind the SMV).

Neck

• Lies directly anterior to the portal-splenic confluence (where SMV + splenic vein form the portal vein).

Body

• Posterior border: Splenic vein runs along it.

• Anterior relation: Lies over the aorta and superior mesenteric artery (SMA).

Tail

• Extends to the splenic hilum.

• Posterior border: Splenic vein continues here as well.

Congenital anomalies

• Agenesis- Complete failure of the pancreas (or part of it) to develop. Partial can cause diabetes/ GI issues.

• Pancreas divisum (most common)- failure for ventral/ dorsal ducts to fuse. Can lead to obstruction.

• Ectopic pancreatic tissue- Pancreatic tissue located outside the normal pancreas. At stomach wall, duodenum, small intestine

• Annular pancreas (rare)- pancreatic tissue encircles the second portion of the duodenum.

What hormones the pancreas produces- regulates blood sugar

-Beta (Insulin)- Lowers blood glucose by promoting uptake into cells and storage as glycogen.

                                           Think: storage hormone.

-Alpha (glucagon) – Raises blood glucose by stimulating glycogen breakdown and gluconeogenesis.

Think: release hormone

-Delta (Somatostatin)- Inhibits both insulin and glucagon secretion. Helps regulate balance between them.

Types of Pancreatitis

Acute Pancreatitis

• Cause: Gallstones (most common), alcohol abuse, trauma, surgery, drugs.

• Pathology: Pancreatic enzymes (amylase, lipase) escape and autodigest the gland.

• Symptoms: Severe epigastric pain radiating to back, nausea/vomiting, ↑ amylase & lipase.

• Sonographic features:

  • Enlarged, hypoechoic pancreas.

  • Blurred margins.

  • Peripancreatic fluid collections.

  • Possible gallstones.

2. Chronic Pancreatitis- inflammation

• Cause: Long-standing inflammation, most often alcoholism.

• Pathology: Irreversible fibrosis, scarring, and loss of function.

• Symptoms: Chronic pain, malabsorption, diabetes.

• Sonographic features:

  • Small, echogenic gland (fibrosis).

  • Irregular borders.

  • Calcifications common.

  • Dilated pancreatic duct.

 Pseudocysts- Acquired. Walled off fluid collections rich in pancreatic enzymes, blood, and necrotic tissue.

• Cause: Complication of acute or chronic pancreatitis (enzymes leak out and become walled off by fibrous tissue).

• Not true cysts because they lack an epithelial lining (hence “pseudo”). Often form in lesser sac.

• Symptoms: Abdominal mass, pain, nausea/vomiting, persistent elevated amylase.

• Sonographic features:

  • Well-defined, anechoic or complex fluid collection.

  • May contain debris.

  • Most often found in the lesser sac (anterior to pancreas, posterior to stomach).

Types of pancreatic neoplasms

A)      Exocrine Neoplasms (most common)

Arise from the ductal or acinar cells (the enzyme-producing part).

1. Adenocarcinoma (ductal carcinoma)

   • Most common pancreatic malignancy (≈ 90%).

   • Typically in the head of the pancreas.

   • Aggressive, poor prognosis.

   • Causes painless jaundice, weight loss, dilated bile/pancreatic ducts (“double duct sign”).

2. Cystic Neoplasms

   • Serous cystadenoma (benign, “honeycomb” appearance, older women).

   • Mucinous cystadenoma/cystadenocarcinoma (premalignant/malignant potential, usually body/tail, women 40–60).

3. Acinar cell carcinoma

   • Rare, malignant, arises from enzyme-producing cells.

B)       Endocrine Neoplasms (Islet Cell Tumors)

Arise from islet of Langerhans cells (hormone-secreting).

1. Insulinoma

   • Most common islet cell tumor.

   • Causes hypoglycemia (too much insulin).

2. Gastrinoma

   • Produces excess gastrin → Zollinger–Ellison syndrome (ulcers, diarrhea).

3. Other rare islet tumors: glucagonoma, somatostatinoma, VIPoma.

• Can be benign or malignant.

• Often small, hypervascular masses in body/tail.

🔹 Metastatic Tumors

• Pancreas can be site of metastasis (lung, breast, melanoma, kidney).

• Appear as focal masses, often multiple.