Pancreatic, biliary tree, and salivary diseases

Question 1

Describe the normal pancreas and it’s anatomical location

Answer 1

• Lobulated organ situated posterior to the stomach and anterior to the thoracic spine and ribs
  
  • Retroperitoneal structure
  • Traverses abdomen from left to right infero-diagonally, with the tail situated immediately medial to the splenic hilum and the head sandwiched within the C-loop of the duodenum
  • Blood supply is dereived from branches of the superior pancreatoduodenal and splenic arteries off the celiac axis
  • And Inferior pancreatoduodenal artery off the SMA
  • Lies immediately anterior to SMV-PV confluence and SMA
  • Immediately inferior/anterior to splenic artery and vein

Question 2

What do acinar cells produce?

Answer 2

• A multitude of digestive pro-enzymes that are secreted across the apical cell membrane into a tiny ductule at the center of each acinus
  
  • Ductules coalesce into the larger exocrine duct system of the pancreas that ultimately leads to the main (ventral) duct and ampulla of Vater
  • In about 10% of people the dominant route of flow is dorsal duct and empties into minor papilla

Question 3

Over 80% of the pancreas is what cell type?

Answer 3

• 80% of pancreateic cells are epithelial in origin and comprise the acinar glands
  
  • Form the exocrine component and are of import in this first unit

Question 4

What are the proteases secreted by the pancreas?

Answer 4

• Trypsinogen
  
  • Chymotrypsinogen
  • Proelastase
  • Procarboxypeptidase A
  • Procarboxypeptidase B

Question 5

What are the ‘other’ enzymes secreted by the pancreas?

Answer 5

• Amylase
  
  • Deoxyribonuclease
  • Ribonuclease
  • Procolipase
  • Trypsin inhibitors
  • Monitor peptide

Question 6

What are the lipases secreted by the pancreas?

Answer 6

• Lipase
  
  • Lipase-related proteins
  • Prophospholipase A1, A2
  • Nonspecific esterase

Question 7

Why are the bicarbonate and water secretions of the pancreas important?

Answer 7

• They help move all the enzymes down to where they need to (flow is important, stasis is bad)
  
  • They also provide a high pH environment to discourage the activation of the zymogens

Question 8

What is going on in acute pancreatitis?

Answer 8

• Occurs when pancreatic enzymes are inappropriately and prematurely activated resulting in autolysis of the gland
  
  • May result in severe inflammation and/or necrosis of pancreatic tissue
  • Most commonly occurs when pancreatic duct becomes obstructed, resulting in stagnation of pancreas enzymes within the organ and activation of enzyme activation cascade

Question 9

Why might alcohol intake precipitate pancreatitis?

Answer 9

• Direct toxic effect on pancreatic acinar cells
• Premature release and activation of trypsinogen and stagnant flow of pancreatic juice
*alcohol abuse will often result in pancreatitis (if it does) within 3-5 days of the binge

Question 10

Some people do have premature enzyme activation, but what keeps this from being a problem normally?

Answer 10

• Peristalsis of duct
  
  • Sphincer of oddi relaxation
  • Bicarbonate and water secretion and flow
  • Trypsin inhibitor function

Question 11

What congential ductal abnormalities would you find obstructing the pancreatic outflow and thus being associated with pancreatitis?

Answer 11

• Pancreas divisum
• Annular pancreas
○ Usually these just increase the risk of alcohol use precipitating the event

Question 12

Hyperlipidemia is associated with what pancreatic disease?

Answer 12

• Severe hyperlipidemia may precipitate acute pancreatitis for numerous reasons which remain poorly understood

Question 13

What are the less common, but still testable causes of acute pancreatitis?

Answer 13

• Drug induced
		○ Thiazide diruetics
		○ Azathioprine
		○ Anti-retroviral drugs
	• Hypercalcemia
	• Infectious
		○ Mumps
		○ Coxsackievirus
	• Cystic fibrosis

Question 14

What does the pancreas look like macroscopically and grossly in severe pancreatitis?

Answer 14

• Lipase released from dying acinar cells breaks down fat, liberating free fatty acids that precipitate with calcium ad form insoluble soaps
  
  • Frank coagulation necrosis of the gland and/or hemorrhage into retroperitoneum
  • Microscopically, necrosis of pancreatic tissue is associated with intense infiltrates of neutrophils and apoptosis of epithelial cells

Question 15

What diagnostic tests are performed with clinical suspicion of pancreatitis?

Answer 15

• Blood test
○ Serum level of amylase and lipase
○ Elevated greater than 3 times the upper limit of normal
• Lipase more specific for pancreatitis and equally to slightly more sensitive than serum amylase
○ Rises 1-2 hours and decreases over following week
• Serum amylase rises and falls within 24-48 hours but its specificity is imperfect
○ Mumps, sjorgrens, penetrating peptic ulcer, intestinal trauma or ischemia, ectopic pregnancy
○ All these can confuse the findings

Question 16

What imaging modalities can be used to help confirm the diagnosis of pancreatitis?

Answer 16

• Ultrasound and CT
• Ultrasound is cheaper and 90% accurate at detecting gallstones
○ BUT not great at looking at pancreas and ducts
• Contrast CT in severe cases or questionable situations
○ Shows inflammatory changes within and surrounding the pancreas-
§ gland edema, fat stranding, fluid accumulation
○ Can sometimes show the tumor cause
○ Certainly good for hemorrhage

Question 17

What is ERCP?

Answer 17

Endoscopic retrograde cholangio-pancreatography (ERCP) is a diagnostic test to examine:

the duodenum (the first portion of the small intestine),
the papilla of Vater (a small nipple-like structure with openings leading to the bile ducts and the pancreatic duct),
the bile ducts, and
the gallbladder and the pancreatic duct.

Question 18

How is acute pancreatitis treated?

Answer 18

• Hospital admission just in case things go south
• NPO status
• IV pain meds
• Time
○ Lame, yes, but majority of uncomplicated acute pancreatitis will improve with these supportive measures alone
• MUST avoid alcohol to prevent disease recurrence or progression to chronic pancreatitis
• Cholecystectomy later to remove source of obstruction
○ Otherwise healthy patients
• Stone removal by ERCP
• Can also be done surgically but that’s more messy

Question 19

Describe (general) the disease state of chronic pancreatitis

Answer 19

• Condition that develops after repeated bouts of acute pancreatitis
• Commonly occurs as a result of chronic alcohol abuse
• Macrospic
○ Characterized by replacement of healthy pancreatic tissue by hard fibrous tissue
○ There may be atrophy of the gland as well
• Pancrease juice may become viscous, and calcifications/stones may devleop within duct if these clumps of protein precipitate with calcium salts
• Microscopic
○ Broad bands of scar tissue replace lost lobular tissue
○ Can show presence of lymphocytes and plasma cells
• There is usually sparing of islet cells
• Fibrous tissue can cause strictures of duct
• Calcified stones can precipitate obstruction
• Malabsorption, pain, malnutrition

Question 20

What is the most common cause of CP in the west?

Answer 20

• CP = chronic pancreatitis
  
  • Chronic alcohol abuse
  • Cigarette smoking also contributed to fibrosis, and particularly in alcoholics

Question 21

What are the inherited conditions that predispose people to chronic pancreatitis?

Answer 21

• CFTR mutations
	• Trypsinogen gene mutations
		○ PRSS
	• Trypsin inhibitor mutations
		○ SPINK
	• Familial hypertriglyceridemia
	• Equatorial countries - idiopathic variant that has extensive calcifications, called tropical pancreatitis

Question 22

Why do pancreatic stellate cells have an important role in chronic pancreatitis?

Answer 22

• They, when stimulated, proliferate and transform into collagen-synthesizing cells
  
  • Can contribute to the ductal obstruction

Question 23

Fat malabsorption is a marker of what degree of pancreatic damage?

Answer 23

• 90% of the organ is destroyed before fat malabsorption is seen
  
  • 95% for carbs and proteins because trypsin and amylase are produced elsewhere as well

Question 24

What are the clinical manifestations of chronic pancreatitis?

Answer 24

• Steatorrhea is important finding
  
  • Epigastic pain that radiates directly to back
  • Can just present as back pain alone
  • Pain will wax and wane but never truly disappear

Question 25

What is steatorrhea

Answer 25

* Fatty diarrhea * Frequent, oily, foul-smelling, and/or buoyant stools * Increased flatulence and weight loss

Question 26

What might patients with chronic pancreatitis have B12 deficiency?

Answer 26

* Pancreatic proteases are required to cleave the R-protien-cobalamin complex * This allows for intrinsic factor to bond to B12 * Thus, pancreatic duct obstruction or atrophy will result in a loss of B12 binding to IF, and thus a malabsorption of B12 * Eventually causes macrocytic anemia

Question 27

Why might bleeding diathesis develop in chronic pancreatitis?

Answer 27

• A result of fat-soluble vitamin malabsorption, specifically vitamin K

Question 28

What diagnostic tests for chronic pancreatitis are available?

Answer 28

• History and physical can be highly suggestive • Plain x-ray of abdomen can show calcifications scattered over epigastrium in severe calcific disease • Rapid fat stool stain ○ Sudan stain, qualitiative • Definitive is 72-hour quantitative stool collection for fat analysis ○ High fat diet of over 100g of fat/day ○ 72 hour stool collection should who over 10-20% fecal fat excretion or 50 g of fat

Question 29

Pancreatic cancer is a major US killer. From what cells does this cancer arrive?

Answer 29

* Vast majority (90-95%) arise from ductal epithelial cells * Remaining come from acinar cells * Both carry a bad prognosis * Cancer usually forms primitive, mucin-positive, gland-like structures * Cells elicit a strong, fibrotic reaction known as desmoplasia, texture very hard and cancer cells less permeable to chemotherapy drugs * Often have microscopic tumor tendrils that are not seen by imaging

Question 30

What are the much more rare pancreatic tumors?

Answer 30

``` • Mucinous cystadenocarcinomas • Intraductal papillary mucinous tumors ○ IPMTs • Arise from cystic lesions in pancreas and much less common than ductal adenocarcinoma • More favorable prognosis ```

Question 31

What are the risk factors for pancreatic adenocarcinoma?

Answer 31

``` • Positive family history • Tobacco abuse • Chronic pancreatitis • Obesity • Ocassionally a genetic syndorme ○ Peutz-Jeghers ○ Von Hippel-Lindau ```

Question 32

What is tousseau's syndrome?

Answer 32

* Associated with pancreatic adenocarcinoma | * Hypercoagulable state associated with neoplasm and decrease in physical activity

Question 33

What imaging studies can result in dx of pancreatic adenocarcinoma?

Answer 33

• Contrast abdominal CT scan ○ 80-90% sensitivity ○ Shows pancreas, bile ducts and pancreatic duct very well ○ Also decent for detecting distant metastasis • Ultrasound ○ Less accurate because of fat and air surrounding pancreas

Question 34

What imaging studies can result in dx of pancreatic adenocarcinoma?

Answer 34

• Contrast abdominal CT scan ○ 80-90% sensitivity ○ Shows pancreas, bile ducts and pancreatic duct very well ○ Also decent for detecting distant metastasis • Ultrasound ○ Less accurate because of fat and air surrounding pancreas • Biopsy or fine-needle aspiration ○ FNA = fine needle aspiration • Endoscopic ultrasound is the up and coming modality • Also helps with pre-op tumor staging as it shows borders and lymph nodes in the region very well

Question 35

Insulinomas, glucoagonomas, gastrinomas, VIPomas and somatistatinomas all have what in common?

Answer 35

• They are neuroendocrine tumors that secrete a given hormone in excess that forms a particular clinical picture *found by imaging and by fine needle aspiration

Question 36

What might glucoagonomas cause?

Answer 36

* Hyperglycemia * Deiabetes * Weight loss * Diarrhea

Question 37

What might somatistatinomas cause?

Answer 37

``` • These are rare • Weight loss • Malabsorption • Acalculous cholecystitis ○ Decreasing GI motility and exocrine secretion ```

Question 38

What might VIPomas cause?

Answer 38

• Severe, chronic, secretory type diarrhea with hypokalemia and weight loss

Question 39

What might gastrinomas cause?

Answer 39

* GERD or peptic ulcers * Diarrhea * Fat malabsorption

Question 40

Why is surgery recommended for anybody with an NET that can handle the surgery?

Answer 40

* NET = neuroendocrine tumor * These cannot be graded/staged for metastatic nature by histology * You can only watch them as they invade * Thus, get them out. Not all have the worst metastatic abilities, but glucagonoma and somatistatinoma are almost always malignant

Question 41

How do you treat autoimmune pancreatitis?

Answer 41

• 6 week course of PO corticosteroids ○ Prompt and effective • Jaundice and pruritis (itchy) patients may benefit from ERCP with placement of a temporary biliary stent. • Immunomodulators can be used…but that's a case by case basis and in refractory cases

Question 42

What studies are done to show autimmune pancreatitis?

Answer 42

* Serum IgG-4 is elevated in about 80% of patients * Imaging shows an enlarged pancreas with decreased enhancement and loss of the lobular contour * ERCP will show narrowed pancreatic duct and sometimes a bile duct stricture * EUS-guided or percutaneous biopsy of the pancreas and IgG-4 staining can be definitive dx modality

Question 43

What does a patient with AIP usually look like?

Answer 43

• NOT your typical chronic pancreatitis patient • No alcohol abuse usually • 45-70 year old males • No history of pancreatitis at all, not even acute • Present with chronic epigastric or diffuse abdominal pain and nearly half also develop cholestasis ○ Jaundice, dark urine, itching • Associated with other auto-inflammatory diseases like RA, IBS, lupus or sjorgren's syndrome

Question 44

What immune-associated factors and cells are implicated in the disease process of autoimmune pancreatitis?

Answer 44

• AIP = autoimmune pancreatitis • IgG-4 and plasma cells and lymphocytes infiltrate the pancreas and its vessels • Results in localized or diffuse enlargement of pancreatic parenchyma and narrowing of pancreatic duct and/or bile duct • YOU WILL NOT FIND ○ Glandular atrophy, ductal dilation, calcifications and steatorrhea are features of chonic pancreatitis but NOT features of AIP

Question 45

What does the gallbladder normally do?

Answer 45

• Storage place for bile, so that it can be released in higher amounts when the diet calls for it • Bile is a yellow liquid with amphopathic properties that contributes to excretion of various compounds ○ Cholesterol, copper, medications • Also helps with lipid digestion within the small bowel • Contains water, bile acids, cholesterol, phospholipids, lecithin, electrolytes • Bile acids are main active ingredient in bile and contribute the most to lipid digestion

Question 46

What are the constituents of bile?

Answer 46

* cholesterol, phospholipids, lecithin, electrolytes | * Bile acids are main active ingredient in bile and contribute the most to lipid digestion

Question 47

Describe the pathway of bile formation and movement into the gall bladder

Answer 47

* Made by hepatocytes and secreted into the cannaliculi * Drain into peripheral intrahepatic bile ducts * Intrahepatic bile ducts coalesce into the right and left hepatic ducts, which fuse to form the common hepatic duct

Question 48

Describe the gall bladder during both fasting and fed states.

Answer 48

• Fasting ○ Vagal tone and CCK levels are decreased ○ Sphincter of Oddi is closed ○ Gallbladder and bile duct peristalsis are inhibited ○ Secretions of bile from liver hit the sphincter and retrograde flux into gallbladder for storage • Fed ○ Vagal tone and CCK levels are increased ○ Sphincter of Oddi is openend and the gall bladder and bile duct peristaltic movements are increased ○ Results in flow from gallbladder into the duodenum through cystic duct

Question 49

What happens to the bile while it sits in the gallbladder?

Answer 49

* There is constant transport of sodium from the lumen of the gallbladder into the bloodstream * Water will follow this passively * End result here is concentration of the bile

Question 50

What are the risk factors for generation of cholesterol stones?

Answer 50

* Obesity * Rapid weight gain or loss * Female gender * Age over 30 * Latin American or Native American ethnicity * Estrogen/contraceptive use

Question 51

What is the process behind gallstone formation?

Answer 51

• There has to be supersaturation ○ Can be from too little water or too much cholesterol ○ Could be both processes as well • Supersaturation of bile with cholesterol first results in formation of cholesterol crystals ○ Microlithiasis • Eventually clinically significant stones can develop • Numerous factors contribute: ○ Stasis in gallbladder or bile duct, hereditary mutations in cholesterol chain structure, inflammation of gallbladder

Question 52

What are the different types of gallstones?

Answer 52

• 3 different types ○ Cholesterol, brown and pigment • Cholesterol stones ○ Cholesterol, bile acids, phospholipids and lecithin ○ White or yellow, soft and greasy • Pigment stones ○ More common in asians ○ Predominantly of calcium bilirubinate salts which coalesce around a mucin nidus ○ Come from increased concentrations of bilirubin in bile § Hemolytic states like sickle cell anemia ○ Can develop in gallbladder OR straight into cystic duct ○ Think about the parastic infections like clonorchis that can result in cholangitis and stasis § Endemic in Asia so these stones are more common in asia • Brown stones ○ Hybrid of cholesterol and pigment stone crystals ○ Develop de novo within bile duct as a result of infection in patients with prostheses § Tubes or stents ○ Can develop due to a downstream obstruction

Question 53

What is the best diagnostic study (at least initially) for gallstones?

Answer 53

* Abdominal ultrasound * Over 90% accurate for gallbladder stones or cholecystitis * Good for seeing bile duct diameter, and possible ductal dilation * Not as good for seeing stones in the bile duct itself

Question 54

How might you treat a bile duct obstruction?

Answer 54

• ERCP • Retrograde cholangiopancreatography • Essentially a scope, and they can protrude needles from it for biopsies or minor surgeries • Can remove stones or place stents during procedure • Less invasive ○ Potential risk of pancreatitis

Question 55

What is biliary colic?

Answer 55

• Occludes the gallbladder intermittently • Usually when patient consumes a meal (particularly fatty meal b/c of CCK release) • Dull or crampy pain in the epigastrium or upper right upper quadrant which occurs within an hour of eating and resolves spontaneously ○ Typically within 3-5 hours ○ Has to do with time for hormone to go down or stone to move

Question 56

What is acute cholecystitis?

Answer 56

• Stone has compacted the bile duct and now there is a bacterial superinfection of gallbladder • Severe inflammation and/or ischemia of the gallbladder, usually associated with infection • Symptoms ○ Severe RUQ pain ○ Radiation to right flank or shoulder ○ Focal tenderness to deep palpation of the RUQ and palpation during expiration ○ Murphy's sign - strongly suggestive of cholecystitis

Question 57

What is the treatment paradigm for acute cholecystitis

Answer 57

• Similar to acute pancreatitis • Hospitalization for pain, but not much else • IV fluids • NPO for gallbladder rest • IV antibiotics (is this controversial too?) • Pain mediations ○ Cholecystectomy is treatment of choice for all surgical candidates within 1-2 weeks of event

Question 58

What serum tests will be affected by acute cholecystitis?

Answer 58

• Neither cholecystitis or gallbladder stones will significantly elevate liver enzymes • Exception - Mirizzi's syndrome ○ Stone lodged in cystic duct causes severe, localized edema and inflammation to develop in the region ○ Leads to benign obstructino of common bile duct or common hepatic duct ○ The other way this can happen is a very fat and enflamed gallbladder physically pushing on the ducts and obstructing them • Treatment is cholecystectomy

Question 59

What is acalculous cholecystitis?

Answer 59

• Similar to stone-caused or calculous cholecystitis, but it's an ischemic process not an obstructive process • Vasculitis (polyarteritis nodosa) • Hypoperfusion event ○ DIC, sepsis, MI, burns, severe trauma and blood loss, etc.

Question 60

What does choledocholithiasis mean?

Answer 60

• Gallstones migrating past cystic duct into common bile duct • If they get lodged in or before the ampulla of vater they can cause ○ Ascending cholangitis and/or acute pancreatitis What does RUQ pain, jaundice and dark urine suggest to you? • This constellation of symptoms looks like choledocholithiasis

Question 61

What is the treatment for ascending cholangitis?

Answer 61

* Remember charcot's triad and reynold's pentad * Admission to hospital and IV antibiotics * Urgent ERCP with stone extraction or stent replacement is necessary often

Question 62

Chorcot's triad can progress to Reynold's pentad which is…?

Answer 62

* Triad + hypotension and confusion * Fever * Pain * Jaundice * Hypotension * Confusion

Question 63

What is Charcot's triad?

Answer 63

* Indicative of ascending cholangitis * RUQ pain * Jaundice * Fever

Question 64

What is up with gallbladder cancer?

Answer 64

* Adenocarcinoma is the only one we talked about * Risk factors are gallstones and chronic cholecystitis * Infection with liver flukes (parasites) may also cause recurrent cholecystitis and chronic cholecystitis enough to present a risk factor * Poor survival rate as this is usually caught pretty late in the disease process * If cancer causes obstruction it can be diagnosed sooner on cholecystectomy * Gallblader cancers are also similar to pancreatic carcinomas as they produce thick stroma connective tissue

Question 65

What is primary sclerosing chlangitis?

Answer 65

* PSC = primary sclerosing cholangitis * Remember UC predisposes you to this * Predominantly affects caucasian males 30-60 * Gallbladder is usually spared * Lots of strictures through the biliary tree * Higher risk of developing cholangiocarcinoma

Question 66

What are gray/white colored stools called?

Answer 66

* Acholic | * Absence of bilirubin in the stools

Question 67

In a patient that has already had a cholecystectomy and they are still having symptoms of biliary colic, what are you thinking?

Answer 67

Sphincter of Oddi problems * there can be a dysfunction of the sphincter of oddi that keeps it spasming and not allowing bile to flow through * can cause ascending cholangitis in really bad cases, even in a patient with absolutely no way to form gall stones

Question 68

What are the 8 salivary gland diseases covered in our notes?

Answer 68

* Mumps * CMV sialadenitis * Bacterial Sialadenitis * Sarcoidosis * Sjorgren's Syndrome * Salivary Lymphoepithelial Lesion * Xerostomia (dry mouth) * Halitosis

Question 69

Because salivary glands are ductal tissue, what disease are they predisposed to?

Answer 69

* Ductal neopslams | * Adenoma or adenocarcinoma

Question 70

What is pleomorphic adenoma?

Answer 70

• Salivary neoplasm discussion here • Diverse microscopic pattern is characteristic • Islands of cuboidal cells arranged in ductlike structures is a common finding • Loose chondromyxoid stroma, connective tissue, cartilage and even osseous tissue ○ Thus pleomorphic • Typically encapsulated ○ Tumor islands may be found within fibrous capsule

Question 71

What's up with Warthin's tumor?

Answer 71

* Benign papillary cystadenoma lymphomatosum * Second most common benign tumor of parotid gland * 2-10% of all parotid gland tumors * Bilateral in 10% of cases * Mucoid brown fluid in FNA (fine needle aspiration)

Question 72

What two components need be present to diagnose warthin's tumor?

Answer 72

• Lymphoid and epithelial components • Epithelial - papillary fronds with two layers of oncocytic epithelial cells ○ Cytoplasm pink b/c lots of mitochondria ○ Occasionally looks like squamous metaplasia, and often confused for SCC • Lymphoid component ○ Occasional germinal centers are seen ○ Lymphoid tissue forms core or papillary structures ○ This is more present than the epithelial or oncocytic component

Question 73

Besides pleomorphic adenoma, what else can be found in the mouth?

Answer 73

• Monomorphic adenoma, usually salivary gland presence • Composed of uniform basaloid epithelial cells with monomorphous pattern • Absence of the many different types of stromal cells • Much more uniform in appearance, ducts surrounded by stroma *important because they have a malignant potential. Still not majority, but something to be aware of

Question 74

What are the malignant neoplasms associated with salivary glands in order of frequency?

Answer 74

``` • Mucoepidermoid carcinoma • Polymorphous low grade adenocarcinoma • Adenoid cystic carcinoma • Clear cell carcinoma • Acinic cell carcinoma (most common) ○ No glycogen, fat and mucin ○ 3% malignant and bilateral) ```

Question 75

What is the most common malignant neoplasm with the salivary gland?

Answer 75

• Acinic cell carcinoma (most common) ○ No glycogen, fat and mucin ○ 3% malignant and bilateral)

Question 76

A patient has a bump around where the salivary glands are. What items in their history and physical would make you concerned for malignancy?

Answer 76

* Induration/hardness of lump * Fixed to overlying skin or mucosa * Ulceration of skin or mucosa * Rapid growth * Short duration * Pain (usually out of proportion) * Facial nerve palsy

Question 77

Swiss cheese pattern is a buzz word for what condition?

Answer 77

* Adenoid cystic carcinoma * Salivary gland neoplsm * Second most common salivary gland neoplasm * Submandibular, sublingual and minor glands

Question 78

you see on histology a gland filled with a thick substance. What are you thinking?

Answer 78

Mucoid Adenocarcinoma. | *either high or low grade depending on how well circumscribed the tumor is

Question 79

What are the exocrine pancreatic cancers in descending order of frequency that we discussed?

Answer 79

``` • Adenocarcinoma (ductal) ○ 90% of all pancreatic cancer starts in the duct • Adenosquamous carcinoma ○ Glands flatten out as they grow • Intraductal papillary-mucinous neoplasm ○ Finger-like projections into duct ○ Prelude to malignancy • RARE ○ Mucinous cystadenocarcinoma § Spongy cystic tumor ○ Pancreatoblastoma § KIDS, suspect in infancy ○ Acinar cell carcinoma § Look for too much lipase chronically due to overproduction by tumor ```