Pathology-Pancreas Flashcards

1
Q

What is the most common congenital anomaly you see with the pancreas?

A

Pancreatic agenesis and annular pancreas are both very rare. Ectopic pancreas can be seen in 2% of the population in the stomach, duodenum or jejunum.

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2
Q

What is the most common complication of ectopic pancreatic tissue?

A

Bleeding, most often it is exocrine ectopic pancreas.

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3
Q

What congenital anomaly can cause pancreatitis?

A

Pancreas divisum. This happens as a result of failure of the dorsal and ventral pancreas to fuse. Instead of secretions draining through the duct of Wirsung like normal, they drain through the minor sphincter, which can become blocked easily.

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4
Q

A patient presents with congenital, non-neoplastic cysts on the pancreas. What are two causes of this?

A

AD PKD and Von Hipple-Lindau disease.

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5
Q

How can you tell the difference between a patient with acute pancreatitis vs. one with chronic pancreatitis by looking at pancreatic acini?

A

Acute: despite acute inflammation & clotting cascade, pancreatic acini will completely resolve. Chronic: repeated damage to pancreas results in pancreatic fibrosis and breakdown of acinar units.

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6
Q

What makes up 80% of acute pancreatitis etiologies? What are some things that make up the other 20%?

A

Alcoholism (mostly males) and gallstones (mostly females) make up 80%. 10-20% are genetic mutations in PRSS1 and SPINK1 (trypsinogen and trypsin inhibitor).

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7
Q

What is the spectrum of acute pancreatitis?

A

Mild: abdominal pain w/some inflammation. Severe: edema, ischemic damage (activation of clotting cascade), fat necrosis and hemorrhage.

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8
Q

What is this section indicative of?

A

Fat necrosis in acute pancreatitis. Note the dark purple edge indicating hemorrhage and saponification peripherally to it.

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9
Q

Mechanism of acute pancreatitis

A

Obstruction -> edema -> activation of clotting cascade -> ischemia -> release of proteolytic enzymes w/toxic damage from proteolysis (protease), fat necrosis (lipase) and hemorrhage (elastase)

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10
Q

When is acute pancreatitis a medical emergency?

A

Acute abdomen, shock

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11
Q

Hemoperitoneum signs of acute pancreatitis

A

*

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12
Q

Which lab test can you do quickly to assess for pancreatitis?

A

P-amylase rises quicker than lipase.

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13
Q

Why are pancreatic pseudocysts not real cysts?

A

They do not have an epithelial border.

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14
Q

Is pseudocyst specific for chronic pancreatitis?

A

No, it can also form in acute pancreatitis

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15
Q

How does fat necrosis differ in chronic vs. acute pancreatitis?

A

Chronic has fat necrosis through the pancreatic parenchyma. Acute has fat necrosis in the periphery.

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16
Q

Hallmark histological sign of chronic pancreatitis.

A

Loss of glands, fibrosis and little acinar units. Islets of Langerhans may persist.

17
Q

Clinical aspects that will help you pin down acute pancreatitis.

A

Shock, ARDS, renal failure, DIC, pancreatic abscess, pancreatic pseudocyst and duodenal obstruction.

18
Q

Clinical aspects that will help you pin down chronic pancreatitis.

A

Pseudocyst, duct obstruction, malabsorption, steatorrhea, secondary diabetes

19
Q

Treatment of acute pancreatitis.

A

IV rehydration and pancreatic rest (no oral intake)

20
Q

Cystic pancreatic neoplasms most often found in the tail of the pancreas. How do you cure these?

A

1) Well-circumscribed serous cystadenoma (flat & cuboidal) 2) Well-circumscribed mutinous cyst adenoma (lots of mucus) 3) Solid-pseudopapillary neoplasm (very rare, female predominance). Surgery is curative for all of these.

21
Q

Pancreatic carcinoma

A

1) Ductal (main tumor) 2) Acinar 3) Pancreatoblastoma (seen in kids)

22
Q

Lifestyle risk factors for ductal pancreatic carcinoma

A

Cigarette smoking, chronic pancreatitis, diabetes, high fat diet.

23
Q

Hereditary risk factors for ductal pancreatic carcinoma

A

Hereditary non-polyposis colorectal carcinoma (Lynch II), hereditary breast/ovarian carcinoma (BRCA 2), hereditary pancreatitis (PRSS1, SPINK 1), Peutz-Jeghers (LKB1).

24
Q

Pancreatic cancer progression

A

Normal -> Pancreatic intraepithelial neoplasia (PanIN) 1A -> K-RAS mutation and telomere shortening -> PanIN-1B -> Inactivation of p16 -> PanIN-2 -> Inactivation of p53, SMAD4, BRCA2 -> PanIN-3 -> Invasive carcinoma

25
Q

Where do you see most ductal carcinomas?

A

60% Head > 15% body >5% tail. Consequently most present with obstructive jaundice as their first symptom.

26
Q

Why is pancreatic cancer so deadly?

A

The infiltrate deeply into the lymphatics from the get-go, metastasizes early and presents late.

27
Q

A patient who had a long history of chronic pancreatitis, weight loss, jaundice and abdominal pain dies. Autopsy is shown below of his pancreas. What did he die from?

A

Pancreatic adenocarcinoma. Note lots of space between acinar units indicating chronic pancreatitis and infiltrating malignant glands in the top image. Note how the tumor migrates along the nerves in the pancreas in the bottom image.

28
Q

Vascular symptoms that may accompany pancreatic adenocarcinoma.

A

Migratory thrombophlebitis

29
Q

How do you treat pancreatic adenocarcinoma?

A

Take out the head of pancreas, duodenum and gallbladder…Whipple procedure.

30
Q

Why is pancreatic carcinoma the 4th leading cause of death?

A

Less than 20% resectable and less than 5% 5 year survival rate…everyone who is diagnosed with this will die.