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Pancreas Flashcards

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1
Q

Pancreatic neoplasms overview

  • Draw the flowchart of pancreatic neoplasms.
  • Common Ix presentation of ductal adeno?
  • What can acinar cell cause?
    • Mnemonic.
  • Mnemonic for serous cystic?
  • Mnemonic for SPEN?
  • PNETs: most common, 2nd, 3rd.
    • US-2
    • CT-3; how they differ from adenos.
A
  • See chart below.
  • Biliary obstruction, as they invade (double duct sign).
  • Acinar = fat necrosis; as some have paraneoplastic syndrome w/hypersecretion of lipase.
    • Lipase makes your ASSinar thin.
  • Serous cystic: grandmothers are serious and small.
  • SPEN: young ladies like to SPENd their $$.
  • PNETs: insulinoma most common, gastrinoma, then glucagonoma.
    • US: well circumscribed, hypoechoic.
    • CT: hypervascular, homogenous when small; heterogeneous or cystic/necrotic when large; unlike adenocas, they have a capsule, so displace, rather than invade hepatic parenchyma, so don’t usually present w/biliary obstruction.
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2
Q

Solid panc neoplasms: adenocarcinoma:

  1. From what portion of the panc are these?
  2. What % of all panc tumours are these?
  3. Ex-2
  4. RFs-3
  5. Typical CT protocol.
    1. Best phase for detecting adeno? How is this different from PNETs?
  6. Most common adeno location?
  7. MR app-1.
  8. If double duct sign is present but no mass visible, what should you be thinking?
  9. Defn unresectable adenoca (4).
A
  1. Exocrine pancreas, i.e., digestive enzymes (you know this as the PNETs are all endocrine).
  2. 80-90%.
  3. >60yo, slight male predominance.
  4. RFs: pancreatitis, EtOH, smoking.
  5. CT protocol: unenhanced, late arterial, PV.
    1. Arterial phase as adeno doesn’t enhance as much as the panc parenchyma. PNETs avidly enhance, so they’re easier to spot on PV phase.
  6. Panc head.
  7. T1 hypo.
  8. It’s an occult adeno–10% are these.
  9. SMA >180º, celiac invasion, venous invasion, mets.
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3
Q

DDx panc mass w/o ductal dilation:

A
  1. Pancreatitis: autoimmune or groove.
  2. Pancreatic tumour: cystic or PNET.
  3. Pancreatic met: RCC, thyroid, melanoma.
  4. Lymphoma (see below)
  5. Peripancreatic LN
  6. Duodenal GIST.
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4
Q

Whipple procedure

  • Aka.
  • Indications-3.
  • What is resected? Anastomosed-3?
  • 3 most common complications.
A
  • Aka: partial pancreaticoduodenectomy.
  • Indications: panc head mass, periampullary or duodenal carcinoma.
  • Resected: duodenum, panc head, gastric antrum, GB.
  • 3 anastomoses; blind ending jejunal loop is brought up to the RUQ:
    • Liver/jejunum: hepaticojejunostomy.
    • Stomach or duodenum & jejunum: gastro/duodeno-jejunostomy.
    • Pancreas/jejunum: pancreaticojejunostomy.
  • Complications:
  1. Delayed gastric emptying: NG tube needed for >1 day.
  2. Pancreatic fistula: clinical Dx of amylase through drain, >50ml for >7-10 days.
  3. Wound infection: 5-20% of pts.
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5
Q

Solid panc neoplasms: acinar cell carcinoma

  • Cell type
  • Demographic
  • Syndrome caused & reason
A
  • Aggresive adenocarcinoma, rare.
  • Only in elderly men.
  • Lipase hypersecretion syndrome (paraneoplastic):
    • subcutaneous fat necrosis w/red skin nodules.
      • Lipase makes your ASSinar thin.
    • bone infarcts causing arthralgias
    • eosinophilia
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6
Q

Cystic pancreatic epithelial neoplasms: general

  1. Which of the 4 is the most common?
  2. Which is the only of the 4 without a capsule?
  3. Which is the only of the 4 without malignant potential?
  4. Which is associated w/vHL?
  5. Which is hypervascular?
A
  1. Mucinous cystic neoplasm (mother tumour).
  2. Serous cystadenoma: it’s a cluster of benign cysts.
  3. Serous cystadenoma.
  4. Serous cystadenoma.
  5. Serous cystadenoma.
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7
Q

Cystic panc epithelial neoplasms: serous cystadenoma

  1. Nickname, Ex, mnemonic.
  2. Capsule? General morphology & nickname.
  3. Malignant?
  4. Typical location?
  5. Classic Ix features-2.
  6. How to confirm Dx?
  7. How it differs from adeno?
A
  1. Grandmother tumour, as it’s predominantly in elderly ladies; “grandmothers are serous and central to the family” (serous, central scar/calc)
  2. No capsule. Bunch of cysts, i.e., bunch of grapes.
  3. No malignant potential.
  4. 40% in panc head.
  5. Classic Ix: central scar, sometimes calcified; and sponge-like appearance w/myriad small cysts.
  6. Endoscopic sonographic aspiration of lesion fluid to look for tumour markers. If none, then benign.
  7. No duct dilation nor tail atrophy.
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8
Q

Cystic panc epithelial neoplasms: mucinous cystic neoplasm

  1. Ex & nickname.
  2. Malignant pot? Capsule?
  3. Typical morphology. Typical location?
    1. Morphology of the lesion interior.
A
  1. Middle-aged women, mother tumour.
  2. Does have malignant potential and a capsule.
  3. Morphology: 1 to a few large cysts (<6 cysts >2cm). Typically in the body/tail, unlike the grandmother tumour, which is typically in the head/uncinate.
    1. Thick-walled, hypovascular septations dividing the mass into locules >2cm, often w/mural nodules & papillary projections.
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9
Q

Cystic panc epithelial neoplasms: SPEN

  1. Ex, nickname.
  2. Capsule? Malignant potential?
  3. Typical location.
  4. Typical appearance? Classic feature. Enhances like?
  5. DDx includes lymphoma, but how to differentiate?
A
  1. Young, non-Caucasian women & kids, granddaughter tumour.
  2. Yes to capsule & low malignant potential.
  3. Location: panc tail.
  4. App: large mass w/heterogenous solid/cystic components. Often contains hemorrhage or central necrosis.
    1. Enhances like a hemangioma.
  5. Lymphoma should have nodes, SPEN will not.
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10
Q

Cystic panc epithelial neoplasms: IPMN

  1. Which type (main or side branch) has a higher risk of evolving into carcinoma?
  2. Typical Ix app.
  3. DDx & how to differentiate.
A
  1. Main duct! They are horrible.
  2. Uniformly dilated panc duct, parenchymal atrophy, absence of mass.
  3. Chronic pancreatitis can also have a dilated duct and atrophy, but the duct may be more beaded and calcs will likely be present.
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11
Q

IPMN: Fukuoka/Tanaka guidelines

*

A
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12
Q

Pancreatic endocrine neoplasms: insulinoma

*

A

*

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13
Q

Pancreatic endocrine neoplasms: gastrinoma

*

A

*

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14
Q

Pancreatic endocrine neoplasms: others

*

A

*

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15
Q

Congenital panc anomalies: divisum

  1. Classic Ix appearance.
  2. Sequelae?
  3. Tx.
A
  1. Crossing ducts sign (see below).
  2. Repeated bouts of pancreatitis which can lead to a CBD stricture, and CBD dilation.
  3. Tx: ERCP cannulation of the minor papilla w/papillotomy & temporary papillary stenting.
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16
Q

Congenital panc anomalies: annular pancreas

  1. Gamesmanship: what sequence of images should make you think of this?
  2. Characteristic ERCP image?
  3. How is this treated if a problem in infancy?
A
  1. UGIS followed by any cross-sectional imaging. The UGIS will show narrowed duodenal 2nd segment (see below).
  2. Duct circling endoscope & insufflated duodenum.
  3. Surgical division of the pancreatic head.
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17
Q

Congenital panc anomalies: common channel syndrome/pancreaticobiliary maljunction:

*

18
Q

Systemic diseases affecting panc: vHL

*

19
Q

Systemic diseases affecting panc: cystic fibrosis

*

20
Q

Cystic fibrosis & the pancreas:

  1. In what % of CT pts is the pancreas involved?
  2. 2 CF-related pancreatic changes & why?
  3. Who does worse: CT pts diagnosed as kids or adults?
  4. The most common finding in adult CF?
  5. What colonic finding is common in CF?
  6. Describe DIOS.
Study These Flashcards
A
  1. 85-90%.
  2. Pancreatic exocrine function is disabled, so pancreatic secretions are inspissated and block the ducts leading to fibrosis & fatty replacement.
  3. Diagnosis as an adult is worse as they likely had residual pancreatic function, so are more likely to have gotten pancreatitis.
  4. Complete fatty replacement.
  5. Fibrosing colonopathy: wall thickening of the proximal colon 2dry to lipase replacement Tx; Ix: long or short segment colon stricture, usually on the right (see below).
  6. DIOS: distal intestinal obstruction syndrome: happens in CF kids; if they aren’t compliant w/their enzymes the get blockages, often just after lung transplant.
21
Q

Systemic diseases affecting panc: Schwachman-Diamond:

*

22
Q

Systemic diseases affecting panc: obesity/exogenous steroids

*

23
Q

Misc. pancreatic lesions: intra-pancreatic accessory spleen

*

24
Q

Pancreatitis: acute

*

25
**Pancreatitis: Atlanta criteria** *
*
26
* What is the standard surgical Tx for pancreatic pseudocyst drainage?
* Cystogastrostomy: surgical opening is created b/w the posterior gastric wall & the pseudocyst. * Internal stent drainage can also be done, which is less invasive & less expensive.
27
**Pancreatitis: chronic** 1. Typical findings of chronic pancreatitis?
1. Ductal dilation; panc calcs; atrophy, typically at the tail.
28
**Pancreatitis: autoimmune** 1. Which conditions can accompany IgG4 pancreatitis if multisystemic IgG4?
1. PSC, thyroiditis.
29
**Pancreatitis: groove** *
*
30
**Pancreas transplant:** 1. What 2 vessels make up the donor Y-graft? 2. What vessels supply the transplant head vs. body/tail? 3. What is the venous drainage? 4. Exocrine drainage? 5. #1 cause of graft failure? #2? 1. When does #2 normally happen? 2. Why is venous thrombosis much more common than arterial compared to other xplants? 3. From where do the clots typically form? 4. Why is arterial thrombosis less of a problem here? 6. Ix signs of venous thrombosis & rejection. 7. Why are RI values irrelevant here? 8. At what time point is the xplant susceptible to pancreatitis? 9. What is a sign of chronic rejection?
1. Donor SMA + splenic artery. 2. dSMA supplies the head; dSA supplies the body/tail. 3. Venous: dPV, which is plugged into the recipient common iliac vein. 4. Into the rbowel via a segment of the dduodenum. 5. #1: acute rejection; #2: dSV thrombosis. 1. w/in first 6 weeks. 2. B/c the veins are so small. 3. From the tied-off stump vessels (dSMV). 4. B/c of dual supply via the Y-graft. 6. Reversed diastolic flow. 7. B/c the pancreas has no capsule. 8. W/in 4 weeks. 9. The shrinking xplant.
31
* What part of the pancreas may be intraperitoneal?
* Tail.
32
* How are hyperlipidemia & the pancreas linked?
* Hyperlipidemia is a RF for acute pancreatitis.
33
* What is the most common hypervascular lesion found in the pancreatic body?
* PNET! * Not an accessory spleen as these are most commonly found in the tail.
34
Dx? 78yo male w/wt loss & abdo pain, thought to be related to chronic pancreatitis:
Dx: IPMN. * Classic appearance: gross panc duct dilation + intraductal tumour. * Pancreas is remarkably atrophic. * Gross duct dilation w/low density material, consistent w/mucus. * However, there is an enhancing soft tissue tumour w/in the duct. * This is not pancreatic adenocarcinoma as that would encase the duct, not be within it. If an IPMN extended through the duct wall, it may be indistinguishable from ductal adeno.
35
Dx? 63yo F s/p L nephrectomy for RCC 10 years prior.
Dx: RCC met to the pancreas. * Hypervascular mass in the panc neck, causing marked pancreatic atrophy & duct dilation. * These findings mimic that of a PNET, but isolated panc mets from RCC, even many years following resection, is a well-recognized phenomenon, even in the absence of mets elsewhere. * RCC mets are very amenable to resection.
36
1. What lines a true pancreatic cyst?
1. Epithelium.
37
38
* Serous cystadenomas of the pancreas have no malignant potential, so are not resected. However, there is one case where they may be--what is it?
* If they are causing obstructive symptoms.
39
1. What is the most common US appearance of a pancreatic adeno? 2. Why do they cause the double duct sign when at the pancreatic head?
1. Hypoechoic & hypovascular. 2. B/c they can cause considerable desmoplastic reaction, which results in obstruction & dilation of the ducts.
40

KB-GI radiology (11 decks)

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