33: Pancreas Flashcards
Where do pancreatic pseudocysts most often occur?
Head of the pancreas
[UpToDate: A pancreatic pseudocyst is an encapsulated collection of fluid with a well defined inflammatory wall usually outside the pancreas with minimal or no necrosis. Pancreatic pseudocysts usually occur more than four weeks after the onset of interstitial edematous pancreatitis.]
What percent of pancreatic adenocarcinoma invades the portal vein, superior mesenteric vein, or the retroperitoneum at the time of diagnosis?
50%
[Unresectable disease]
Where is heterotopic pancreas most commonly found?
Duodenum
What percent of patients with acute pancreatitis get pancreatic necrosis?
15%
[UpToDate: Pancreatic and peripancreatic necrosis occur in approximately 20% of patients with pancreatitis, as a result of inflammation and vascular compromise.
Pancreatic necrosis can lead to secondary infection or symptomatic sterile necrosis, which is characterized by chronic low grade fever, nausea, lethargy, and inability to eat. Both infected pancreatic necrosis and symptomatic sterile necrosis are accepted indications for debridement.
The goal of pancreatic debridement is to excise all dead and devitalized pancreatic and peripancreatic tissue while preserving viable functioning pancreas, controlling resultant pancreatic fistulas, and limiting extraneous organ damage. For patients with biliary pancreatitis, cholecystectomy with intraoperative cholangiography is an important secondary objective of the surgery because it will prevent recurrent disease.]
Which 3 lab values are typically elevated in acute pancreatitis?
- Amylase
- Lipase
- WBCs
[UpToDate: Serum amylase rises within 6 to 12 hours of the onset of acute pancreatitis. Amylase has a short half-life of approximately 10 hours and in uncomplicated attacks returns to normal within 3 to 5 days. Serum amylase elevation of greater than three times the upper limit of normal has a sensitivity for the diagnosis of acute pancreatitis of 67% to 83% and a specificity of 85% to 98%.
However, elevations in serum amylase to more than three times the upper limit of normal may not be seen in approximately 20% of patients with alcoholic pancreatitis due to the inability of the parenchyma to produce amylase, and in 50% of patients with hypertriglyceridemia-associated pancreatitis as triglycerides interfere with the amylase assay. Given the short half-life of amylase, the diagnosis of acute pancreatitis may be missed in patients who present >24 hours after the onset of pancreatitis. In addition, elevations in serum amylase are not specific for acute pancreatitis and may be seen in other conditions.
Serum lipase has a sensitivity and specificity for acute pancreatitis ranging from 82% to 100%. Serum lipase rises within 4 to 8 hours of the onset of symptoms, peaks at 24 hours, and returns to normal within 8 to 14 days.
Lipase elevations occur earlier and last longer as compared with elevations in amylase and are therefore especially useful in patients who present >24 hours after the onset of pain. Serum lipase is also more sensitive as compared with amylase in patients with pancreatitis secondary to alcohol.
However, nonspecific elevations of lipase have also been reported.]
What is the most common cause of splenic vein thrombosis?
Chronic pancreatitis
What are 3 palliative options for patients with unresectable pancreatic adenocarcinoma?
- Biliary stents or hepaticojejunostomy (for biliary obstruction)
- Gastrojejunostomy (for duodenal obstruction)
- Celiac plexus ablation (for pain)
What gastrin levels would be seen in a patient with a gastrinoma?
Usually greater than 200
[1000s is diagnostic]
What are the 2 surgical treatment options for controlling pain in patients with chronic pancreatitis?
- Bilateral thoracoscopic splanchnicectomy or celiac ganglionectomy
- Hepaticojejunostomy or choledochojejunostomy (For common bile duct stricture)
[UpToDate: Most afferent nerves emanating from the pancreas pass through the celiac ganglion and splanchnic nerves. Thus, interruption of these nerve fibers has the potential to alleviate pain originating from the pancreas. Interruption of these pathways also occurs with pancreaticoduodenectomy and with resection of the pancreatic head, which may in part explain the pain relief achieved with these procedures.
Denervation has been accomplished using an open surgical approach and using thoracoscopic surgery. However, in most series, pain relief with thoracoscopic splanchnicectomy was incomplete and of short duration with only about one-half of patients noting a benefit after two years.
The overall benefit from denervation surgery is uncertain. While a response rate as high as 90% has been reported, patients in this series also underwent additional procedures. Which patients may benefit the most from this option is incompletely understood. One study suggested a higher response rate in patients who had not undergone prior operative or endoscopic procedures.]
What happens to endocrine and exocrine function in chronic pancreatitis?
Endocrine function is usually preserved (islet cell preservation) but exocrine function is decreased
Where do functional pancreatic endocrine neoplasms most commonly occur?
Head of the pancreas
What is Cullen’s sign?
periumbilical ecchymosis in a pancreatitis patient that indicates bleeding
[UpToDate: Patients with severe pancreatitis may have fever, tachypnea, hypoxemia, and hypotension. In 3% of patients with acute pancreatitis, ecchymotic discoloration may be observed in the periumbilical region (Cullen’s sign) or along the flank (Grey Turner sign). These findings, although nonspecific, suggest the presence of retroperitoneal bleeding in the setting of pancreatic necrosis.]
What are the symptoms of gastrinoma?
Refractory or complicated ulcer disease and diarrhea
[Improved with PPI]
[UpToDate: Abdominal pain (75%) and chronic diarrhea (73%) are the most common symptoms in patients with Zollinger-Ellison syndrome (ZES). Nearly half of patients have heartburn due to gastroesophageal reflux. Other symptoms include weight loss (17%) and gastrointestinal bleeding (25%).
Approximately 1% to 10% of patients, especially with metastatic disease or multiple endocrine neoplasia type 1 (MEN1), have symptoms due to a second hormonal syndrome (eg, VIPoma, somatostatinoma, glucagonoma, ACTH).]
What is the Grey Turner sign?
Flank ecchymosis in a pancreatitis patient that indicates bleeding
[UpToDate: Patients with severe pancreatitis may have fever, tachypnea, hypoxemia, and hypotension. In 3% of patients with acute pancreatitis, ecchymotic discoloration may be observed in the periumbilical region (Cullen’s sign) or along the flank (Grey Turner sign). These findings, although nonspecific, suggest the presence of retroperitoneal bleeding in the setting of pancreatic necrosis.]
Which pancreatic bud forms the uncinate process and inferior portion of the head?
Ventral pancreatic bud
Pancreatic pseudocysts are most commonly associated with which condition?
Chronic pancreatitis
What is the treatment for pancreatic pseudocyst?
Expectant management for 3 months
[Most will resolve on their own. Those that don’t resolve will have time to mature if cystogastrostomy is required]
[UpToDate: Watchful waiting is an appropriate option in patients with walled-off pancreatic fluid collections with minimal or no symptoms and no evidence of a pseudoaneurysm:
A retrospective review of 68 patients with a walled-off pancreatic fluid collection followed conservatively showed a 9% incidence of serious complications, with the majority occurring in the first 8 weeks after diagnosis. Complications included pseudoaneurysm formation in three patients, free perforation in two, and spontaneous abscess formation in one. An additional third of the patients underwent elective surgery, generally for fluid collection enlargement associated with pain. However, 43 patients (63%) either had spontaneous fluid collection resolution or remained well without symptoms or complications at a mean follow-up of 51 months.
A similar experience was noted in a series of 75 patients. Surgery was undertaken only for significant abdominal pain, complications, or progressive enlargement of a fluid collection. 52% of the patients underwent surgery for these indications, while the remaining patients were followed conservatively. Among patients in the latter group, 60% had complete resolution at one year, and only one had a fluid collection-related complication. The other patients in the conservatively-followed group had no symptoms, with either persistence of their fluid collections or a gradual decrease in size. It was not possible to predict which patients would completely resolve based on the etiology of the fluid collection or computed tomography (CT) criteria but, in general, walled-off pancreatic fluid collections were smaller in the conservatively-managed group than in patients requiring surgery.
We obtain follow-up abdominal imaging with a CT scan or magnetic resonance imaging (MRI) every three to six months. Imaging should be repeated sooner if the patient develops symptoms such as abdominal pain, chills, jaundice, early satiety, or fever. We stop obtaining follow-up imaging if the cyst resolves or stabilizes at an asymptomatic small size, provided we are confident in the diagnosis.
If a pseudoaneurysm is present but the patient has minimal or no symptoms, we recommend embolization of the aneurysm followed by expectant management.]
What is the most common islet cell tumor of the pancreas?
Insulinoma
What percent of gastrinomas are malignant?
50%
[UpToDate: Although gastrinomas are one of the most common functional pancreatic neuroendocrine tumors, only 25% of gastrinomas arise in the pancreas. Approximately 50% to 88% of patients with sporadic ZES, and 70% to 100% of patients with ZES associated with MEN1, have duodenal gastrinomas. Duodenal gastrinomas are predominantly found in the first part of the duodenum. As compared with pancreatic gastrinomas, duodenal gastrinomas are usually small (<1 cm), are often multiple, and are less likely to have metastasized to the liver at diagnosis (0% to 10% vs 22% to 35%). In 5% to 15% of patients, gastrinomas arise in non-pancreatic, non-duodenal abdominal (stomach, peripancreatic lymph nodes, liver, bile duct, ovary), and extra-abdominal (heart, small cell lung cancer) locations.]
What is the treatment for pancreatitis-associated pleural effusions (or ascites)?
Thoracentesis (or paracentesis) followed by conservative treatment (NPO, TPN, and octreotide)
[Amylase will be elevated in the fluid]
[UpToDate: Initial management of pancreatic fistulas and resultant complications of pancreatic ascites and pleural effusion include reduction of pancreatic stimulation and octreotide (a long-acting somatostatin analogue) to decrease pancreatic secretion. However, the long-term success of these approaches is limited, and only 50% to 65% of fistulas close over 4 to 6 weeks. Patients with persistent symptoms require endoscopic stents, preferably bridging the ductal disruption. Surgery for a persistent pancreatic fistula is indicated when endoscopic management fails or is technically unfeasible.]
CCK and secretin are mostly released by cells located where?
Duodenum
What do PP or F cells of the pancreas secrete?
Pancreatic polypeptide (PP)
[The function of PP is to self-regulate pancreatic secretion activities (endocrine and exocrine); it also has effects on hepatic glycogen levels and gastrointestinal secretions. Its secretion in humans is increased after a protein meal, fasting, exercise, and acute hypoglycemia and is decreased by somatostatin and intravenous glucose.]
[UpToDate: PP has a number of inhibitory actions that are believed to be important for both pancreatic and gastrointestinal function. Because many of its actions are local, it has been difficult to assess the magnitude of PP’s effects in the pancreas; however, it is well recognized to inhibit pancreatic exocrine secretion. In addition, PP has inhibitory effects on gallbladder contraction and gut motility, and may influence food intake, energy metabolism, and the expression of gastric ghrelin and hypothalamic peptides. PYY inhibits vagally stimulated gastric acid secretion and other motor and secretory functions. PYY-producing cells of the ileum are stimulated by incompletely digested nutrients, particularly fats. PYY released into the bloodstream can inhibit several gastrointestinal processes, including gastric emptying and intestinal motility, thus delaying the delivery of additional food to the intestine. This concept is known as the “ileal brake” and is believed to be mediated largely by PYY. Like PP, PYY also signals to the brain to reduce food intake by acting on Y2 receptors in the hypothalamus. In the periphery, PYY induces lipolysis and improves glycemic control by increasing insulin sensitivity through a reduction in circulating fatty acids.]
Which 2 lab values are typically elevated in pancreatic adenocarcinoma?
- Bilirubin
- Alkaline phosphatase
[UpToDate: Routine laboratory tests are often abnormal but are not specific for pancreatic cancer. Common abnormalities include an elevated serum bilirubin and alkaline phosphatase levels, and the presence of mild anemia.]
What is the treatment for pancreas divisum?
ERCP with sphincteroplasty
[Open sphincteroplasty if that fails]
Non-functional pancreatic endocrine neoplasms most commonly metastasize to where?
The liver
What are the 2 most common etiologies for acute pancreatitis in the United States?
- Gallstones (obstructs ampulla of vater causing impaired extrusion of zymogen granules and activation of degradation enzymes)
- ETOH (Causes auto-activation of enzymes while still in pancreas)
[Other etiologies: ERCP, trauma, hyperlipidemia, hypercalcemia, viral infection, medications]
[UpToDate: Gallstones (including microlithiasis) are the most common cause of acute pancreatitis in most areas of the world accounting for 35% to 40% of cases. However, only 3% to 7% of patients with gallstones develop pancreatitis
Alcohol is responsible for approximately 30% of cases of acute pancreatitis in the United States. Approximately 10% of chronic alcoholics develop attacks of clinically acute pancreatitis that are indistinguishable from other forms of acute pancreatitis.
Alcohol may act by increasing the synthesis of enzymes by pancreatic acinar cells to synthesize the digestive and lysosomal enzymes that are thought to be responsible for acute pancreatitis or over-sensitization of acini to cholecystokinin. However, the exact mechanism of pancreatic injury, the genetic and environmental factors that influence the development of pancreatitis in alcoholics, and the reason why only a small proportion of alcoholics develop pancreatitis, are unclear.]
What are the 6 Ranson’s Criteria after 48 hours?
- Hct drop more than 10% from admission
- BUN increase more than 5 mg/dL from admission
- Ca less than 8 mg/dL within 48 hours
- PaO2 less than 60 mmHg within 48 hours
- Base deficit (24 - HCO3) more than 4 mg/dL within 48 hours
- Fluid needs more than 6L within 48 hours
[UpToDate: A score based upon Ranson’s criteria is one of the earliest scoring systems for severity in AP. Ranson’s criteria consist of 11 parameters. Five of the factors are assessed at admission and six are assessed during the next 48 hours. A later modification for biliary pancreatitis included only 10 points. Mortality increases with an increasing score. Using the 11 component score, mortality was 0% to 3% when the score was <3, 11% to 15% when the score was ≥3, and 40% when the score was ≥6. Although the system continues to be used, a meta-analysis of 110 studies found the Ranson score to be a poor predictor of severity.]
What is the treatment for a duodenal gastrinoma?
Resection with primary closure (Be sure to check pancreas for primary tumor)
[May need a whipple if extensive]
[UpToDate: Patients with a sporadic gastrinoma who do not have evidence of metastatic spread of disease should be offered exploratory laparotomy and resection with curative intent, even in the event of negative imaging studies in approximately 17% of patients. This recommendation is derived from the observation that in addition to eliminating or at least decreasing the need for antisecretory medical therapy, successful resection of sporadic gastrinomas protects against the possibility of eventual morbidity and death from metastatic spread of the tumor. In the hands of an experienced surgeon, up to 50% of these patients will be cured. Lymphadenectomy exceeding more than 10 lymph nodes at the time of surgery has been shown to achieve a higher biochemical cure as compared with selective or no lymphadenectomy.
The likelihood for surgical cure is especially high for extrapancreatic gastrinomas (eg, those in the duodenum or peripancreatic lymph nodes). In contrast, laparotomy is not routinely recommended for patients with Zollinger-Ellison syndrome (ZES) as part of MEN 1 since the multifocal nature of the tumors in this disorder almost uniformly precludes cure of gastrin hypersecretion. However, because a minority of MEN-1 tumors can have aggressive growth patterns, some recommend imaging techniques or even surgical exploration to identify those exceeding 2 cm with the intent of resecting them.
80% of curable gastrinomas lie within the gastrinoma triangle comprised of the head of the pancreas and the duodenal sweep. The combination of preoperative localization techniques makes it possible for the experienced surgeon to identify over 90% of sporadic gastrinomas. Intraoperative transduodenal illumination and duodenotomy are of particular value in detecting very small gastrinomas arising in the wall of the duodenum. In the unlikely event that a sporadic gastrinoma cannot be identified at surgery, we suggest deferring a Whipple’s procedure in favor of closure, with the intent of serial imaging every 6 months to try to localize the neoplasm.
Gastric secretion may not return to the normal range following gastrinoma resection because of a residual excess of gastric parietal cells, a consequence of the trophic effect of chronically elevated gastrin levels. Up to 40% of patients will require prolonged antisecretory therapy to control hyperacidity following curative resection, and such patients need continued monitoring for acid hypersecretion. Of 50 patients who underwent curative resection for ZES, gastric hypersecretion was observed for a mean of 8 years in 62% of patients and was judged to be extreme in 28% despite normal blood gastrin levels.
A parietal cell (proximal gastric) vagotomy performed at the time of tumor resection has been advocated to reduce (and in some cases obviate) the need for postoperative medical therapy, particularly when complete resection of the gastrinoma tissue cannot be accomplished. However, it is currently uncommonly performed because of the efficacy of proton pump inhibitors. Furthermore, relatively few surgeons currently perform this procedure.
The reduction in mortality associated with surgical therapy for patients without metastatic disease was illustrated in a prospective study of 124 patients with gastrinoma presumed to be free of metastasis by imaging studies. Only 3% of the 98 patients who underwent resection developed liver metastases during a mean follow-up period of 6.3 years. By contrast, 23% of 26 patients treated medically developed metastatic disease over a slightly longer follow-up period (8.7 years). Two deaths due to metastatic gastrinoma occurred in the medically treated group compared with no disease-specific deaths in the operative group.]
Chronic pancreatitis is characterized by which irreversible macroscopic change?
Parenchymal fibrosis
[UpToDate: Morphologically, chronic pancreatitis is a patchy focal disease characterized by a mononuclear infiltrate and fibrosis. In contrast, acute pancreatitis diffusely involves a large portion of the entire pancreas with a predominantly neutrophilic inflammatory response.]
What are the 6 endocrine products of the pancreas?
- Glucagon
- Insulin
- Somatostatin
- Pancreatic polypeptide
- Vasoactive intestinal peptide (VIP)
- Serotonin
What is the first imaging test one should obtain when working up jaundice?
Ultrasound
[Positive common bile stones and no mass = ERCP, No common bile stones and no mass = MRCP, Positive for mass = MRCP]
[UpToDate: The diagnostic approach to the jaundiced patient begins with a careful history, physical examination, and initial laboratory studies. A differential diagnosis is formulated based on those results and additional testing is performed to narrow the diagnostic possibilities.
If there is evidence of biliary obstruction or intrahepatic cholestasis (eg, elevated conjugated bilirubin and alkaline phosphatase), the first step in the evaluation is hepatic imaging (eg, ultrasound, magnetic resonance cholangiopancreatography [MRCP], endoscopic retrograde cholangiopancreatography [ERCP]) to look for evidence of intra- or extrahepatic bile duct dilation. If imaging is negative, the evaluation typically will also include obtaining an antimitochondrial antibody to evaluate for primary biliary cholangitis.]
What do alpha cells of the pancreas secrete?
Glucagon
What are 3 symptoms of VIPoma
- Watery diarrhea
- Hypokalemia (from diarrhea)
- Achlorhydria
[UpToDate: The majority of patients with VIPoma have VIPoma syndrome, which is also called the pancreatic cholera syndrome, Verner-Morrison syndrome, and the watery diarrhea, hypokalemia, and hypochlorhydria or achlorhydria (WDHA) syndrome. VIPoma syndrome is characterized by watery diarrhea that persists with fasting. Stools are tea-colored and odorless with stool volumes exceeding 700 mL/day. In 70% of patients, stool volume can exceed 3000 mL/day. Abdominal pain is mild or absent. Associated symptoms include flushing episodes in 20% of patients and symptoms related to hypokalemia and dehydration, such as lethargy, nausea, vomiting, muscle weakness, and muscle cramps.]
What is the single best study for localizing a gastrinoma?
Octreotide scan
[UpToDate: After the diagnosis of Zollinger-Ellison syndrome (ZES) is made, the gastrinoma must be located and staged. Tumor localization begins with an upper endoscopy if not already performed, cross-sectional imaging with helical, contrast-enhanced, triple-phase computed tomography (CT) or magnetic resonance imaging (MRI), and somatostatin receptor scintigraphy (SRS)/Gallium-68-DOTA-D-Phe1-Tyr3-Octreotate (Gallium Ga-68 DOTATATE PET/CT). Because of its greater sensitivity, 68-Ga DOTATATE PET/CT is preferred over conventional SRS with 111-In pentetreotide.
If CT/MRI and SRS/68-Ga DOTATATE PET/CT are negative, and surgery is being considered, an endoscopic ultrasound (EUS) should be performed because of its greater sensitivity in detecting small tumors. EUS also permits fine-needle aspiration for histological identification.]
Which duct is a small accessory pancreatic duct that drains directly into the duodenum?
Duct of Santorini
During which decades of life does pancreatic adenocarcinoma occur?
6th and 7th decade of life
[UpToDate: In the United States, approximately 53,070 patients are diagnosed with cancer of the exocrine pancreas annually, and almost all are expected to die from the disease. Pancreatic cancer is the fourth leading cause of cancer-related death in the United States among both men and women. The majority of these tumors (85%) are adenocarcinomas arising from the ductal epithelium.
Worldwide, pancreatic cancer is the eighth leading cause of cancer deaths in men (138,100 deaths annually) and the ninth in women (127,900 deaths annually). In general, pancreatic cancer affects more individuals inhabiting the Western/industrialized parts of the world; the highest incidence is reported among Maoris in New Zealand, native Hawaiians, and Black American populations, while people living in India and Nigeria have the lowest reported incidence.
The disease is rare before the age of 45, but the incidence rises sharply thereafter. Incidence and death rates vary by sex and race. The incidence is greater in males than females (male-to-female ratio 1.3:1) and in blacks than in whites (14.8 per 100,000 in black males compared with 8.8 per 100,000 in the general population). However, more recent data suggest that these racial differences may be diminishing.]
Which medication should be avoided in patients with pancreatitis?
Morphine (it can contract the spincter of Oddi and worsen attack)
What effect does CCK have on pancreatic excretion?
Increases pancreatic enzymes
What are the 5 surgical indications for treating chronic pancreatitis?
- Pain that interferes with quality of life
- Nutrition abnormalities
- Addiction to narcotics
- Failure to rule out cancer
- Biliary obstruction
Which chemotherapeutic drug is commonly used in combination with XRT following resection of pancreatic adenocarcinoma?
Gemcitabine
[Gemcitabine monotherapy represents a standard approach. FOLFIRINOX (leucovorin, 5-FU, Irinotecan, Oxaliplatin) is an option for patients with good ECOG status. Gemcitabine plus Paclitaxel or Capecitabine represent acceptable and potentially less toxic alternatives to FOLFIRINOX. For patients with ECOG status of 0-1 Gemcitabine alone is recommended. Radiotherapy as a single modality may be considered in the setting of palliation of pain for a nonresectable patient.]
[UpToDate: In general, multiagent regimens are associated with higher response rates than single-agent gemcitabine, and at least two combinations, leucovorin plus short-term infusional fluorouracil (FU) plus oxaliplatin and irinotecan (FOLFIRINOX) and gemcitabine plus nanoparticle albumin-bound paclitaxel (nabpaclitaxel), have been associated with significantly prolonged survival as compared with gemcitabine alone. However, combination therapy is also associated with more adverse effects, which can have a negative impact on quality of life (QOL). As a result, single-agent therapy, typically with gemcitabine alone, remains a reasonable first-line therapy option.]
What are the 4 main symptoms of acute pancreatitis?
- Abdominal pain radiating to back
- Nausea
- Vomiting
- Anorexia
[Can also get jaundice, left pleural effusion, ascites, or sentinel loop (dilated small bowel near the pancreas as a result of the inflammation)]
When should cholecystectomy be performed in a patient with acute pancreatitis?
Patients with gallstone pancreatitis should undergo cholecystectomy when recovered from pancreatitis (same hospital admission)
Coagulopathy associated with acute pancreatitis is caused by what?
Release of proteases
What proportion of pancreatic endocrine neoplasms are functional endocrine neoplasms?
2/3
[UpToDate: One-third to one-half of PNETs have no defined clinical syndrome and no elevated hormone levels. As such, the presentation of nonfunctional PNETs is often delayed. Patients often present late in their course with symptoms of mass effect or with symptoms related to metastases including abdominal pain, weight loss, and jaundice. But patients with nonfunctional tumors can also present with an incidental finding on cross-sectional imaging performed for an unrelated reason.
Patients with functional (ie, hormone-secreting) tumors present clinically with syndromes of excess gastrointestinal hormone production (insulin, serotonin, gastrin, VIP (vasoactive intestinal peptide), glucagon, or somatostatin). In general, the aggressiveness of PNETs (grade based on histologic features) does not correlate with presence or type of hormone production. Once a diagnosis of a functional tumor has been made biochemically, it is generally unnecessary to repeat any studies.]
What do acinar cells of the pancreas secrete?
Digestive enzymes
[The pancreatic acinar cell is the functional unit of the exocrine pancreas. It synthesizes, stores, and secretes digestive enzymes. Under normal physiological conditions, digestive enzymes are activated only once they have reached the duodenum.]
What is heterotopic pancreas?
Pancreatic tissue outside boundaries of pancreas without anatomic or vascular connections to pancreas
What is good at differentiating between dilated ducts secondary to chronic pancreatitis vs cancer?
MRCP
[Signs of cancer on MRCP include: duct with irregular narrowing, displacement, destruction; MRCP can also detect vessel involvement]
[UpToDate: An alternative to diagnostic ERCP is MRCP. MRCP uses magnetic resonance technology to create a three-dimensional image of the pancreaticobiliary tree, liver parenchyma, and vascular structures. MRCP is better than CT for defining the anatomy of the biliary tree and pancreatic duct, has the capability to evaluate the bile ducts both above and below a stricture, and can also identify intrahepatic mass lesions. It is at least as sensitive as ERCP in detecting pancreatic cancers, and unlike conventional ERCP, it does not require contrast material to be administered into the ductal system. Thus, the morbidity associated with endoscopic procedures and contrast administration is avoided.]
What is pancreas divisum?
Failure of the pancreatic ducts to fuse
[Can result in pancreatitis from duct of Santorini stenosis]
What do ductal cells of the pancreas secrete?
HCO3 solution (have carbonic anhydrase)
When are antibiotics indicated in the treatment of acute pancreatitis?
Stones, severe pancreatitis, failure to improve, or suspected infection
[UpToDate: Up to 20% of patients with acute pancreatitis develop an extrapancreatic infection (eg, bloodstream infections, pneumonia, and urinary tract infections). Extrapancreatic infections are associated with an increase in mortality. When an infection is suspected, antibiotics should be started while the source of the infection is being determined. However, if cultures are negative and no source of infection is identified, antibiotics should be discontinued.
Prophylactic antibiotics are not recommended in patients with acute pancreatitis, regardless of the type (interstitial or necrotizing) or disease severity (mild, moderately severe, or severe).]
What is the leading cause of death in acute pancreatitis?
Infection
[Usually gram negative rods]
[UpToDate: The occurrence of pancreatic infection is a leading cause of morbidity and mortality in acute necrotizing pancreatitis. Approximately 1/3 of patients with pancreatic necrosis develop infected necrosis. There is no correlation between the extent of necrosis and the risk of infection. Although infection can occur early in the course of necrotizing pancreatitis, it is more often seen late in the clinical course (after 10 days). The majority of infections (approximately 75%) are monomicrobial with gut-derived organisms (eg, Escherichia coli, Pseudomonas, Klebsiella, and Enterococcus).]
How is a glucagonoma diagnosed?
Fasting glucagon level
[UpToDate: The diagnosis of a glucagonoma requires the demonstration of increased plasma glucagon levels (>500 pg/mL). Plasma glucagon levels are usually elevated 10- to 20-fold in patients with glucagonoma (normal <50 pg/mL). Concentrations above 1000 pg/mL are virtually diagnostic of glucagonoma. However, up to 70% of the immunoreactive glucagon may be biologically inactive.
Conditions other than glucagonoma that can induce moderate elevations in the serum glucagon concentration (<500 pg/mL) include hypoglycemia, fasting, trauma, sepsis, acute pancreatitis, abdominal surgery, Cushing’s syndrome, and renal and hepatic failure. Idiopathic hyperglucagonemia syndrome, either familial or sporadic, is associated with a large molecular weight form of the peptide. In addition, other neuroendocrine tumors, such as carcinoid tumors, insulinomas, and gastrinomas, can secrete glucagon, although rarely in high enough levels to cause the classic clinical syndrome.
However, some glucagonomas are associated with serum levels of the peptide in the “physiologically elevated” range, even in the presence of necrolytic migratory erythema. Thus, in patients with the classic syndrome, a serum glucagon concentration below 500 pg/mL does not exclude a glucagonoma.]
How do normal patients and patients with a gastrinoma respond to a secretin stimulation test?
- Nomal patients respond with a reduction in gastrin levels
- Gastrinoma patients respond with increased gastrin levels
[UpToDate: The secretin stimulation test is used to differentiate patients with gastrinomas from other causes of hypergastrinemia. Secretin stimulates the release of gastrin by gastrinoma cells, and patients with ZES tumors have a dramatic rise in serum gastrin. In contrast, normal gastric G cells are inhibited by secretin.
False-negative response can occur in 6% to 20% of patients. False-positive results occurred in 15% to 39% of patients with achlorhydria induced by PPIs or due to chronic atrophic gastritis. However, if PPIs are discontinued abruptly, patients with ZES are at high risk to develop complications (such as acute bleeding and perforation) during the interim week. One week prior to the secretin study we substitute PPIs with high-dose H2 receptor antagonists (eg, ranitidine 450 to 750 mg every 6 hours until 24 hours prior to the test). Oral antacids are then taken as needed until midnight prior to the study. Patients should be advised to seek immediate medical attention for nasogastric aspiration if they develop significant exacerbation of ZES symptoms (eg, vomiting, pain, diarrhea) during the taper period.
The secretin stimulation test is performed by administering 2 units/kg by rapid infusion intravenously over one minute; a baseline serum gastrin is measured twice before the secretin is administered and 2, 5, 10, 15, and 20 minutes later. Several criteria have been proposed to define a positive test; an increase in gastrin levels of greater than 120 pg/mL over basal fasting levels has a sensitivity and a specificity of 94% and 100%, respectively. Serum gastrin levels usually peak by 10 minutes.
The secretin stimulation test should not be performed in patients with severe manifestations of ZES. This includes patients with severe abdominal pain, vomiting and diarrhea to the point of dehydration, or endoscopic findings of thickened gastric folds or multiple ulcers, as they are at particular risk for life-threatening consequences of discontinuing acid suppression. In such patients, tumor localization studies should be performed.]
For non-metastatic pancreatic adenocarcinoma, what is the prognosis dependent upon?
Nodal invasion and ability to get a clear margin
[UpToDate: Even in the setting of completely resected, node-negative pancreatic cancer, the majority of patients die of their disease. The most important prognostic factor for completely resected patients is nodal status. 5-year survival after pancreaticoduodenectomy is only about 10% for node-positive disease (even if only one node is positive), while it is 25% to 30% for node-negative disease.]
Do most pancreatic fistulas close spontaneously or require treatment?
Close spontaneously
[Especially if low output less than 200 cc/day]
[UpToDate: With supportive care, case series have reported fistula closure in approximately 80% of external and 50% to 65% of internal fistulas over 4 to 6 weeks. We obtain follow-up abdominal imaging with an abdominal computed tomography (CT) scan or magnetic resonance imaging (MRI) in 6 to 8 weeks to evaluate the size of peripancreatic fluid collections. Imaging should be repeated sooner if the patient develops abdominal pain, fever, chills, jaundice, or early satiety. In patients with clinical symptoms, sepsis physiology, or increasing white blood cell count, pancreatic fluid should be sent for Gram stain and culture to rule out an infection. Systemic antibiotics should be administered in patients with evidence of infected pancreatic fluid collections.]
Where do most somatostatinomas occur?
Head of pancreas
[UpToDate: Somatostatinomas are rare neuroendocrine tumors with an annual incidence of 1 in 40 million. The mean age at diagnosis of somatostatinomas is 50 to 55 years (range 26 to 84), with a roughly equal gender distribution. Approximately 55% of somatostatinomas are in the pancreas, and, of these, two-thirds arise within the head of the pancreas. The remainder arises in the ampulla and periampullary region of the duodenum or rarely in the jejunum. Other rare primary sites include the liver, colon, and rectum. Approximately 75% of somatostatinomas are malignant, and 70% to 92% present with metastatic disease.
Although 45% of somatostatinomas occur in association with multiple endocrine neoplasia (MEN)-1 syndrome, somatostatinomas are among the least common functioning pancreatic neuroendocrine tumors in patients with MEN-1 syndrome, occurring in less than 1% of patients. Up to 10% of patients with neurofibromatosis I (NF-1; von Recklinghausen disease) develop somatostatinomas. NF-1-associated somatostatinomas are characteristically duodenal, are rarely associated with somatostatinoma syndrome, and are less likely to metastasize as compared with sporadic somatostatinomas.]
The uncinate process of the pancreas is positioned anterior to which vessel and posterior to which vessel?
- Anterior to aorta
- Posterior to superior mesenteric vein
What do islet cells of the pancreas secrete?
- Alpha cells: Glucagon
- Beta cells: Insulin
- Delta cells: Somatostatin
- PP or F cells: Pancreatic polypeptide
[Vasoactive intestinal peptide (VIP) and serotonin are also secreted by pancreatic islet cells.]
What is the treatment for a pancreatic abscess?
Surgical debridement (gas is indication for open debridement)
[CT-guided drainage of pancreatic abscess is generally not effective]
What are the 3 surgical treatment options for chronic pancreatitis with normal or small ducts?
- Distal pancreatic resection (Only distal portion of the gland affected)
- Whipple (Isolated pancreatic head disease)
- Beger-Frey procedures (Isolated pancreatic head enlargement)
[UpToDate: A duodenal-preserving pancreatic head resection (DPPHR) technique was described by Beger in 1980 for CP in an effort to decrease the morbidity of pancreatic head resection. In DPPHR, the pancreas neck is transected, followed by a subtotal resection of the head. A rim of pancreatic parenchyma along the duodenal wall, which contains the arcade of duodenal arterial blood supply, is preserved. A Roux-en-Y limb of jejunum is then used to create a pancreaticojejunostomy.
In 1987, Frey described a technique that opens the pancreatic duct along its length and into the head and uncinate process of the pancreas for drainage, “cores” out the overlying fibrotic pancreatic head tissue without transecting the pancreatic neck, and preserves the pancreatic parenchyma along the posterior and lateral margin of the pancreatic head and the duodenum to minimize long-term gastrointestinal dysfunction.]
What are the boundaries of the gastrinoma triangle where the majority of gastrinomas occur?
- Common bile duct
- Neck of the pancreas
- Third portion of the duodenum
[90% of gastrinomas occur in this region]
[Radiopaedia.org: The triangle is formed by joining the following three points:
- superiorly: confluence of the cystic and common bile ducts
- inferiorly: junction of the second and third portions of the duodenum
- medially: junction of the neck and body of the pancreas]
[UpToDate: 80% of curable gastrinomas lie within the gastrinoma triangle comprised of the head of the pancreas and the duodenal sweep. The combination of preoperative localization techniques makes it possible for the experienced surgeon to identify over 90% of sporadic gastrinomas. Intraoperative transduodenal illumination and duodenotomy are of particular value in detecting very small gastrinomas arising in the wall of the duodenum. In the unlikely event that a sporadic gastrinoma cannot be identified at surgery, we suggest deferring a Whipple’s procedure in favor of closure, with the intent of serial imaging every 6 months to try to localize the neoplasm.]
Where do most VIPomas occur?
Distal pancreas
[10% extrapancreatic (retroperitoneal, thorax)]
[UpToDate: VIPomas are detected in 1 in 10 million people per year. The majority of VIPomas arise within the pancreas, and are classified as functioning pancreatic neuroendocrine (islet cell) tumors. In adults, VIPomas are intrapancreatic in over 95% of cases. However, other VIP-secreting tumors have been reported, including lung cancer, colorectal cancer, ganglioneuroblastoma, pheochromocytoma, hepatoma, and adrenal tumors. In children, VIPomas can occur in sympathetic ganglia and the adrenal glands.
VIPomas are usually diagnosed between 30 and 50 years of age in adults and between two and four years of age in children. Symptomatic pancreatic VIPomas are usually solitary, more than 3 cm in diameter, and occur in the tail of the pancreas in 75% of patients. Approximately 60% to 80% of VIPomas have metastasized by the time of diagnosis. VIPomas usually occur as isolated tumors, but in 5% of patients they are part of the multiple endocrine neoplasia syndrome type 1 (MEN1) and occur in association with parathyroid and pituitary tumors, gastrinoma, and other tumors.]
Where does venous blood from the pancreas drain?
Into the portal system
What do beta cells of the pancreas secrete?
Insulin
Which tests should be performed on a patient with suspected acute pancreatitis?
- Ultrasound (needed to check for gallstones and possible CBD dilatation)
- Abdominal CT (to check for complications such as necrotic pancreas (will not uptake contrast))
What is the treatment for pancreatic pseudocyst that does not resolve with expectant management for 3 months?
Cystograstrostomy (open or percutaneous)
[Cysts that are growing must be resected to rule out cancer]
[UpToDate: Surgical management can be performed with an open surgical procedure or with a laparoscopic approach.
Most of the surgical literature is based on open surgical drainage procedures. Open surgical drainage can be accomplished via cystgastrostomy, cystenterostomy (direct drainage or via a Roux limb), or resection. However, these approaches are associated with substantial morbidity and mortality (25% and 5%, respectively).
Drainage can also be accomplished laparoscopically. Laparoscopic cystgastrostomy can be performed via an anterior transgastric approach, which requires an anterior gastrotomy for access and cystgastrostomy creation through the posterior gastric wall, or a posterior approach through the lesser sac (requiring only a single gastrotomy in continuity with the walled-off pancreatic fluid collection). It can also be performed through a lesser sac approach, which is considered technically easier and is associated with less intraoperative bleeding.
Walled-off pancreatic fluid collections that are not in close proximity to the stomach require creation of a cystojejunostomy. The cystojejunostomy is sometimes created via a Roux limb of jejunum. Left-sided pancreatectomy, either open or laparoscopic, may be preferred in the setting of a communicating walled-off pancreatic fluid collection in the tail, particularly in the setting of chronic pancreatitis or disconnected pancreatic tail syndrome.]
What is the mortality rate associated with acute pancreatitis?
10%
[UpToDate: Advances in diagnostic and therapeutic interventions have led to a decrease in mortality from acute pancreatitis, especially in those with severe, often necrotizing pancreatitis. Mortality in acute pancreatitis is usually due to systemic inflammatory response syndrome and organ failure in the first two-week period, while after two weeks it is usually due to sepsis and its complications.
A multicenter prospective study of 1005 patients with acute pancreatitis reported overall mortality of 5% (1.5% in mild acute pancreatitis and 17% in severe pancreatitis). While the overall mortality in all hospitalized patients with acute pancreatitis is approximately 10% (range 2% to 22%), the mortality in the subset with severe acute pancreatitis may be as high as 30%.]
What is the most common islet cell tumor of the pancreas in MEN-1 patients?
Gastrinoma (Zollinger-Ellison syndrome)
Do most pancreatic pseudocysts resolve spontaneously or do they require treatment?
Resolve spontaneously
[Especially if under 5cm]
[UpToDate: Watchful waiting is an appropriate option in patients with walled-off pancreatic fluid collections with minimal or no symptoms and no evidence of a pseudoaneurysm:
A retrospective review of 68 patients with a walled-off pancreatic fluid collection followed conservatively showed a 9% incidence of serious complications, with the majority occurring in the first eight weeks after diagnosis. Complications included pseudoaneurysm formation in three patients, free perforation in two, and spontaneous abscess formation in one. An additional third of the patients underwent elective surgery, generally for fluid collection enlargement associated with pain. However, 43 patients (63%) either had spontaneous fluid collection resolution or remained well without symptoms or complications at a mean follow-up of 51 months.]
Are Somatostatinomas usually benign or malignant?
Malignant
[UpToDate: Somatostatinomas are rare neuroendocrine tumors with an annual incidence of 1 in 40 million. The mean age at diagnosis of somatostatinomas is 50 to 55 years (range 26 to 84), with a roughly equal gender distribution. Approximately 55% of somatostatinomas are in the pancreas, and, of these, two-thirds arise within the head of the pancreas. The remainder arises in the ampulla and periampullary region of the duodenum or rarely in the jejunum. Other rare primary sites include the liver, colon, and rectum. Approximately 75% of somatostatinomas are malignant, and 70% to 92% present with metastatic disease.
Although 45% of somatostatinomas occur in association with multiple endocrine neoplasia (MEN)-1 syndrome, somatostatinomas are among the least common functioning pancreatic neuroendocrine tumors in patients with MEN-1 syndrome, occurring in less than 1% of patients. Up to 10% of patients with neurofibromatosis I (NF-1; von Recklinghausen disease) develop somatostatinomas. NF-1-associated somatostatinomas are characteristically duodenal, are rarely associated with somatostatinoma syndrome, and are less likely to metastasize as compared with sporadic somatostatinomas.]
What is the treatment for chronic pancreatitis?
Supportive (pain control and nutritional support with pancrelipase)
[Surgery if indicated]
[UpToDate: Chronic pancreatitis typically presents as chronic unrelenting pain with episodic flares. Although it is sometimes stated that chronic pancreatitis “burns out” over time, the duration of time over which this may occur is highly variable, if it occurs at all. In addition, pancreatic endocrine and exocrine dysfunction may develop as the disease progresses, and a variety of complications can occur, including pseudocysts, bile duct or duodenal obstruction, pancreatic ascites, splenic vein thrombosis, and pseudoaneurysms.
Thus, the natural history of chronic pancreatitis is relatively bleak. Most therapies are aimed at “resting” the pancreas by minimizing exocrine pancreatic secretion; unfortunately, this is relatively ineffective. The goals of treatment include pain management, correction of pancreatic insufficiency, and management of complications. Therapy is similar in patients with acquired and hereditary pancreatitis.]
What percent of insulinomas are benign?
90%
[They are usually evenly distributed throughout the pancreas]
What is the treatment for pancreatic necrosis?
- Sterile necrosis should be left alone
- Infected necrosis (fever, sepsis, positive blood cx) requires surgical debridement
- Gas in infected necrosis requires open surgical debridement
[CT-guided drainage of infected pancreatic necrosis is generally not effective]
[UpToDate: Pancreatic necrosis can lead to secondary infection or symptomatic sterile necrosis, which is characterized by chronic low grade fever, nausea, lethargy, and inability to eat. Both infected pancreatic necrosis and symptomatic sterile necrosis are accepted indications for debridement.
The goal of pancreatic debridement is to excise all dead and devitalized pancreatic and peripancreatic tissue while preserving viable functioning pancreas, controlling resultant pancreatic fistulas, and limiting extraneous organ damage. For patients with biliary pancreatitis, cholecystectomy with intraoperative cholangiography is an important secondary objective of the surgery because it will prevent recurrent disease.
Secondary infection of the necrotic pancreatic or peripancreatic tissue with either bacteria or fungus occurs soon after the initial inflammatory reaction subsides and is heralded by tachycardia, hypotension, fevers, and/or deteriorating organ function. Bacterial or fungal infections occur either by bacterial translocation from the gastrointestinal tract or via seeding through transient bacteremia that can occur in the setting of invasive intravenous lines, endotracheal intubation, or prolonged bladder catheterization. The risk of secondary bacterial infections can be minimized with early enteral feeding, central line catheter maintenance programs, ventilator protocols, and early urinary catheter removal.
There is no benefit from probiotics, protease inhibitors, or early surgical debridement for the prevention of infected pancreatic necrosis. The use of prophylactic systemic antibiotics in acute pancreatitis is controversial.]
Which vessel supplies blood to the superior portion of the head of the pancreas?
Pancreaticoduodenal arteries off of the gastroduodenal artery
Which vessel supplies blood to the inferior portion of the head of the pancreas?
Pancreaticoduodenal arteries off of the superior mesenteric artery
Which duct is the major pancreatic duct that merges with the common bile duct before entering the duodenum?
Duct of Wirsung
What are the lab values required to diagnose insulinoma?
- Insulin to glucose ratio greater than 0.4 after fasting
- Increased C peptide and proinsulin (if not elevated, suspect Munchaussen’s syndrome)
[UpToDate: Fasting for a maximum of 72 hours has been the standard test for the diagnosis of insulinoma. A 48-hour maximum has been proposed as a simpler alternative based upon a report of 127 patients with insulinoma in which adequate information was obtained for diagnosis in all patients. The fast was terminated because of hypoglycemia (plasma glucose ≤45 mg/dL [2.5 mmol/L]) in 43% by 12 hours, 67% by 24 hours, and 95% by 48 hours.
However, in our series of 205 patients with insulinoma, 14% did not develop Whipple’s triad until after 48 hours of fasting. Thus, to avoid misdiagnosis, we recommend the standard 72-hour fast.
The decision to end the fast may not be easy. Some patients have slightly low plasma glucose values, but no symptoms or signs of hypoglycemia, while others have the same symptoms during fasting that they have in ordinary life at a time when plasma glucose values are normal. In the latter patients, the symptoms cannot be attributed to hypoglycemia. To complicate matters further, young, lean, healthy women may have plasma glucose concentrations in the range of 40 mg/dL (2.2 mmol/L) or even lower after prolonged periods of fasting.
Careful questioning and testing for subtle symptoms or signs of hypoglycemia should be conducted repeatedly when the patient’s plasma glucose is near or in the hypoglycemic range. To end the fast solely on the basis of a low plasma glucose value (except in those patients who have had Whipple’s triad documented previously), in the absence of symptoms or signs of hypoglycemia, jeopardizes the possibility of discriminating between normal persons and those with hypoglycemia not mediated by insulin. A low plasma glucose value is a necessary but not sufficient finding for the diagnosis of hypoglycemia.
The absence of symptoms or signs of hypoglycemia and lack of a low plasma glucose concentration during a 72-hour fast indicates a normal 72-hour fast, but does not preclude the existence of a hypoglycemic disorder that causes only postprandial symptoms.
Interpretation of the data obtained at the end of the 72-hour fast is the same as that performed during the occurrence of a spontaneous hypoglycemic episode or during a postprandial evaluation (mixed meal test). These data will help distinguish hyperinsulinemia (endogenous or exogenous) from other causes of hypoglycemia.
Ratios of insulin-to-glucose or of glucose-to-insulin are not helpful in the establishment of hyperinsulinemia; absolute values for insulin are preferable.]
What activates trypsinogen to trypsin?
Enterokinase (Released by the duodenum)
[Trypsin activates other pancreatic enzymes including trypsinogen]
What is Whipple’s triad?
- Fasting hypoglycemia (less than 50)
- Symptoms of hypoglycemia (palpitations, Tachycardia, diaphoresis)
- Relief with glucose
[Indicative of insulinoma]
[UpToDate: The presence of a hypoglycemic disorder in a person without diabetes should not be suspected solely on the basis of a low plasma glucose concentration, as this observation is necessary but insufficient for a diagnosis and in some cases may be misleading. Only those patients in whom Whipple’s triad is documented require evaluation and management of hypoglycemia.
In the patient without diabetes, the definition of hypoglycemia is based upon the presence of Whipple’s triad: symptoms, signs, or both consistent with hypoglycemia, a low plasma glucose concentration at the time of symptoms, and resolution of those signs and symptoms after raising the plasma glucose concentration.]
What effect does secretin have on pancreatic excretion?
Increases HCO3 excretion
What is the serum marker for pancreatic cancer?
CA 19-9
Do the superior mesenteric vein and artery run anterior or posterior to the neck of the pancreas?
They lay posterior to the neck of the pancreas
How is pancreas divisum diagnosed?
ERCP
[Minor papilla will show long and large duct of Santorini, major papilla will show short duct of Wirsung]
What happens to result in annular pancreas?
It forms from the ventral pancreatic bud failing to rotate clockwise
[Double bubble sign on abdominal xray]
[UpToDate: In symptomatic neonates, a plain abdominal radiograph will show the classic “double bubble” sign with air in the stomach and duodenum. However, the double bubble sign is not specific for annular pancreas since it can also be seen in other conditions including duodenal atresia and intestinal malrotation.]
Which pancreatic bud is connected to the duct of Wirsung and migrates posteriorly, to the right, and clockwise to fuse with the other pancreatic bud?
Ventral pancreatic bud
What is the double-duct sign?
Dilation of both the pancreatic duct and the common bile duct dues to pancreatic head tumor
Are VIPomas usually benign or malignant?
Malignant
[UpToDate: VIPomas are detected in 1 in 10 million people per year. The majority of VIPomas arise within the pancreas, and are classified as functioning pancreatic neuroendocrine (islet cell) tumors. In adults, VIPomas are intrapancreatic in over 95% of cases. However, other VIP-secreting tumors have been reported, including lung cancer, colorectal cancer, ganglioneuroblastoma, pheochromocytoma, hepatoma, and adrenal tumors. In children, VIPomas can occur in sympathetic ganglia and the adrenal glands.
VIPomas are usually diagnosed between 30 and 50 years of age in adults and between two and four years of age in children. Symptomatic pancreatic VIPomas are usually solitary, more than 3 cm in diameter, and occur in the tail of the pancreas in 75% of patients. Approximately 60% to 80% of VIPomas have metastasized by the time of diagnosis. VIPomas usually occur as isolated tumors, but in 5% of patients they are part of the multiple endocrine neoplasia syndrome type 1 (MEN1) and occur in association with parathyroid and pituitary tumors, gastrinoma, and other tumors.]
Which 3 vessels supply blood to the body of the pancreas?
- Great pancreatic artery
- Inferior pancreatic artery (Also known as transverse pancreatic artery)
- caudal pancreatic artery
[These are branches off of the splenic artery]
How is chronic pancreatitis diagnosed?
- Abdominal CT (Pancreas will be shrunken with calcifications)
- Ultrasound (Pancreatic ducts greater than 4mm, cysts, atrophy)
- ERCP (very sensitive for chronic pancreatitis)
[UpToDate: The diagnosis of chronic pancreatitis can be challenging since laboratory studies and imaging procedures may be normal. In addition, patients may have symptoms suggestive of chronic pancreatitis but in fact have pancreatic carcinoma. On the other hand, the classic triad of pancreatic calcifications, steatorrhea, and diabetes mellitus strongly suggests the diagnosis, but are usually seen together only in late, very advanced disease. The diagnosis is confirmed if there are calcifications within the pancreas on abdominal plain films or computed tomography (CT) scan, an abnormal pancreatogram revealing beading of the main pancreatic duct or ectatic side branches, or an abnormal secretin pancreatic function test.]
Which pancreatic bud forms the body, tail, and superior aspect of the pancreatic head?
Dorsal pancreatic bud
Which 3 vessels supply blood to the tail of the pancreas?
- Splenic artery
- Gastroepiploic artery
- Dorsal pancreatic artery
[UpToDate: The arterial supply to the duodenum and pancreas is derived from the celiac artery, providing the superior pancreaticoduodenal arteries (anterior and posterior branches), and the superior mesenteric artery, providing the inferior pancreaticoduodenal arteries (anterior and posterior branches). The splenic artery supplies primarily the body and tail of the pancreas. The venous drainage follows the arteries to provide tributaries to the splenic vein and superior mesenteric vein which drain into the portal vein.]
What do delta cells of the pancreas secrete?
Somatostatin
Functional pancreatic endocrine neoplasms most commonly metastasize to where?
The liver
Infection from acute pancreatitis is usually caused by which group of bacteria?
Gram negative rods
What are 4 symptoms of a glucagonoma?
- Diabetes
- Stomatitis
- Dermatitis (Rash - Necrolytic migratory erythema)
- Weight loss
[UpToDate: As the clinical features of glucagonoma syndrome are non-specific, the majority of patients are diagnosed late when the disease has metastasized.
Weight loss, often significant, is the most common presenting feature, occurring in 80% of patients with glucagonoma syndrome.
Necrolytic migratory erythema (NME) is the presenting feature of glucagonoma syndrome in approximately 70% of patients. Although the rash can occasionally be the only symptom, in most cases patients have associated systemic symptoms. NME characteristically begins as erythematous papules or plaques involving the face, perineum, and extremities. Over the ensuing 7 to 14 days, the lesions enlarge and coalesce. Central clearing then occurs, leaving bronze-colored, indurated areas centrally, with blistering, crusting, and scaling at the borders. The affected areas are often pruritic and painful. The same process often affects the mucous membranes, resulting in glossitis, angular cheilitis, stomatitis, and blepharitis. Patients with NME often have associated hair loss and nail dystrophy.
Glucose intolerance occurs in 75% to 95% of patients with glucagonoma. However, clinically significant hyperglycemia with diabetes mellitus is present at diagnosis in approximately 40% of patients. Hyperglycemia due to glucagonoma syndrome does not usually result in diabetic ketoacidosis, since beta cell function is preserved and insulin secretion is normal.]
Which pancreatic bud has the duct of Santorini?
Dorsal pancreatic bud
[The ventral bud has the duct of Wirsung.]
What is the surgical treatment option for chronic pancreatitis with enlarged ducts (greater than 8mm)?
Puestow procedure: Pancreaticojejunostomy (Open along main pancreatic duct and drain into jejunum)
[Most patients improve]
[UpToDate: Decompression procedures have generally been recommended for patients with refractory pain who have a dilated main pancreatic duct. The normal pancreatic duct ranges from 2 to 4 mm in diameter (most narrow in the tail, enlarging as it passes toward the ampulla). A dilated duct (from a surgical standpoint) is one that would permit anastomosis to a loop of jejunum. Consensus has not been achieved at the threshold at which this can be achieved; some surgeons will perform such a procedure in those with ducts that are only 5 to 6 mm in diameter, while others require dilation to around 10 mm.
Multiple series have described the outcome of this procedure and its variants. A review of these data in a consensus statement from the American Gastroenterological Association (AGA) focused on five reports that were selected because of their relatively large numbers of patients, longer follow-up, and methodologic quality. The data suggest that short-term pain relief is achieved in approximately 80% of patients. Morbidity and mortality related to the operation are generally low when the procedure has been performed by experienced surgeons (0% to 5%).
However, pain relief persists for more than two years in only about 60% of patients. Patients with recurrent pain may require additional surgery. The cause of pain recurrence is unclear. It may be related to progressive pancreatic injury or inadequate drainage of secondary ducts.
How these outcomes compare with resection procedures has not been extensively studied in randomized studies, but tend to favor drainage approaches.]
What are the Ranson’s criteria used for?
Predicting the severity of acute pancreatitis
[Nearly 100% mortality if 8 Ranson’s criteria met]
What procedure should be done in conjunction with somatostatinoma resection?
Cholecystectomy
[UpToDate: In patients with somatostatinomas, cholelithiasis may result from inhibition of cholecystokinin release, which reduces gallbladder contractility. Diminished insulin secretion leads to glucose intolerance/diabetes. Inhibition of pancreatic enzyme and bicarbonate secretion and intestinal absorption of lipids causes diarrhea and steatorrhea.]
What is the treatment for annular pancreas?
Duodenojejunostomy or duodenoduodenostomy (Possible sphincteroplasty)
[Pancreas is not resected]
[UpToDate: Most patients with annular pancreas are asymptomatic, and thus the presence of annular pancreas does not necessarily indicate that symptoms can be attributed to it. Surgery remains the procedure of choice in patients in whom symptoms can be attributed to annular pancreas. The goal of surgery is to relieve duodenal or gastric outlet obstruction by bypassing the annulus. Resection of the annulus should be avoided since it is associated with pancreatitis, pancreatic fistula formation, and incomplete relief of obstruction.
In neonates, relief of obstruction is accomplished with a duodenoduodenostomy. In adults, a duodenojejunostomy or gastrojejunostomy is recommended as the duodenum is less mobile. In patients with annular pancreas associated with obstructive jaundice, biliary bypass with choledochoenterostomy or placement of a biliary stent may be necessary to relieve the obstruction. Pancreaticoduodenectomy has been recommended when annular pancreas is associated with obstructive pancreatic duct stones in the setting of chronic pancreatitis or a periampullary lesion that is suspicious for a malignancy.]
What percent of gastrinomas are spontaneous vs MEN-1 related?
- 75% are spontaneous
- 25% are MEN-1 related
Where is enterokinase released?
Duodenum
What are the 5 Ranson’s Criteria on admission?
- Age over 55
- WBC over 16
- Glucose over 200
- AST over 250
- LDH over 350
[UpToDate: A score based upon Ranson’s criteria is one of the earliest scoring systems for severity in AP. Ranson’s criteria consist of 11 parameters. Five of the factors are assessed at admission and six are assessed during the next 48 hours. A later modification for biliary pancreatitis included only 10 points. Mortality increases with an increasing score. Using the 11 component score, mortality was 0% to 3% when the score was <3, 11% to 15% when the score was ≥3, and 40% when the score was ≥6. Although the system continues to be used, a meta-analysis of 110 studies found the Ranson score to be a poor predictor of severity.]
Are glucagonomas usually benign or malignant?
Malignant
[UpToDate: Glucagonomas are rare, with an annual incidence of 0.01 to 0.1 new cases per 100,000. Glucagonomas are usually solitary, and the majority are located in the distal pancreas. Patients typically present in their fifth decade. While most glucagonomas are sporadic, up to 20% may be associated with the multiple endocrine neoplasia syndrome type 1 (MEN1). However, glucagonomas occur in only 3% of MEN1 patients. Glucagonomas are usually large (>3 cm), and approximately 50% to 80% are metastatic at diagnosis. Unlike carcinoid tumors, however, liver metastases are not a prerequisite for the clinical syndrome.]
Where do most glucagonomas occur?
Distal pancreas
[UpToDate: Glucagonomas are rare, with an annual incidence of 0.01 to 0.1 new cases per 100,000. Glucagonomas are usually solitary, and the majority are located in the distal pancreas. Patients typically present in their fifth decade. While most glucagonomas are sporadic, up to 20% may be associated with the multiple endocrine neoplasia syndrome type 1 (MEN1). However, glucagonomas occur in only 3% of MEN1 patients. Glucagonomas are usually large (>3 cm), and approximately 50% to 80% are metastatic at diagnosis. Unlike carcinoid tumors, however, liver metastases are not a prerequisite for the clinical syndrome.]
