Pancreas Flashcards
RUSH–Pancreas
Which of the following vascular relationships is not an important consideration during resection of the head of the pancreas?
A. Arterial supply of the pancreatic head from the splenic artery
B. Confluence of the splenic vein and SMV dorsal to the pancreatic neck
C. Absence of ventral portal vein branches doral to the pancreatic neck
D. Origin of the R hepatic artery from the SMA
E. Origin of the middle colic artery from the SMA
A
Arterial supply to the head of the gland is derived from both from the GDA and SMA via the anterior and posterior pancreaticoduodenal arcades. For the most part, head of the pancrease and duodenum have a shared blood supply so they must be resected together. Techniques for duodenal sparing pancreatetcomy and pancreatic sparing duodenectomy in select circumstances
Body and tail of pancreas receive blood supply from multiple brances of splenic artery, which also connect with superior mesenteric sources.
Variations in major arteries such as origin of R hepatic artery from SMA and origin of middle colic artery from SMA or dorsal pancreatic artery pleave these vessels in close proximity to head and neck of pancreas, where they are subject to injury during pancreatectomy
Junction of splenic vein and SMV to from the portal vein lies behind the neck of the pancreas. Usually these vessel do not have large anterior tributaries in this area.
RUSH–Pancreas
Endoscopy demonstrates a 1 cm submucosal nodule with central umbilication in the second portion of the duodenum. This finding is usually associated with which of the following?
A. Peptic ulceration B. Increased risk for pancreatic cancer C. Islet cell hyperplasia D. Absence of symptoms E. Intussuscption
D
Heterotopic pancreas is pancreatic tissue located at sites other than the normal location of the gland. Ectopic pancreatic tissue has been described at many anatomic locations but is typically found in the stomach, duodenum or Meckel’s diverticulum.
Theories of origin include metaplasia and transplantation. Histologic findings range from rudimentary structure to a fully formed gland. Most heterotopic rests contain ducts and both endocine and exocrine elements may be present.
Not uncommon, in 1-2% of autopsies. Usually asymptomatic. When symptoms occurs, they are related to location of the ectopic site and include obstruction (as a results of intussusception), ulceration, and bleeding. Malignancy has been reported, there is no evidence that heterotopic pancreatic tissue is predisposed to cancer.
Typical gross appearance is submucosal nodule, often with central umbilication. Resection is indicated for symptomatic lesions and is appropriate diagnostically for incidental lesions discovered during operations for other reasons
RUSH–Pancreas
The embryologic ventral pancreas forms which area of the fully developed gland?
A. Superior head B. Uncinate process C. Neck D. Body E. None of the above
B
Pancreas is forms from two outpouching of the primitive gut. Dorsal pancreas originates from the duodenum and ventral pancreas begins as a bud from the hepatic diverticulum, which itself is an outpouching of the duodenum. Other outgrowths from the hepatic diverticulum mature into the liver, gallbladder and bile ducts.
During normal fetal development, ventral pancreas rotates along with the primitive gut and fuses with the dorsal component. Ventral pancreas constitutes the uncinate process and the inferior portion of the head of the gland in the fully developed state. The dorsal pancreas forms the remainder of the gland.
Abnormalities in this development process result in recognized congenital anomalies that can be clinically important.
RUSH–Pancreas
The uncinate process of the pancreas is adjacent and dorsal to which of the following?
A. Splenic vein B. IVC C. SMA D. Left renal vein E. 4th portion of the duodenum
C
Pancreas divided into head, uncinate, neck, body and tail.
Uncinate process is the portion of the gland that extends to the left, dorsal to the portal vein and SMA. It lies ventral to the aorta and IVC. Located caudad and ventral to the L renal vein and cephalad to the 4th part of the duodenum.
Blood supply of uncinate is derived from numerous short branches of the SMA and portal vein. When performing a Whipple, these branches must be controlled to prevent bleeding and avoid injury to the SMA and portal vein
RUSH–Pancreas
What is the recommended treatment of duodenal obstruction caused by annular pancreas?
A. Endoscopic division of the associated duodenal web
B. Gastrojejunostomy
C. Duodenoduodenostomy
D. Surgical division of the annular tissue
E. Pancreaticoduodenectomy
C
Annular pancreas is a congenital anomaly involving a band of pancreatic tissue encircling the 2nd portion of the duodenum. Appears to originate from the embryologic ventral pancreas. Causal theories include abnormal fixation of the ventral pancreatic primordium before gut rotation, failure of involution of part of the ventral pancreas, and the development of heterotopic pancreatic tissue in the duodenum.
1/2 of these cases are dx in infants and the remainder in adults, with a peak during 4th decade of life. Most patients are asymptomatic. Clinical findings are obstruction in infants & children and obstruction, ulceration, or pancreatitis in adults. Associated anomalies include duodenal stenosis or atresia and Down’s syndrome.
Tx of symptomatic patients consists of surgical bypass by duodenoduodenostomy or duodenojejunostomy. Gastrojejunostomy can also alleviate obstruction but risks marginal ulceration.
Resection or division of the annular band is not advised because it risks the develop of a pancreaticfistula and may fail to relieve the obstruction
RUSH–Pancreas
Which of the following developmental anomalies best characterizes pancreas divisim?
A. Aplasia of the dorsal pancreatic anlage
B. Aplasia of the ventral pancreatic anlage
C. Incomplete rotation of the ventral pancreatic anlage
D. Failed fusion of the ventral and dorsal pancreatic parenchyma
E. Failed fusion of the ventral and dorsal pancreatic ducts
D
Pancreatic division refers to congenital variation of the pancreatic ducts that result from failed or incomplete fusion of the embryologic ventral and dorsal ductal systems.
There may be complete separation of the ducts, an absent or minimal ventral duct, or only a few meagre connections between systems. As a consequence, most of the pancreatic duct drainage is through the dorsal duct joining the duodenum at the minor papilla. Any existing ventral ducts (Wirsung) drain only the uncinate process and the caudal head of the gland rather than the bulk of the gland at the major papilla, as when normally developed.
Some variation of pancreatic divism is present in 10% of the population. In some individuals, it is clinically significant if the relatively stenotic mior papilla imposes an obstruction to ductal flow. This can potentiall reuslt in recurrent abdominal pain, acute pancreatitis or chronic pancreatitis.
RUSH–Pancreas
The diagnosis of pancreas divisim is usually made by which of the following?
A. Laparoscopic exploration B. Endoscopic U/S C. CT D. ERCP E. Genetic testing
D
Dx of pancreas divisim is usually made by ERCP and cannulation of the minor papilla may be required to image the dorsal duct.
MRCP might also demonstrate this ductal anatomy.
RUSH–Pancreas
Which of the following is appropriate treatment of a patient with pancreas divism, chronic abdominal pain, a dilated dorsal pancreatic duct and an enlarged calcified pancreatic head?
A. Pancreaticoduodenectomy B. Endoscopic dorsal sphincterotomy C. Operative dorsal sphincterotomy D. Endoscopic or operative ventral sphincterotomy E. Sphlanchnic nerve ablation
A
Vast majority of patients with pancreatic divism are asymptomatic. Symptomatic patients with pancreas divism require evaluation of nature of their symptoms and for any other causes of abdo pain or pancreatitis.
WHen it is reasonable to suspect that a stenotic lesser papilla is the cause of recurrent abdo pain or pancreatitis, therapeutic considerations include endoscopic treatments (dilation, stenting, sphinterotomy) or operative sphincterotomy/sphincteroplasty, which may be combind with cholecystectomy and sphincteroplasty of major papilla
Occasionally, there are patients with established findings of chronic pancreatitis and pancreas divism. Sphincter operations are not successful in this setting. Rather, surgical treatment involving resection or decompression of the pancreatic head may be indicated
RUSH–Pancreas
Which of the following is not characteristic of pancreatic acinar cells?
A. Zymogen granules B. Carbonic anhydrase C. Golgi apparatus D. Rough endoplasmic reticulum E. Contractile proteins
B
Twofold function of the exocrine pancreas–secrete bicarbonate rich fluid and to synthesize digestive enzymes.
Acinar cells, which elaborate and secrete digestive enzymes, are designed for protein synthesis. Contain abundant RER, Golgi apparatus and secretory zymogen granules. Contractile proteins are also abundant near the apical membrane of the cell and facilitate exocytosis of the enzyme bundles into the ductal lumen.
The centroacinar cells are part of the ductal system. They secrete bicarbonate and therefore contain carbonic anhydrase, which dissociates carbonic acid into bicarbonate and hydrogen ion. Some ductal cells also contain synthetic and secretory organelles for the production of mucoproteins
RUSH–Pancreas
The bicarbonate concentration of pancreatic secretions is:
A. Primarily increased by CCK
B. Primarily decreased by secretin
C. Independent of acinar cell secretion
D. Reciprocally related to the chloride concentration
E. Reciprocally related to the sodium concentration
D
The centroacinar cells secrete a bicarbonate rich solution by an active transport mechanism primarily in response to secretin. CCK is the primary stimulatn in enzume secretion from the acinar cells.
The bicarbonate and chloride contents of pancreatic juice are reciprocally related. As ductal flow rates increase, the bicarbonate concentration increases and the chloride concentration decreases. This is the result of two processes: 1) changes in passive exchange of intraductal bicarbonate for intracellular chloride and 2) changes in the relative contribution of acinar cell secretion. Acinar cells secrete fluid high in chloride in addition to digestive enzymes. In contradistinction to anion concentrations, the concentration of sodium and potassium in pancreatic duct secretions remain relatively constant despite the flow rate and are similar to their concentrations in plasma
RUSH–Pancreas
Normally, activation of pancreatic trysinogen involves which of the following?
A. Pancreatic amylase B. pH greater than 7.0 C. Lysosomal hydrolase D. Pancreatic enterokinase E. Duodenal enterokinase
E
Pancreatic acinar cells secrete digestive enzymes for fats, carbohydrates and proteins. Except amylase, these enzymes are secreted in inactive forms to protect the pancreas from autodigestion. Activation of the proenzymes trypsinogen to trypsin is the primary event that leads to activation of the other various proteases and phospholipases. It occurs in the duodenum via the action of enterokinase. Trypsinogen activation can also occur in acidic environments (pH <7.0). With acute pancreatitis, intranglandular activation can take place when the inactive enzymes are exposed to lysosomal hydrolases
RUSH–Pancreas
Which pancreatic islet cell type produce a hormonal peptide to stimulate glycogenolysis and gluconeogenesis?
A. Alpha cell B. Beta cell C. Delta cell D. F cell E. PP cell
A
Endocrine pancreas is composed of various cells located in the islets of Langerhans, approx 1 million of which are interspersed with the acinar and ductal elements throughout the gland.
Primary function of the endocrine pancreas is to regulate glucose homeostasis. Beta cells, which are the most numerous, produce insulin. Insulin promotes glucose transport, stimulates protein synthesis, and inhibits glycogenolysis and lipolysis. Alpha cells secrete glucagon which counterbalances insulin by stimulating hepatic glycogenolysis, guloconeogenesis, ketogenesis, and lipolysis. Glucagon also inhibits intestinal mobility and gastric acid and pancreatic exocrine secretion.
Pancreatic delta cells secrete which inhibitory peptide?
A. Bombesin B. Glucagon C. Somatostatin D. Insulin E. Pancreatic polypeptide
C
Somatostatin produced by delta cells, has a broad range of inhibitory effects on the GI tract including inhibition of secretion of other pancreatitic peptides; inhibition of gastric, biliary, intestinal, and pancreatic exocrine secretions; and inhibitions of GI motility.
PP cells are the source of pancreatic polypeptides. Pancreatic polypeptide inhibits pancreatic exocrine secretion and biliary and gut motility. Clinically, deficiency of pancreatic polypeptide has been linked to diabetes following resection of the pancreatic head or chronic pancreatitis. Because postprandial secretion of pancreatic polypeptide is dependent on vagal innervation, it has been used to assess the completeness of vagotomy
RUSH–Pancreas
Which is the principal cell type located at the center of the islets of Langerhans?
A. Alpha cell B. Beta cell C. Delta cell D. F cell E. Varies according to the location of the islet in the pancreas
B
Each islet of Langerhans is composed of an average of 3000 cells. Beta cells are located at the core and make up about 70% of the islet. The other cell types are located at the periphery of the islet. The cellular anatomy has potential functional implications that are as yet not well understood.
The distribution of cell types within the islet varies in different areas of the gland. Islets in the uncinate process derived from the embryologic ventral pancreas contain PP cells but few alpha cells. Islets in the body and tail of the gland have abundant alpha cells but no PP cells.
RUSH–Pancreas
Which of the following statements is true regarding blood flow to the pancreas?
A. Islet cells receive a greater proportion of pancreatic blood flow than do the exocrine elements
B. CCK and secretin regulate secretion by altering blood flow
C. Fragile anastomotic networks predispose the gland to ischemia
D. The blood supply to the islet cells is independent of the acinar supply
E. Pancreatic blood flow is highly sensitive to changes in systemic blood flow
A
Microcirculation of the pancreas is complex and has important correlated with endocrine and exocrine functions of the gland. Rich anastomotic supply from various sources makes pancreatic ischemia unusual
The islets receive is disproportionately large amount of total pancreatic blood flow (10-25%) relative to their mass (1-2%). Both the islets and exocrine tissues have arteriolar blood supply. The acinar tissue is also perfused by blood that drains from the islets, a mechanism referred to as the islet-acinar or insuloacinar portal system. This system is the structural basis for endocrine regulation of exocrine function. Insulin receptors are present on acinar cells, and the density of receptors is highest on acini located near the islets. Because the islets themselves often have a central to peripheral pattern of perfusion, insulin from the centrally located beta cells can influence the other peripheral islet cell types. In addition, some islets are apparently perfused in a peripheral to central pattern.
CCK and secretin have relatively little effect on blood flow and thus exert their stimulatory effects independently.
Pancreatic blood flow is maintained relatively constant despite changes in arterial pressure.
RUSH–Pancreas
Which of the following events occurs in acinar cells with acute pancreatitis?
A. Accelerated extrusion of zymogen granules
B. Impaired syntehsis of zymogen granules
C. Fusion of lysosomes and zymogen granules
D. Fusion of mitochondria and zymogen granules
E. Impaired protein synthesis
C
Pathogenesis of pancreatitis involves intra pancreatic activation of digestive enzymes that are normally secreted in inactive form. This results in “autodigestion” of the gland.
Although the mechanism by which the various causes of clinical pancreatitis lead to this state are incompletely understood, experimental observations have identified certain derangements in acinar cell biology that may be the underlying common pathway to pancreatic injury. The primary defects involve blocked extrusion of zymogen granules containing inactive digestive enzymes and alterations in intracellular transport that result in fusion of zymogen granules with lysosomes to form large cytoplasmic vacuoles. This sequence results in co-localization of digestive enzymes and lysosomal hydrolases. Lysosomal enzymes, such as cathepsin B, activate trypsinogen and initiate a cascade of intracellular digestive enzyme activation.
Amino acid uptake and protein synthesis are not impaired during this process.
RUSH–Pancreas
The mechanism of alcohol induced acute pancreatitis is thought to involve all of the following except:
A. Pancreatic ductal obstruction B. Pancreatic exocrine hypersecretion C. Hypertriglyceridemia D. Acetaldehyde toxicity E. Genetic defect in lysosomal membranes
E
EtOH is the prevalent etiologic factor in acute pancreatitis. Several contributory mechanisms by which EtOH induced pancreatic injury occurs. EtOh causes pancreatic ductal HTN by increasing ampullary resistance and by intraductal deposition of stone proteins. Concomitantly, it stimulates gastric acid secretion and increases pancreatic exocrine secretion via release of secretin. The combination of ductal obstruction with stimulated secretion may result in enzyme extravasation.
Acetaldehyde, the metabolic product of ethanol, injures acinar cells by increasing membrane permeability and disrupting the microtubular structure.
The elevated levels of serum triglycerides induced by alcohol are a source of cytotoxic free fatty acids.
Alcohol also impairs normal trypsin inhibition and reduces pancreatic blood flow.
All of these effects may contribute to intraglandular enzyme activation and development of alcholic pancreatitis
RUSH–Pancreas
Hyperamylasemia is diagnostic of acute pancreatitis when associated with which of the following lab findings?
A. Hyperlipasemia B. Increased urinary amylase levels C. Amylase-creatnine clearance ration (ACCR) >5% D. Hypocalcemia E. None of the above
E
The dx of acute pancreatitis is based on signs and symptoms, supported by biochemical findings and morphologic abnormalities seen on imaging studies such as CT
No biochemical feature is pathognomonic of acute pancreatitis. Hyperamylasemia, hyperlipasemia and elevations in urinary-amylase levels and the ACCR are typical of acute pancreatitis but are not specific or sensitive, and they can occur with other abdmoinal and extra-abdominal disorders. There is no absolute level of serum amylase or lipase that is diagnostic of acute pancreatitis. Marked elevations are more indicative of pancreatitis but not themselves diagnostic. Both amylase and lipase levels may be elevated in a number of conditions that can be confused with acute pancreatitis, such as cholecystitis, perforated peptic ulcer, and intestinal infarction. Moreover, severe pancreatitis can occur without substantial elevations in these serum enzymes
Hypocalcemia may occur as a consequence of pancreatitis but it is also non specific
RUSH–Pancreas
A patient with abdo pain is found to have a serum amylase of 1200 IU/L, a normal urinary amylase level, and an ACCR of <2%. Based on these findings, the probably diagnosis is which of the following conditions?
A. Acute pancreatitis B. Chronic pancreatitis C. Renal failure D. Choledocholithiasis without pancreatitis E. Macroamylasemia
E
Elevations of serum and urinary amlyase levels and in the ACCR are typical of acute pancreatitis.
Elevation of amylase-creatnine ratio above normal 2-5% is not specific for pancreatitis, but a normal ratio in the presence of hyperanlyasemia suggests that hyperamylasemia is the result of something other than pancreatitis.
Serum and urinary amylase levels and the ACCR may be normal in patients with chronic pancreatitis or elevated during an acute exacerbation.
Renal disease may be associated with low urinary amylase levels and an elevated ACCR. CBD stones may produce hyperamylasemia without true pancreatitis. Urinary amylase is elevated, although the ACCR may be normal. With macroamylasemia, amylase forms complexes with serum proteins too large for glomerular filtration. The serum amylase level is elevated but urinary amlyase levels and the ACCR are low. The dx can be confirmed by electrophoresis. Abdo pain has been reported in >1/2 of patients with macroamylasemia, although the biochemical abnormality is probably not etiologically related to the pain. Hyperamylasemia predominantly caused by salivary amylase may also be assoc with a low urinary amylase level and ACCR because the salivary isoenzyme is cleared more slowly by the kidneys than the pancreatic isoenzyme
RUSH–Pancreas
Which of the following is an unfavorable prognostic factor in patients with acute alcoholic pancreatitis?
A. Initial WBC >16
B. Elevated serum triglycerides during the initial 48 hrs
C. Serum amylase > 1200 on admission
D. Serum lipase more than 3x normal
E. Serum BUN elevated more than 2mg/dL during the initial 48 hrs
A
Ranson critera include 11 parameters determined at the time of admission or during the subsequent 48 hours
Patients with 3 or more criteria have more severe disease and are at increased risk for septic complicaions and death. Criteria reflect the patient’s underlying status, severity of retroperitoneal inflammatory process, and effects on renal and respiratory function. The Ranson criteria were originally developed for alcoholic pancreatitis and have been modified for gallstone pancreatitis. A rise in the serum BUN of more than 2 mg/dL is one of the 10 criteria for gallstone pancreatitis but the rise must be more than 5 mg/dL to meet the criteria for alcoholic pancreatitis.
RUSH–Pancreas
What is the leading cause of death from acute pancreatitis?
A. Hemorrhage B. Pseudocyst rupture C. Secondary pancreatic infection D. Biliary sepsis E. Renal failure
C.
Formerly, death from acute pancreatitis often occurred early in the course of the disease as a result of the acute effects of hypovolemia and inadequate resuscitation.
In the current era, about 80% of death are attributed to secondary pancreatic infection, which develops in ~10% of patients with acute pancreatitis. Fatal pancreatic sepsis typically progresses to multisystem organ failure, and deaths occur later in the course of the disease. To have an impact on this disease, therapeutic effects have therefore focused on the prevention and early diagnosis of pancreatic infection and on more effective methods of surgical therapy
RUSH–Pancreas
Which of the following complications of acute pancreatitis is associated with the highest mortality rate?
A. Peripancreatic abscess B. Infected pancreatic pseudocyst C. Infected pancreatic necrosis D. Sterile pancreatic necrosis E. Bile duct obstruction
C
Retroperitoneal infection is a serious, often fatal complication of acute pancreatitis.
Pancreatic abscess best describes a localized collection of drainable pus in or around the pancreas. Pancreatic abscess and infected pseudocyst can be treated effectively by external drainage and the anticipated mortality rate for each is 5%.
Pancreatic necrosis is a manifestation of severe pancreatitis. When accompanies by infection, it has been associated with a mortality rate that may exceed 40% which is higher than noninfected necrosis. Infected pancreatic necrosis is treated by operative debridement and open or closed retroperitoneal drainage. Patient with sterile necrosis may require operative intervention as well but are generally treated nonoperatively with intensive support as long as their condition permits
RUSH–Pancreas
A 45M is admitted with severe alcoholic pancreatitis. 40% pancreatic necrosis is estimated on CT .Which of the following statements best describes the current use of antibiotics for this patient?
A. Systemic Abx are not indicated unless his condition deteriorates
B. Systemic Abx are indicated for coverage of gut derived bacteria
C. Systemic Abx are indicated for coverage of gut derived bacteria and fungal organisms
D. Nonabsorbable Abx are indicated for gut decontamination
E. Systemic Abx are not indicated if enteric feeding can be tolerated
B
Risk for infected pancreatic necrosis is related to the clinical severity and duration of disease and to the extent of necrosis. Strategies to decr secondary pancreatic infection focus on patients at higher risk. RCTs of systemic Abx for ppx against secondary infection have yielded conflicting results. Differences are probably b/c of numerous factors, including heterogeneity in the severity of disease, patient characteristics, and concomitant therapy among those studied as well as methodologies.
Current practice favors systemic Abx for patients with severe disease and more extensive (>30%) necrosis based on studies demonstrating fewer septic complications and perhaps decreased mortality. However, not all studies have shown benefit, and the risk for subsequent infection with multiresistant bacteria or fungal organisms may be increased, particularly if ppx abx use is prolonged. B/x the gut is typically the source of the organisms, the use of nonabsorbable enteral abx for selective gut decontamination has some appeal. The effect of this measure remains unclear, and is not typically used. Enteric feeding are beneficial to maintain the gut mucosal barrier to bacterial translocation. However, the efficacy of enteric feeding alone for prevention of secondary pancreatic infection has not been demonstrated
