PANCREAS Flashcards

1
Q

The time course of amylase levels with pancreatitis

A

Amylase levels rise within several hours after onset of symptoms

remain elevated for 3 to 5 days during uncomplicated episodes of mild acute pancreatitis.

Because of the short serum half-life of amylase (10 hours), levels can normalize as soon as 24 hours after disease onset.

The magnitude of the increases in amylase or lipase concentrations has no correlation with the severity of pancreatitis. he is in

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2
Q

Serum lipase concentrations with pancreatitis

A

increase with kinetics similar to those of amylase.

Lipase has a longer serum half-life than amylase,

may be useful for diagnosing acute pancreatitis late in the course of an episode (at which time serum amylase concentrations may have already normalized).

Although lipase is more specific than amylase in the diagnosis of acute pancreatitis, lipase is produced at a range of nonpancreatic sites, including the intestine, liver, biliary tract, stomach, and tongue.

The magnitude of the increases in amylase or lipase concentrations has no correlation with the severity of pancreatitis.

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3
Q

why does Orally administered glucose has a greater effect on insulin secretion than an equivalent amount of glucose administered intravenously

A

This effect is called the enteroinsular axis

related to the release of enteric hormones in response to glucose that also potentiate insulin secretion.

Gastric inhibitory polypeptide (GIP) is an important regulator of this effect.

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4
Q

Additional gut peptides and hormones that stimulate insulin secretion include

A

glucagon, glucagonlike peptide-1, and cholecystokinin (CCK), while somatostatin, amylin, and pancreastatin inhibit insulin secretion.

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5
Q

Compare her mortality rate is with chronic pancreatitis general population

A

“Patients with chronic pancreatitis have a decreased survival compared with the general population; most patients die of cirrhosis, diabetic complications, or aerodigestive cancers”

chronic pancreatitis have an excess mortality of 36% over 20 years compared with the general population.

A minority of patients with chronic pancreatitis die secondary to their disease.

The primary causes of death in this population may be attributed to associated:
tobacco and alcohol use and their sequelae, including aerodigestive cancers and cirrhosis.

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6
Q

indications for pancreatic duodenectomy for chronic pancreatitis

A

Pancreatoduodenectomy may be used to treat:
disease confined to the head of the pancreas that is not amenable to a drainage procedure.

when associated with:
biliary obstruction,
duodenal obstruction,
pseudocysts located in the pancreatic head,
poorly drained head and uncinate process after a longitudinal pancreaticojejunostomy.

considered in:
all patients with disease in the head of the pancreas when malignancy cannot be definitively ruled out.

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7
Q

is there association with chronic pancreatitis and developing pancreatic cancer?

A

chronic pancreatitis carries a 4% risk of pancreatic cancer over 20 years.

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8
Q

blood supply of the pancreas

A

The pancreas blood supply
both the celiac axis and superior mesenteric artery.

celiac axis:
splenic artery posterior pancreatic body and tail

head of the pancreas, from the splenic artery form collaterals with the inferior pancreaticoduodenal arcades.

gastroduodenal artery (is first branch off the common hepatic artery):
superior pancreaticoduodenal artery 
(divides into anterior and posterior branches)

supplying both the duodenum and head of the pancreas.

superior mesenteric artery:
inferior pancreaticoduodenal artery
(anterior and posterior branches)

supplying both the duodenum and head of the pancreas.

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9
Q

Variations or anomalies in the pancreatic and biliary blood supply

A

20% to 30%

The most common anomaly is a replaced right hepatic artery arising from the superior mesenteric artery in approximately 20% of people.

In the case of a replaced right hepatic artery arising from the superior mesenteric artery, the GDA arises from this replaced vessel and enters the pancreas posterior to the bile duct.

replaced right hepatic artery courses to the liver LATERAL (instead of normal medial position) to the bile duct – can easily be injured during dissection of the pancreatic uncinate process off of the superior mesenteric vessels.

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10
Q

large named vessel taken during Whipple

A

The GDA is the largest named artery taken during pancreaticoduodenectomy.

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11
Q

The most common neoplasms of the exocrine pancreas are

A

ductal adenocarcinomas.

Cystic neoplasms also arise from the exocrine pancreas. Cystic neoplasms are must less common than ductal adenocarcinomas, tend to occur in women, and are evenly distributed throughout the gland. Serous cystadenomas or microcystic adenomas are more common in women than in men. Most serous cystic neoplasms are benign, although malignant behavior has been rarely reported. Mucinous cystic neoplasms are also more common in women than in men. They can be divided into three types: (a) mucinous cystadenoma, (b) the intermediate or borderline tumor, and (c) mucinous cystadenocarcinoma. The prognosis for patients with resected, benign, or borderline tumors is excellent. Patients with mucinous cyst adenocarcinoma tend to do better than patients with ductal adenocarcinoma, with a 5-year survival of approximately 50%. Intraductal papillary mucinous neoplasms are soft villous tumors that are found in mucus-filled dilated pancreatic ducts. They show great degrees of cellular atypia. Intraductal papillary mucinous neoplasms appear to be more common in the head, neck, and uncinate process of the pancreas but can be found diffusely throughout the whole gland. These tumors may contain areas of invasive carcinoma and should be considered premalignant. Aggressive surgical resection is recommended if possible.

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12
Q

list most common locations of the pancreas or ductal cancer to develop

A

65% of the pancreatic ductal cancers arise in the head, neck, or uncinate process of the pancreas;

20% diffusely involve the whole gland

15% originate in the body or tail of the gland

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13
Q

Gastric acid is the primary stimulus for release of

A

secretin,

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14
Q

secretin

A

stimulates the secretion of pancreatic FLULID

water, electrolytes, and bicarbonate.

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15
Q

stimulus for the release of CCK

A

In response to the presence of long-chain fatty acids, some essential amino acids (methionine, valine, phenylalanine, and tryptophan), and gastric acid, the duodenum and jejunum release cholecystokinin (CCK).

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16
Q

CCK

A

stimulates ENZYME secretion from the pancreas.

also gallbladder contraction and sphincter of Odie relaxation

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17
Q

The presence of bile salts in the intestine also stimulates

A

pancreatic secretion, integrating the function of the pancreas, biliary tract, and small intestine.

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18
Q

Vagal (parasympathetic) afferent and efferent pathways and effects on the pancreas

A

Vagal (parasympathetic) afferent and efferent pathways

synergistically with CCK

stimulate pancreatic secretion.

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19
Q

secretion of enzyme-rich fluid is largely dependent on

A

secretion of enzyme-rich fluid is largely dependent on

on the vagal stimulation,

whereas fluid and electrolyte secretion are more dependent on the direct hormonal effects of the secretin and CCK.

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20
Q

vasoactive intestinal peptide (VIP) is released by what stimulus

A

Parasympathetic stimulation also causes the release of vasoactive intestinal peptide (VIP),

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21
Q

mechanism of vasoactive intestinal peptide

A

VIP

stimulate secretin secretion.

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22
Q

inhibitors of pancreatic secretion

A
somatostatin, 
pancreatic polypeptide, 
peptide YY, 
calcitonin gene-related peptides, 
neuropeptide Y, 
pancreastatin, 
enkephalin, 
glucagon,
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23
Q

The initial imaging technique used to localize a pancreatic endocrine neoplasm and stage the disease is

A

a high-quality spiral or multidetector three-dimensional CT scan.

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24
Q

The accuracy of CT in detecting primary pancreatic endocrine neoplasms

A

The accuracy of CT in detecting primary pancreatic endocrine neoplasms

varies widely from 35% to 85%,

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25
Q

Somatostatin receptor scintigraphy or octreotide scan

A

Somatostatin receptor scintigraphy or octreotide scan

sensitivity may be greater than 70%,

NOT for insulinoma
Nonfunctional tumors and insulinomas seem to be localized less frequently by somatostatin receptor scintigraphy than by CT scan or ultrasonography.

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26
Q

somatostatin receptor scintigraphy appears superior for diagnosing what pancreas and the tumor(s)

A

somatostatin receptor scintigraphy appears superior for

gastrinoma,

endoscopic ultrasonography has also shown utility in localizing pancreatic endocrine neoplasms.

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27
Q

endoscopic ultrasonography for pancreas endocrine tumors workup

A

endoscopic ultrasonography localization procedure in patients with

insulinoma
or
gastrinoma.

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28
Q

Selective transhepatic portal venous hormone sampling

A

may help in localizing the occult neoplasm.

This invasive test is designed to demonstrate an increase in hormone concentration at the site where its hormonal product drains into the portal system.

The overall accuracy of this test ranges from 70% to greater than 95% depending on the number of samples obtained, the persistence of autonomous hormone production by the tumor, and the careful handling and assaying of all specimens.

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29
Q

diagnosis of pancreatic cancer with Ultrasonography

A

CT scan first choice

ultrasound:
although operator dependent, can demonstrate dilated intrahepatic and extrahepatic bile ducts, liver metastasis, pancreatic masses, ascites, and enlarged pancreatic lymph nodes.

Ultrasonography will reveal a pancreatic mass in 60% to 70% of patients with pancreatic cancer.

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30
Q

diagnosis of pancreatic cancer with CT scan

A

CT scan just plain better

Helical or spiral CT is currently the preferred noninvasive imaging test for the diagnosis of pancreatic cancer.

just as sensitive as ultrasonography

provides more complete information about surrounding structures and the local and distant extent of the disease, ultrasonography has largely been replaced by CT.

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31
Q

diagnosis of pancreatic cancer with MRI

A

Magnetic resonance imaging

no significant advantage over CT because of the lower signal-to-noise ratio, motion artifacts, lack of bowel opacification, and low spacial resolution.

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32
Q

Patients with chronic pancreatitis, significant ductal dilatation, and minimal head involvement are candidates for ductal drainage procedures, with

A

longitudinal pancreaticojejunostomy being the procedure of choice.

Immediate pain relief can be achieved in more than 80% of patients, but pain may recur in 25% to 50% of patients over 5 years!

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33
Q

Active trypsin is formed from the proteolytically inactive trypsinogen by the action of enterokinase,where

A

a brush border enzyme in the duodenum.

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34
Q

Pepsin is inactivated at a pH level of

A

above 3.5.

pepsin is denatured at a pH level of 5.0.

MOST activated in acid - pepy chief

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35
Q

what is more accureate for dx of acute pancreatitis - amylase of lipase

A

It has been shown that serum lipase is a more accurate biomarker of acute pancreatitis than serum amylase, with 19% of patients with acute pancreatitis having normal serum amylase levels, but only 3% having normal serum lipase levels.

lipase, serum trypsinogen is made only by the pancreas and may serve as a better marker for acute pancreatitis.

.

36
Q

Several tests of pancreatic exocrine function require duodenal intubation:

A

the secretin test,

dimethadione test (DMO),

the Lundh test.

37
Q

greatest discrimination between normal subjects and patients with chronic pancreatitis during secretin stim test

A

The maximal bicarbonate concentration

38
Q

The fecal fat test measures

A

intraluminal digestion products and is used to distinguish between pancreatic dysfunction and malabsorption due to enteric disease.

Steatorrhea from pancreatic dysfunction is the result of lipase deficiency and is usually not present until lipase secretion is reduced by 90%.

Fecal fat content is measured over a 24-hour time period. If the fecal fat is elevated to more than 20 g, this indicates pancreatic insufficiency, whereas steatorrhea in the presence of low levels of fecal fat (<20 g) indicates intestinal dysfunction.

A reduction of fecal fat can be used to demonstrate adequate replacement of pancreatic enzymes in patients with endocrine insufficiency. However, this test is time consuming and disliked by patients, and pancreatic enzyme replacement is often titrated based on symptom relief once the diagnosis of pancreatic insufficiency is made.

39
Q

The centrally located insulin-producing cells or B cells (β) cells make up

A

50% to 70% of the islet population.

distributed evenly across the pancreas - (insulinomas thorughout panc)

40
Q

çThe glucagon-producing cells or A (α) cells make up approximately what percent - where are they

A

10%

of each islet are generally located at the periphery of each islet.

. Islets in the body and tail are rich in A

41
Q

somatostatin-producing cells where in panc and what cells

A

or D (δ) cells

Also located in the periphery of each islet are the (5%)

distributed evenly across the pancreas

42
Q

pancreatic polypeptide where in panc and what cells

A

and (PP)-secreting F (yep, really are the f cells) cells (15%).

uncinate are rich in F cells

43
Q

The main humoral factors include the hormones released from individual islet cell subtypes, including

A

insulin, glucagon, PP, and somatostatin.

44
Q

The principal stimulant for pancreatic water and electrolyte secretion is the hormone

A

secretin.

45
Q

secretin phys - where is it released, what cells, what stim, what action

A

Secretin is derived from mucosal S cells of the crypts of Lieberkühn of the proximal small bowel.

It is released into the blood in the presence of a duodenal luminal pH of less than 3.0 AND BILE

Secretin is the principal stimulant of pancreatic water and electrolyte secretion

46
Q

The WHO well-differentiated endocrine tumors are further subclassified as having predicted benign behavior or uncertain behavior. This subdivision (benign vs. uncertain) is based on

A

size (<2% or ≥2%), and absence or presence of perineural and vascular invasion.

The presence of biologically active hormones does not predict malignant behavior.

47
Q

Local factors that preclude pancreatoduodenal resection include

A

retroperitoneal extension of the tumor to involve the inferior vena cava or aorta

or

direct involvement or encasement of the
superior mesenteric artery,
superior mesenteric vein,
portal vein.

Although isolated focal involvement of the portal vein/superior mesenteric vein can be managed with venous resection, most patients with venous involvement have extension that involves the superior mesenteric artery, making isolated vein resection inappropriate.

48
Q

the largest source of post op comp after whipple

A

The pancreaticojejunostomy is the most problematic anastomosis in the reconstruction.

Traditionally, much of the morbidity and mortality associated with this operation was related to problems with this anastomosis. T

49
Q

advantage and disadvantage of pylorus preserving

A

reduce the incidence of troublesome postgastrectomy problems, including marginal ulceration.

he pylorus-preserving modification spares the antrum and pylorus

no survival benifit

50
Q

pancreatic endocrine neoplasms asso inherited familial syndromes such as

A

MEN-1,
VHL syndrome,
NF-1,
TSC.

MEN-1 is associated with gastrinoma,

while NF-1 is associated with somatostatinomas.

VHL and TSC are both associated with increased pancreatic endocrine neoplasms.

CAREFUL - not Peutz-Jeghers syndrome

51
Q

Ranson determined that a patient with three or more abnormal factors

A

has an increased risk both for infectious complications and for mortality.

52
Q

Gastric ileus resolves by at what time frame

A

six weeks postoperatively in nearly all patients. A response to metoclopramide is seen in only about 20% of patients, and relapse is common when the drug is stopped. Nasogastric suction is the traditional treatment, but addition of a prokinetic agent such as erythromycin should be considered. Erythromycin 150acts by binding to motilin receptors to stimulate intestinal smooth muscle contraction. The addition of a jejunal feeding tube at operation may allow enteral feeding to continue while recovery from gastric atony occurs.

53
Q

The bentiromide test measures

A

he excretion of para-aminobenzoic acid after administration of a precursor compound that requires chymotrypsin cleavage.

This test appears ONLY to be most sensitive in patients with severe chronic pancreatitis.

Endoscopic retrograde pancreatography is the current “gold standard” for diagnosis

54
Q

best test to dx chronic panc

A

Endoscopic retrograde pancreatography is the current “gold standard” for diagnosis, with high sensitivity and specificity. Importantly, endoscopic retrograde pancreatography allows the opportunity to distinguish chronic pancreatitis from periampullary cancer, provides important anatomy of the pancreatic duct that may aid in planning surgical treatment, and may include placement of pancreatic or biliary duct stents for treatment in specific cases.

Other imaging modalities that are being used more frequently include magnetic resonance pancreatography with secretin stimulation and endoscopic ultrasonography, both of which are less invasive than endoscopic retrograde pancreatography.

55
Q

Management of an insulinoma

A

is surgical in nearly all cases. Insulinomas are evenly distributed in the pancreas;

ninety percent of patients have a benign solitary adenoma amenable to surgical cure.

Small benign insulinomas not close to the pancreatic duct can be removed by means of enucleation, independent of location within the gland.

In the body and tail of the pancreas, insulinomas larger than 2 cm in diameter and those close to the pancreatic duct are most commonly excised by means of a distal pancreatectomy.

Large insulinomas deep in the head of pancreas or uncinate process of the pancreas may not be amenable to local excision and may necessitate pancreaticoduodenectomy.

56
Q

Secretin is found where

A

localized to specialized cells of the

duodenal

and

proximal jejunal
(S cells).

released by duodenal acidification or by contact with bile and perhaps fat. The primary role of secretin is to stimulate the release of water and bicarbonate from pancreatic ductal cells. This action facilitates the entry of pancreatic enzymes and provides a pH favorable for fat digestion. Secretin also acts to stimulate the flow of bile and to inhibit gastrin release, gastric acid secretion, and GI motility.

57
Q

Secretin released by

A

duodenal acidification

or

by contact with BILE

and perhaps fat.

58
Q

The primary role of secretin is to

A

stimulate the release of water and bicarbonate from pancreatic ductal cells.

This action facilitates the entry of pancreatic enzymes and provides a pH favorable for fat digestion.

Secretin also acts to stimulate the flow of bile and to inhibit gastrin release, gastric acid secretion, and GI motility.

CAREFUL: CCK cause GB CONTRACTION (that squirts bile) and responsible for release of enzymes

59
Q

head vs body / tail drainage in the pancreas.

A

head the superior venous arcades drain either directly into the suprapancreatic portal vein or laterally (even though head!) into the retropancreatic portal vein.

The anterior and inferior branches of the pancreaticoduodenal arcades of the pancreatic head drain directly into the infrapancreatic superior mesenteric vein.

The body and tail of the pancreas have many venous tributaries that drain into the splenic vein, which joins the superior mesenteric vein posterior to the pancreatic neck, forming the portal vein.

60
Q

The three named tributaries of the splenic vein are:

A

the inferior pancreatic vein,

the caudal pancreatic vein,

the great pancreatic vein.

The inferior mesenteric vein does not drain the pancreas, but joins the splenic vein posterior to the pancreatic body.

61
Q

Acinar cells

A

20 different digestive enzymes and enzyme precursors

All peptidases synthesized by acinar cells are released into the pancreatic ductal system in an inactive form.

Some enzymes (that are not peptidases) are secreted by acinar cells in their active form, including:

amylase AND lipase.

acinar cells also secrete a trypsin inhibitor, pancreatic secretory trypsin inhibitor, that protects the pancreas from trypsin that is prematurely activated within the pancreas.

62
Q

enterokinase

A

Duodenal mucosal serves to activate trypsinogen to the active enzyme trypsin, which further activates the other peptidases.

63
Q

. Approximately 20% of cases are classified as severe acute pancreatitis, defined as acute pancreatitis associated with one or more of the following:

A

(a) necrosis of greater than one third of the pancreas,
(b) distant organ failure (indicated by systolic blood pressure ≤90 mm Hg, serum creatinine >2.9 mg/dL, gastrointestinal blood loss >500 mL in volume within a 24-hour period, and/or partial pressure of oxygen in arterial blood ≤60 mm Hg), and/or
(c) the development of local complications, such as hemorrhage, abscess, or pseudocyst.

64
Q

The mortality rate associated with severe acute pancreatitis ranges from

A

10% to 20% in contemporary series.

Greenfield’s Surgery: Scientific Principles and Practice, 5th ed. Lippincott, Williams & Wilkins; 2011.

65
Q

Acute fluid collections develop in patients with acute pancreatitis what what percent and what is percent that go on to psudocyst

A

30% to 50%

in up to 10% of patients with acute pancreatitis, these fluid collections progress to develop a wall of fibrous granulation tissue, at which point they are classified as pseudocysts.

The walls of pseudocysts generally require at least 4 weeks from the onset of pancreatitis to develop. Pseudocysts are distinguished from true pancreatic cysts, which have epithelium-lined walls.

66
Q

The most common findings in the glucagonoma syndrome are

A

severe dermatitis, mild diabetes, stomatitis, anemia, and weight loss. T

67
Q

he diagnosis of glucagonoma

A

secured by documentation of high fasting levels of serum glucagon.

but is suggested by the clinical presentation of biopsy of the skin lesions

68
Q

Most glucagonomas are located

A

in the body and tail of the gland.

These tumors are typically large and bulky and surgical resection requires distal pancreatectomy.

69
Q

tx of metastatic glucagonoma

A

Metastases are found in most patients and safety bulking of these should be considered.

70
Q

stim release of CCK and what inhibits

A

Products of fat and protein digestion within the intestinal lumen initiate release of CCK.

intraluminal trypsin and bile acids inversely regulates CCK release.

In addition, CCK stimulates pancreatic bicarbonate secretion and insulin release from the pancreas. (CAREFUL consider SECRETIN the main stim for BICARB and CL release)

Conversely, CCK inhibits contraction of the lower esophageal sphincter (LES) and the sphincter of Oddi.

CCK has a trophic effect on the pancreas as well as CCK receptor—positive GI cancers.

71
Q

The main pancreatic duct

A

extends from the tail of the pancreas toward the head.

In the body of the pancreas, the main duct usually runs midway between the superior and inferior borders and closer to the posterior than to the anterior surface.

The main pancreatic duct normally measures 3 to 4.5 mm in diameter. After passing into the neck of the pancreas, the main pancreatic duct extends in a caudal and posterior direction before joining the distal bile duct at the ampulla.

72
Q

The accessory pancreatic duct usually drains

A

the anterior and superior portions of the pancreatic head through a minor papilla, which enters the duodenum approximately 2 cm proximal and slightly anterior to the ampulla of Vater.

The accessory duct is patent in approximately 70% of autopsy specimens and usually communicates with the main duct.

In 90% of the population, the main and accessory pancreatic ducts join near the junction of the head and neck of the pancreas.

73
Q

The incidence and mortality rates for pancreatic cancer in African Americans

A

higher than the rates for Caucasians. T

74
Q

he most consistently observed environmental risk factor for the development of pancreatic cancer is

A

cigarette smoking can increase the risk of pancreatic cancer between 1.5 and 5 times.

Alcohol consumption does not seem to be a risk factor for pancreatic cancer despite conflicting past reports..

75
Q

exposure to ionized radiation and risk of pancreas cancer

A

NONE

76
Q

most serious complication following pancreaticoduodenectomy,

A

Pancreatic fistula remains the with an incidence ranging from 5% to 15%.

In the past, the development of pancreatic fistula following pancreaticoduodenectomy was associated with mortality rates of 10% to 40%.

ahough the incidence of pancreatic fistula following pancreaticoduodenectomy remains stable, the overall associated mortality rate is diminished owing to improved management.

77
Q

Preoperative radiotherapy for locally advanced tumors.

A

may improve the resectability rate

THIS IS RADATION OF THE PANCREAS

Lillimoe KD: Current management of pancreatic carcinoma. Ann Surg 221:133-148, 1995

Tan HP, Smith J, Garberoglio CA: Pancreatic adenocarcinoma: An update. J Am Coll Surg 183:164-184, 1996
78
Q

Chemotherapy for pancrease cancer

A

NOT effective in the treatment of pancreatic adenocarcinoma.

Multidrug regimens are more toxic than fluorouracil (5-FU) and have not proven more effective than 5-FU alone. Newer agents are being investigated.

Lillimoe KD: Current management of pancreatic carcinoma. Ann Surg 221:133-148, 1995

Tan HP, Smith J, Garberoglio CA: Pancreatic adenocarcinoma: An update. J Am Coll Surg 183:164-184, 1996
79
Q

The pancreas is divided into five parts:

A

the head, uncinate, neck, body, and tail.

head lies adjacent to the second lumbar vertebra and is intimately attached to the C-loop of the duodenum. The distal CBD passes through the pancreatic head (Fig. 18.4B) [View Image], although in approximately 15% of people, the CBD lies in a groove on the posterior aspect of the pancreas. The uncinate process lies adjacent to the third and fourth portions of the duodenum and next to the superior mesenteric vein (SMV). The uncinate process also extends behind the SMV and portal vein to the right edge of the superior mesenteric artery.T

80
Q

The genes involved in the pathogenesis of pancreatic cancer

A

(a) tumor-suppressor genes, (b) oncogenes, and (c) DNA mismatch-repair genes.

Tumor-suppressor genes normally function to control cellular proliferation.

The function of p53 appears to be inactivated in up to 75% of all pancreatic cancers.

The p53 gene product is the DNA-binding protein that acts as a cell cycle checkpoint and an inducer of apoptosis.

The DPC4 is a tumor-suppressor gene that has been identified on chromosome 18q. The chromosome has been shown to be missing in approximately 90% of pancreatic cancers!

The DPC4 gene is inactive in approximately 50% of pancreatic carcinomas. DPC4 mutations are more specific than p53 or p16 mutations for pancreatic cancers.

Oncogenes are derived by normal cellular genes called proto-oncogenes. When expressed or activated by mutation, oncogenes code proteins with transforming properties.

Activating point mutations in the K-ras oncogene are the most common genetic alteration in pancreatic cancer. Mutations of K-ras have been found in 80% to 100% of pancreatic cancers and therefore may be useful in the development of a molecular screening test for pancreatic cancer.

Mismatch-repair genes function to ensure accuracy of DNA replication, and when these genes are mutated, errors in DNA replication are not repaired. Only 4% of pancreatic cancers can be characterized by disorders of DNA mismatch-repair genes.

81
Q

glucagon release is also influenced

A

i) effects on metabolism, including stimulation of glycogenolysis, gluconeogenesis, and ketogenesis in the liver, stimulation of lipolysis in adipose tissue, and stimulation of insulin secretion;
(ii) effects on gastrointestinal secretion, including inhibition of gastric acid and pancreatic exocrine secretion;
(iii) effects on intestinal motility, including inhibition of intestinal peristaltic activity; and (iv) effects on the cardiovascular system,

including increase in heart rate and the force of cardiac contraction!!

82
Q

pancreatic exocrine secretion is divided into three phases:

A

Like gastric acid secretion,

cephalic,

gastric,

intestinal

During the cephalic phase of digestion, stimuli activate vagal efferent signals, which follow parasympathetic pathways to stimulate pancreatic exocrine secretion and account for one fourth to one third of the maximal pancreatic response

stimulation of gastric acid secretion, both by direct cholinergic influence on parietal cells and through the release of antral gastrin, leads to duodenal acidification.

acidification releases secretin, which stimulates pancreatic bicarbonate secretion.

During the gastric phase of digestion, antral distention and the presence of protein in the antrum stimulate the release of gastrin.

Gastrin itself serves as a weak stimulator of pancreatic enzyme secretion because of the sequence homology between gastrin and the C-terminus pentapeptide-amide sequence of CCK.

In addition, gastric distension triggers pancreatic enzyme release through a vasovagal response. These two processes act primarily on the acinar cells themselves giving rise to an enzyme-rich secretion during the gastric phase (40).T

83
Q

he pancreas has a rich blood supply derived from

A

The pancreas has a rich blood supply derived from the gastroduodenal, superior mesenteric, and splenic arteries. The gastroduodenal artery terminates as the superior pancreaticoduodenal artery, which divides into an anterior and posterior branch. The first branch of the superior mesenteric artery is the inferior pancreaticoduodenal artery that divides into an anterior and posterior branch collateralizes with the superior arcade to supply the pancreatic head and duodenum (Fig. 18.5) [View Image]. The neck, body, and tail of the pancreas receive blood from the splenic artery as the dorsal pancreatic artery arising near the celiac trunk, the great pancreatic or pancreatic magna to the body, and the caudal pancreatic artery supplying the tail. These usually arise from the splenic artery and run within the substance of the gland.

84
Q

Obstructive jaundice if left untreated, it can result in

A

progressive liver dysfunction,
hepatic failure,
early death.

85
Q

Nonoperative palliation Obstructive jaundice

A

with endoscopic stenting

appropriate alternative for palliation in patients who do NOT undergo operation!

86
Q

If at the time of laparotomy the patient is found to be unresectable, wit obstructive jaundice and pancrease cancer - what is managment

A

we are surgeons..

hepaticojejunostomy can provide excellent long-term palliation with MINIMAL associated MORDITY and mortality.

Recent prospective randomized trials have confirmed that prophylactic gastrojejunostomy in patients with unresectable cancer can prevent the development of late gastric outlet obstruction and prevent the need for reoperation (EVEN if pt does not present with gastric outlet obstrucion)

Patients with unresectable cancer at the time of surgical exploration should receive a chemical splanchnicectomy with 20 mL of 50% alcohol injected into either side of the aorta at the level of the celiac axis.

87
Q

most common symptom of chronic pancreatits

A

Pain is the most common symptom of chronic pancreatitis, and it is often the most difficult symptom to manage in these patients. Patients with chronic pancreatitis often complain of epigastric pain that radiates to the back. Patients often report that leaning forward or lying prone may relieve that pain, which may be exacerbated in the supine position. Exocrine pancreatic insufficiency, which usually initially presents with fat malabsorption and steatorrhea, is a late symptom of chronic pancreatitis that occurs only after destruction of greater than 90% of the exocrine pancreas. Many patients with chronic pancreatitis have some degree of glucose intolerance, but diabetes mellitus develops in fewer than 60% of patients and is often a late symptom.