Fiser Absite. Ch 33 The Pancreas

Front 1

In regards to the dorsal and ventral buds that become the pancreas, what does the ventral bud give rise to?

Back 1

The uncinate and a portion of the head of the pancreas.

Front 2

What are the two embryologic ducts of the pancreas, and what are their ultimate forms?

Back 2

The main duct (duct of Wirsung) is made by the fusion of the ventral bud duct and the distal portion of the dorsal bud duct. This drains into the common bile duct.

The accessory duct (duct of Santorini) derives itself from the proximal portion of the dorsal bud duct and empties via the minor papilla.

Front 3

What vertebral level does the pancreas live?

Back 3

At the first and second lumbar vertebrae.

Front 4

Describe the uncinate process's position in regards to blood vessels?

Back 4

It lies posterior to the SMA and SMV, but ANTERIOR to the inferior vena cava and aorta.

Front 5

Where do the superior pancreatoicduodenal arteries arise from?

Back 5

Off the gastroduodenal artery that branches off the celiac trunk common hepatic artery.

Front 6

What arterial systems supply the body and tail of the pancreas?

Back 6

Branches of the splenic and left gastroepiploic arteries (the largest branches being the dorsal pancreatic and transverse pancreatic arteries)

Front 7

Where does the portal vein form in relation to the pancreas?

Back 7

Posterior to the neck, as the confluence of the splenic and superior mesenteric vein.

Front 8

What conditions are annular pancreas associated with?

Back 8

Down syndrome, intracardiac defects, or intestinal malrotation in kids.

Front 9

1. What is the overall architectural structure of the pancreatic islets?

2. How do regions of the pancreas vary in makeup?

Back 9

1. A core of Beta cells, and peripheral mantle composed of alpha, delta and pancreatic polypeptide cells.

2. The head is rich in PP cells, while alpha cells predominate the body and tail (beta and delta cells are evenly distributed throughout the pancreas).

Front 10

In regards to the exocrine pancreas, what cells are responsive for enzymatic production, and which for fluid composition?

Back 10

Acinar cells produce enzymes, while ductal cells make the fluid and electrolytes under vagal and humoral control.

Front 11

How do pancreatic digestive fluids alter in composition, depending on varying factors?

Back 11

At low secretory rates concentrations of chloride and bicarbonate equal plasma, but as rate increases (with neurohumoral stimulation) bicarbonate levels increase and chloride decreases (most potently stimulated by Secretin)

Both sodium and potassium concentrations remain the same, and reflect plasma.

Front 12

How does Secretin (the most potent stimulator of bicarbonate secretion) affect the pancreas (pathway)?

Back 12

Mucosal S cells in the proximal small bowel's Crypts of Lieberkuhn are released in the presence of luminal acid and bile, which goes into blood and binds selective receptors on ductal cells.

The increased bicarbonate neutralizes stomach acid that enters the duodenum.

Front 13

What does Lipase do, and how is it secreted from the pancreas?

Back 13

Cleaves fatty acids. Active.

Front 14

What does Trypsinogen​ do, and how is it secreted from the pancreas?

Back 14

A protease (active form trypsin) that activates OTHER digestive enzymes (chymotrypsin, elastase, carboxypeptidase, etc.).

It is secreted in the INACTIVE form, and activated by Enterokinase in the duodenum.

Front 15

What does Colipase​ do, and how is it secreted from the pancreas?

Back 15

Prevents lipase inactivation by bile acids in the duodenum. Active form.

Front 16

What does Cholesterol esterase​ do, and how is it secreted from the pancreas?

Back 16

Cleaves cholesterol ester bonds for cholesterol/FA absorption. Active form.

Front 17

What does amylase​ do, and how is it secreted from the pancreas?

Back 17

Cleaves complex carbs. Active form.

Front 18

What are the three major phases of pancreatic contribution to digestion?

Back 18

1. Cephalic: vagal efferent signal trigger enzyme-rich, bicarbonate-poor secretions

2. Gastric: antral distention, protein delivery triggers gastrin release, which weakly stimulates pancreatic enzyme secretion. Acidification of the duodenum cuases secretin release, which stimulates bicarbonate production/release.

3. Intestinal phase: CCK and Secretin continue to work together to stimulate release of enzymes

Front 19

What does the following cell type secrete? What are it's stimulators and inhibitors? Function?

Alpha cells.

Back 19

Release: Glucagon (glycogenolysis, gluconeogenesis, lipolysis, increased blood sugar)

Release Stimulants: hypoglycemia, arginine, alanine

Inhibitor: Hyperglycemia, insulin, somatostatin

Front 20

What does the following cell type secrete? What are it's stimulators and inhibitors? Function?

Beta cells.

Back 20

Release: Insulin (Protein synthesis and glucose uptake by cells)

Release Stimulants: Hyperglycemia, glucagon, CCK, GIP, choliergic stimulation, B-adrenergic input

Inhibitor: Somatostatin, amylin, panreatin, alpha adrendergic input

Front 21

What does the following cell type secrete? What are it's stimulators and inhibitors? Function?

Delta cells.

Back 21

Release: Somatostatin (inhibit acid production, pancreas/GB secretions, regulates pancreatic endocrine function)

Release Stimulants: Acid in duodenum

Inhibitor: None

Front 22

What does the following cell type secrete? What are it's stimulators and inhibitors? Function?

PP cells.

Back 22

Release: Pancreatic polypeptide (decreases GB, pancreatic secretions, inhibits food intake)

Release Stimulants: food, vagal stimulation, ghrelin

Inhibitor: Somatostatin

Front 23

What does the following cell type secrete? What are it's stimulators and inhibitors? Function?

Delta 2 cells.

Back 23

Release: Vasoactive Inhibitory Peptide aka VIP (Increases gut motility and secretions)

Release Stimulants: Fat in diet, acetylcholine

Inhibitor: Somatostatin

Front 24

What are physical manifestations of hemorrhage with pancreatitis?

Back 24

Turner's Sign: flank ecchymosis

Cullen's Sign: periumbilical ecchymosis

Fox's Sign: ecchymosis below inguinal ligament and/or involving scrotum

Front 25

What percentage of pancreatitis is caused by EtOH or stones?

Back 25

80-90%

Front 26

What percentage of symptomatic cholelithiasis patients will potentially develop pancreatitis?

Back 26

3-8%

Front 27

What autoimmune diseases are linked with pancreatitis?

Back 27

SLE, Sjogren's Syndrome

Front 28

What percentage of pancreatitis is idiopathic?

Back 28

10-15%

Front 29

What admission variables are included in Ransom's criteria?

Back 29

Age

WBC count

Glucose

LDH

AST

< 3 (1%), 3-4 (15%), 5-6 (50%), ≥ 7 (100%)

Front 30

What variables are included at 48 hours in Ransom's Criteria?

Back 30

Hematocrit decrease

BUN increase

Serum calcium

PaO2

Base deficit

Fluid requirement

< 3 (1%), 3-4 (15%), 5-6 (50%), ≥ 7 (100%)

Front 31

In gallstone pancreatitis what is the early recurrence rate if cholecystectomy is not performed?

Back 31

35%

Front 32

What are the major infection-related complications of pancreatitis that may require operation?

Back 32

Infected pseudocyst, necrosis or abscess

Front 33

What is the gene mutation in hereditary pancreatitis?

Back 33

In the cationic trypsinogen gene.

Front 34

What is a simple test to evaluate exocrine pancreatic function in the setting of chronic pancreatitis?

Back 34

Sudan stain of feces, or levels of fecal elastase.

Front 35

By what percentage would endogenous enzyme secretion in chronic pancreatitis have to be reduced to create malabsorption?

Back 35

90%

Front 36

What percentage of acute pancreatitis patients develop pseudocyts?

Back 36

Up to 10%

Front 37

What is the actual definition of a pancreatic pseudocyst?

Back 37

Collection of fluid containing pancreatic enzymes that persist beyond 4 weeks of onset of acute pancreatitis (if before that they are termed acute fluid collections).

Front 38

What percentage of patients see spontaneous resolution of pancreatic pseudocysts?

Back 38

Up to 60%. Pseudocyst size correlates with eventual need for surgery. Of those with lesions > 6 cm, 67% will need surgical intervention.

A trial of 6 weeks - 3 months is usually given before intervention is considered (allows wall to mature). Lesions < 5 cm most likely to resolve.

Surgery is USUALLY an internal drainage procedure (cyst jejunostomy or cyst gastrostomy).

Front 39

What are risk factors in development of pancreatic adenocarcinoma?

Back 39

Increasing age

being black

male

smoking (NUMBER ONE RISK FACTOR!!!!)

HNPCC / FAP / Peutz-Jahger Syndrome

ataxia-telangiectasia syndrome

BRCA2 mutation

FAMM (familial atypical multiple mole melanoma syndrome)

hereditary pancreatitis

chronic pancreatitis

cystic fibrosis

exogenous estrogen intake

pernicious anemia

high meat and fat in diet.

Front 40

Beyond Virchow's nodes (left supraclavicular), Sister Mary Joseph's nodes (periumbilical), what is the name of metastatic lymph nodes found in drop metastases in the pelvis (palpable on rectal exam)?

All indicative of intra-abdominal metastases.

Back 40

Blumer Shelf nodes

Front 41

Of the pancreatic endocrine tumors, which are almost always malignant?

Back 41

Glucagonomas, somatostatinomas. Insulinomas are rarely malignant (85-95% benign)

Front 42

If someone is diagnosed with a pancreatic endocrine tumor, what other work up is required?

Back 42

Serum calcium (concerning for MEN syndrome).

Gastrinomas (25%), Insulinomas (10%) are most commonly associated with MEN syndrome.

Front 43

What are common presenting symptoms, and diagnostic modalities for the following pancreatic endocrine tumor? Where are they most commonly found?

- Insulinoma

Back 43

Symptoms: Whipple's Triad (hypoglycemia while exercising/fasting, plasma glucose level lower than 50 mg/dL, resolution of symptoms with administration of IV glucose).

Diagnosis: Closely monitored fasting exam measuring glucose and insulin levels. EUS is the most sensitive study to locate the insulinoma. Can also perform portal venous sampling (usually for when operation has failed to ID and remove the tumor)

Octreotide scans miss ≥ 40% (BAD TEST).

Location: evenly distributed

Treatment: enucleation if < 2 cm, resection if > 2 cm

Front 44

What is a radiographic sign of an annular pancreas?

Back 44

Double bubble sign (distended stomach, pylorus, and distended early portion of duodenum).

Usually the second portion of the duodenum is trapped. Treatment includes a duodenojejunostomy or duodenoduodenostomy and sphincteroplasty. PANCREAS IS NOT RESECTED.

Front 45

Describe Tropical Pancreatitis.

Back 45

Type of chronic pancreatitis, found in young patients. Associated with SPINK1 mutation, and ingestion of casava root.

Front 46

What is the defective mutation in Hereditary Pancreatitis? What is their overall risk of developing pancreatic cancer?

Back 46

AD mutation in Trypsinogen gene (PR551), that presents in childhood and causes progressive decrease in pancreatic function.

Roughly 40% cancer risk.

Front 47

What are primary treatments for a pancreatic fistula?

Back 47

TPN, allow drainage and Octreotide. If those fail can perform ERCP, sphincterotomy and stent placement (decreases flow resistance into the duodenum).

Front 48

What is a common ERCP finding in patients with chronic pancreatitis?

Back 48

Chain of lakes.

Front 49

What is the most common cause of splenic vein thrombosis?

Back 49

Chronic pancreatitis. This leads to Sinistral HTN (gastric varices without esophageal involvement). Treat with splenectomy.

Front 50

What percentage of pancreatic endocrine tumors are nonfunctional? What percentage of those are malignant? Most common medical treatment?

Back 50

1. Thirty percent.

2. Ninety percent.

3. 5-FU, Streptozocin

Front 51

What are common presenting symptoms, and diagnostic modalities for the following pancreatic endocrine tumor? Where are they most commonly found?

- Gastrinoma (Zollinger-Ellison Syndrome). Roughly 50% are multiple, roughly 50% malignant.

Back 51

Symptoms: persistent reflux despite medical treatment, reflux associated with diarrhea.

Diagnosis: Elevated gastrin (> 1000, not extremely reliable), Secretin stimulation test (Gastrin levels increase with administration of Secretin). Somatostatin receptor scintigraphy (aka Octreotide scan) single best study to localize tumor or mets.

Location: Gastrinoma triangle (most likely to be extra-pancreatic).

Treatment: Enucleation if < 2 cm, formal resection if > 2 cm.

Front 52

What are common presenting symptoms, and diagnostic modalities for the following pancreatic endocrine tumor? Where are they most commonly found?

- Somatostatinoma

Back 52

Symptoms: diabetes, gallstones, steatorrhea, hypochlorhydria

Diagnosis: fasting somatostatin levels

Location: Pancreatic head

Treatment: E

Front 53

What are common presenting symptoms, and diagnostic modalities for the following pancreatic endocrine tumor? Where are they most commonly found?

- Glucagonoma

Back 53

Symptoms: Diabetes, stomatitis (inflammation of oral mucus membranes), dermatitis (necrolytic migratory erythema)

Diagnosis: Fasting glucagon levels

Location: Distal pancreas

Treatment: Zinc, amino acids, or fatty acids can treat skin manifestations.

Front 54

What are common presenting symptoms, and diagnostic modalities for the following pancreatic endocrine tumor? Where are they most commonly found?

- VIPoma (Verner-Morrison Syndrome)

Back 54

Symptoms: Watery diarrhea, hypokalemia, achlorhydria (WDHA).

Diagnosis: R/O other lesions, elevated VIP levels.

Location: Tail

Treatment: Treat with octreotide.