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Pancreas small group

2022
Jobs of the Pancreas
• Secrete bicarbonate (HCO3-):
• Neutralizes gastric acid entering duodenum
• Provides optimal pH for digestive enzymes
• Secrete digestive enzymes:
• Break down nutrients into small particles and absorbable small molecules
• Prevent autodigestion of pancreas by enzymes:
• Enzymes packaged intracellularly as zymogen granules
• Secreted as proenzymes->activated in gut lumen
• Trypsin Inhibitor
• High pH in the duct.
• Release hormones:
• Insulin, Glucagon, Somatostatin
Physiology Review
• Secretion of Pancreatic Enzymes • Secretion of Pancreatic Bicarb
• LCFA, proteins->CCK-RF • H+-> Duodenal S cells to secrete
• CCK-RF-> CCK from I cells (paracrine) secretin.
• CCK-stimulates vagal reflex loop- • Secretin->pancreas to secrete
release of enzymes from pancreas Bicarb via endocrine effect.
(hormone effect)
• CCK->Also causes gall bladder to
squeeze
• Note: Trypsin is activated in
duodenum by enterokinase. Trypsin
then activates other pro-enzymes
Case 1
CC: 54 yo presents to ER with vomiting and severe, constant, midepigastric pain

HPI: Sudden onset 8 hours ago, started in midepigastric area and has now radiated to her back. Eating worsens
the pain.

PMH: Gallstones diagnosed during episodes of RUQ pain 3 years ago – no intervention nor symptoms since
then.
SHx: baker, lives with her sister, no tobacco or EtOH
Meds: daily MVI
NKDA

PE: Distressed and reluctant to move, afeb, 120 bpm, 85/50


Abd: upper abd distension, guarding, tender
How would you acutely manage this patient?
 
Her vital signs are worrisome for impending shock. She needs an IV immediately
and close monitoring. We will get to why she is going into shock soon….
 
What is your differential diagnosis for her pain?
The most likely possibilities are acute pancreatitis, biliary colic (pain from bile
obstruction by a gallstone), and a perforated peptic ulcer. Her history of gallstones

Case 1 favor gallstone-related pancreatitis or biliary colic. However, with biliary colic the
onset of pain is usually more gradual, and the patient is typically restless rather than
reluctant to move. Furthermore, biliary colic does not put her at risk for shock,
unless she has infection in the biliary system that is now spreading into the
bloodstream. Perforated peptic ulcer is less likely in the absence of prior episodes of
peptic ulcer pain or prior GI bleeding, and in the absence of abdominal rigidity.

How does her longstanding pain differ from that of peptic ulcer disease?
It is aggravated by eating and unrelieved by antacids.
What initial tests would you order to evaluate your differential diagnosis?
Most patients who are resuscitated for shock would automatically have a CBC and a Chem 12 (also
called a Comprehensive Metabolic Profile – CMP) drawn. These would provide blood counts, the
Chem-7 (Basic MP), liver function tests (AST,ALT, ALK Phos, Bili), albumin, calcium. To look for
pancreatitis specifically, you would add lipase and amylase. Once the patient is stabilized, you would
order imaging to help create a clear picture of her disease process.

Her labs:
Hct = 40% (normal). WBC = 12 x 103 (high)
Amylase = 500 (normal 25-100)
Lipase = 750 (normal 10-140)
Case 1 Calcium = 7.0 (normal 8.5-10)

These elevations in Amylase and Lipase mean she has ACUTE PANCREATITIS. Her pancreatitis can be
from many things, including gallstones.

Based on your knowledge of pancreatic secretion, how would you propose to treat this patient?
Pancreatitis can be mild to life-threatening. Almost all pancreatitis will need IV hydration and pain
management. Most pancreatitis requires pancreatic rest and fasting of the intestinal system to
eliminate stimulation of pancreatic acinar secretion. A stimulated pancreas secretes about 2 liters
of fluid/day. A fasting pancreas produces about 300 ml of fluid/day. Nasogastric suction reduces
pancreatic secretion to about 75 ml a day and is sometimes used to help rest the pancreas.
Pancreatitis comes in many forms:
Causes of chronic pancreatitis include:
Acute (5% mortality!) • Alcohol (the most common cause)
• Hypertriglyceridemia
Chronic
• Genetic
Chronic with acute exacerbations • Autoimmune
• Recurrent/acute pancreatitis
• Obstruction (tumors, scars, stones, etc)
Causes of acute pancreatitis include: • Multiple etiologies
• Gallstones (the most common cause) ------------------------------------------------------------
• Alcohol
• Hypertriglyceridemia (high triglycerides that can happen as an Smoking greatly increases the risk of chronic
inherited disease or in association with obesity, diabetes, pancreatitis
hypothyroidism, pregnancy, and some medications)
• After an ERCP procedure Chronic pancreatitis increases the risk of
• Genetic causes pancreatic cancer
• Medications
• Trauma
 How would you explain the following phenomena which may occur during an attack of acute
pancreatitis?
 
Jaundice –
Gallstone or edema of pancreatic head obstructs common bile duct

Elevated serum amylase and/or lipase levels –


Inflammation or necrosis of pancreas leads to leakage of pancreatic enzymes into the peripancreatic fat
and retroperitoneal space which then get absorbed into the circulation

Case 1 Fluid in the abdomen –


Peripancreatic edema caused by the inflammation

Hypotension –
2 mechanisms: exudative edema in the peripancreatic spaces and systemic cytokine release

Radiation of pain to the back –


Inflammation of retroperitoneal space

A dilated, fluid-filled stomach seen on abdominal X-ray –


Reflex gastroparesis from peritoneal involvement + inflammation of the celiac plexus
 How would you explain the following phenomena which may occur during an attack of acute
pancreatitis (continued)?

Left pleural effusion –


Extension of inflammation from the tail of pancreas to the area under the diaphragm

Hyperglycemia –
Destruction of pancreatic islets with loss of insulin production

Hypocalcemia –
Precipitation of calcium as calcium-fatty acid soaps in the abdominal cavity and the tissues.
Case 1 Respiratory distress –
Cytokines + lysolecithins destroying alveolar surfactant fluid and stimulating pulmonary edema

A toxic course with fever during the first seven days -


Effects of released cytokines

Painful subcutaneous nodules –


Metastatic fat necrosis from released lipases

Fever, starting after 7 days –


Peripancreatic abscess
Anatomic relationships
Gastroduodenal Artery

Pancreas

Common
Bile Duct
Stomach

Splenic
Gallbladder Flexure

Duodenum Adrenal

Spleen

R. Renal Vein Aorta


Inf. Vena Cava
Sup. Mesenteric Artery
Sup. Mesenteric Vein
CT Scans of Normal Pancreas

CT scan of a normal pancreas at two levels. The dark, curved line running axially through the center of the
pancreas is the main pancreatic duct. Note the contrast-filled splenic artery coursing dorsal to the pancreas.
Case 1: CT Scans of Abdomen
Case 1
Normal

Right panel shows ill defined fluid collections and necrosis in and around the pancreas, characteristic of acute pancreatitis.
Peripancreatic inflammation may involve the duodenum, and/or the transverse colon, to produce paralytic ileus. Left panel:
A normal CT scan for comparison.
Case 1: Spread and Local Effects of
Peripancreatic Enzyme Leakage
Normal Acute Pancreatitis

Pancreatic inflammation and necrosis acts like a severe burn and leads to marked exudation of fluid.
The structures nearby can be greatly effected: sympathetic ganglia, kidneys, adrenals, stomach, biliary tree,
spleen, left lung.
Case 1: Other Complications of
Acute Pancreatitis
Complication Causes

HyperglycemiaIslet destruction  insulin deficiency


Hypocalcemia Low serum albumin
Fat necrosis  precipitation of
fatty acids as calcium soaps
Respiratory Cytokines; Released lecithinases
Distress destroy pulmonary surfactant
Fever Cytokine release
Painful subQ Metastatic fat necrosis
nodules from released lipases
Case 1: CT Scan of Abdomen
Case 1
Normal

Right panel: Shows a large pancreatic pseudocyst posterior to and compressing the barium-containing stomach (radiodense
crescent). The swollen, inflamed pancreas lies within the pseudocyst. Pseudocysts form when a fibrotic capsule develops
around a persistent peri-pancreatic fluid collection
CC: 67 yo presents to his PCP with weight loss, mild mid-back discomfort for 3 months
and now stool changes

HPI: His vague discomfort originally was mild, and he thought it might be arthritis in his
back. He used NSAIDs with some relief, but the discomfort returned and slowly became
more prominent. He has lost 20 pounds in 2 months and has little appetite. His stools
are now light in color with episodes of diarrhea and his eyes have a yellow tint.

PMH: Osteoarthritis of back and hips


Meds: OTC NSAIDs prn
Case 2 NKDA

What is the most likely diagnosis?

An older person with rapid weight loss has cancer until proven otherwise.
The most common presenting symptoms of pancreatic cancer are pain, weight loss and
jaundice.
Pancreatic cancer often presents at a late stage. It is the 4 th leading cause of cancer-
related death in the US.
Case 2
How do we evaluate for the diagnosis?
He needs imaging to define the nature of the cancer –
presumably either pancreatic or biliary carcinoma. The imaging
will also help in “staging” the cancer. Staging determines
where the cancer is and how far it has spread, such as in the
lymph nodes. The treatment depends on the stage.
He will get a CT followed by ERCP (endoscopic retrograde
cholangiopancreatography) and endoscopic ultrasound to
better determine the operability of the lesion, its local invasion
of vascular and other structures, and the presence of nodal
metastases.
In the normal ERCP, note the contrast-filled common bile duct
and pancreatic duct emptying separately into the Ampulla of
Vater. Both ducts, as well as the intrahepatic bile ducts, are
smooth and taper proximally. The spiral cystic duct branches off
the common bile duct into the collapsed gallbladder.

The patient's ERCP reveals a a “double duct sign”, with a


stricture of the lower common duct. The extrahepatic bile ducts
proximal to the obstruction are enormously dilated, the
pancreatic duct less dilated. The metal clips alongside the
common duct are from an earlier cholecystectomy

Normal ERCP
Case 2: Specimen from Whipple Procedure
The operative specimen from
the Whipple procedure,
showing the cancer (white
mass) in the pancreatic head
at the junction of the 2nd and
3rd parts of the duodenum,
and the cystic duct and
gallbladder to the left. The
metal probe is in the opened,
dilated common bile duct.C
Disease Review
• Acute Pancreatitis
• Pancreatic Insufficiency/Chronic Pancreatitis
• Pancreatic Cancer
• Zollinger-Ellison Syndrome

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