PANCREAS

Alvarez, Vinna Lynn P.

Arciaga, Amessa Jamira
GROUP 31 – Dra. Crisostomo

Anatomy
- lies transversely in the upper abdomen at the L1-L2 level.
- head and body are retroperitoneal; tail is intraperitoneal lying in the splenorenal ligament.
- Pancreatic size is variable but normal maximum adult AP measurement is 3.5cm. for the
head, body and tail.

I. Production of digestive enzyme

 A cells,B cells, D cells,PP cells
 Regulate blood glucose level
Beta cells:
 60-80% produce insulin
 Insulin promotes glucose transport, stimulates protein synthesis
 Inhibits glycogenolysis
Alpha cells:
 5-20% seretes glucagon
 Glucagon counterbalance insulin by stimulating hepatic glycogenolysis, ketogenesis and
lipolysis
 Glucagon inhibits intestinal motility ad gastric acid secretion
 The release of glucagon is stimulated by hypoglycaemia, stress, CCK
D cells:
 Secretes somatostatin w/c have inhibotory effect on most GIT hormones
PP cells:
 Source of pancreatic polypeptide
 Decrease exocrine secretions and biliary motility
 Used as tumor markers for pancreatic endocrine tumors

Acute Pancreatitis
 5000 new cases/yr USA
 Over-all mortality – 10%
 Inflammatory disease involves heart, lung and kidney
 2 pathological form:
a. Interstitial – edematous, PMN infiltrates
b. Necrotiing – focal of diffuse necrosis of parenchyma

Etiology:
 Gallstones (40%)
 Alcohol (30%)
 Idiopathic (15%)
 Metabolic (5%)
 Anatomical (<5%)
 Mechanical insults (<5%)
 Drugs (<5%)
 Infection (<5%)
 Hereditary (rare)
 1. Pancreatitis assoc. w/gallstones
 Common channel between CBD and duct of wirsung was thought to cause gallstone
 High proportion of cases with gallstone pancreatitis have recoverable biliary calcium in the
stools
 Reflux of bile into the pancreatic duct can induce pancreatitis (experimental)

2. Alcohol Pancreatitis
 Alcohol causes increase in protein concentration into the pancreatic juice –precipitation of
protein forms a nidus with subsequent calcification w/c in turn can cause duodenal
inflammation with some degree of ductal obstruction or increase intraductal pressure with spasm
of sphincter resulting in pancreatitis

Alcohol-induced Pancreatitis
 Pancreatic duct obstruction
- Increase ampullary resistance
- Protein deposition
 Pancreatic exocrine hypersecretion
- Ethanol stimulates gastric acid secretion
- Activation of secretin – exocrine
 Impairedtrypsin inhibition
 Acetaldehyde
- Injures acinar cells by increasing membrane permeability
 Hypertriglyceridemia
- Source of free fatty acids which are cytotoxic

Clinical Presentation:
 Abdominal pain
 Hx of large quantities alcohol consumption
 Pain typically begins 1-4 hours after meal
 Sudden epigastric pain radiating to the back w/ N&V
 Seere and steady w/o cramping pain
 PE, lying still in bed, febrile, tachycardia
 Mild to moderate abdominal tenderness
 In severe cases, rigid abdomen and rebound tenderness
 Severe pancreatic inflammation and necrosis may cause retroperitoneal haemorrhage whick leads to:
- Large 3rd space fluid loss
 Diminished breath sounds d/t effusion
 Jaundice d/t biliary obstruction
 Stigmata of chronic liver disease eg. Spider angiomata, gynecomastia and parotid enlargement
 Blood dissection along different planes
-Gray Turner’s Sign: Blood extends to the flank tissue resulting to flank ecchymosa
-Cullen’s sign: Blood dissects up to the falciform ligament and create peri-umbilical ecchymosis

Diagnostic evaluation:
1. Serum amylase
-increased in 95% of cases: 5% false negative
(75% of patients with abdominal pain and increase amylase have pancreatitis
-Other causes of hyperamylasemia
 Acute cholecystitis
 CBD stones with or without pancreatitis
 Perforated peptic ulcer
 Strangulated small bowel
  Acute alcoholism
 Cancer of the pancreas
 Mumps
 Ruptured ectopic pregnancy
 ERCP
 Acute appendicitis
-Amylase P level 3x above
-Amylase level over 1000 Somogyi- Nelson Unit often indicates biliary tract disease pancreatitis
-200-500 units indicate alcoholic pancreatitis

2. Lipase
-Longer half- life more specific levels remain high for 12 days
- the level of amylase and lipase has nothing to do with severity and prognosis

3. Serum Calcium
-Values of < 7.5mg/dL generally indicates poor prognosis and reflects extensive disease process

Laboratory Studies
 Liver associated enzymes
-Alk pos total bilirubin SGOT SGPT
-ALT > 150U/L gallstone pancreatitis
 Serum electrolytes, BUN, Creatinine, Glucose and Triglycerides
 C-reactive protein
-24-48 hrs after prognostic value
-Double value= severe pancreatitis
-Acute phase reactant is nonspecific

Imaging techniques
A. Abdominal film – demonstrates pancreatic calcifications.
B. Chest Film- demonstrates pleural effusion, basal atelectasis, elevated diaphragm.
C. Ultrasound- normal pancreas has homogeneous echopattern of slightly higher echogenicity than
the liver.
D. CT scan- more helpful than ultrasound in assessing pancreatic outline and tail, peripancreatic
tissues and blood vessels.
E. ERCP (Endoscopic retrograde cholagiopancreatography)
-endoscopic assessment of upper gastrointestinal tract and ampulla
-contrast assessment of pancreatic and bile ducts.
-most effective method for imaging pancreatic duct.
- therapeutic and diagnostic procedures which may be undertaken at
ERCP
a. sphinoterotomy
b. stone extraction from bile duct and pancreatic ducts
c. biopsy of the gut or ampulla
d. cytology of pancreatic juice and brushings
e. balloon dilatation of benign strictures
f. stent insertion
g. pancreatic cyst drainage
F. Angiography – inferior to CT in assessing respectability of malignant tumors
G. MRI – pancreas is difficult to adequately image because of respiratory motion and peristalsis.
H. Fine needle biopsy – performed under ultrasound , CT or fluoroscopic control
I. CT scan – method of choice in imaging the pancreas.
Common pancreatic diseases
A. Acute pancreatitis
Chest film changes – left pleural effusion with high amylase
 basal atelectasis
 elevated diaphragm
 pulmonary edema
 wide mediastinum (pseudocyst)
Abdominal film changes
- colon cut off sign – transverse colon is dilated but cuts off abruptly at the
splenic flexure.
- sentinel loops
-duodenal ileus – most specific
- small bowel ileus
- gasless abdomen due to persistent vomiting
- gastrocolic separation
- left renal halo sign
- ascites
- obliterated left psoas outline
- gas bubbles in the pancreas
- fat necrosis – mottled shadowing
- bone changes – avascular necrosis
- bone infarcts
- lytic lesions

Barium studies – widened duodenal or C-loop with compressed medial border

 ampullary edema
 thickening of gastric and duodenal folds
Ultrasound findings:
- normal in 30% of cases
- ultrasonic changes may be seen after 12-24 hours
- enlarged and hypoechoic pancreas
- pancreatic duct dilatation may be present complications:
-phlegmon, hemorrhage, abscess, fluid collection and pseudocyst

CT scan changes:
- best imaging technique for demonstrating pancreas and peripancreatic tissues and associated
complications.
- pancreatic enlargement (diffuse or local)
- decreased attenuation
- indistinct outline
- phlegmon – low density mass
- hemorrhage – high density areas
- fluid collections, pancreatic and peripancreatic
- inflammation of peripancreatic tissues
- abscess
- free intraperitoneal fluid

B. Chronic Pancreatitis
plain film changes – pancreatic calcifications –predominant features of alcoholic
pancreatitis.
-bone infarcts

Barium studies hypotonic duodenography: reversed 3 or epsilon sign of duodenal loop

 - effacement or speculation of duodenal folds.
- ampulla edema

Ultrasound and CT scan – enlarged or smaller than normal

- focal and diffuse changes with irregular outline and loss of definition of fascial planes
- pancreatic and common bile duct are frequently dilated
ERCP – irregular and dilated main duct
- irregular filling and cytic dilatation of side branches
- narrowing or smooth stricture of common bile duct

C. Pancreatic Tumors
Barium studies and hypotonic duodenography
-widened duodenal loops
- fixation of the loop
- anterior displacement, speculation of medial mucosal fold
- nodular mucosal filling defects
- inverted 3 or Frostberg sign
Ultrasound findings:
- positive findings in 80-90% of cases
o early – focal bulge to pancreatic outline
o late – irregular lobulated mass of low or mixed echogenicity
- distal chronic pancreatitis
- dilated common bile duct, pancreatic duct, distal to tumor
- signs of spread – liver metastasis, portal and peripancreatic nodes, invasion of retroperitoneal
fat, loss of definition of adjacent tissues, occlusion of splenic and portal veins.
CT-SCAN:
- superior to ultrasound in assessing tumor invasion of peripancreatic structures
- preferred technique for assessing operability