Pancreas Flashcards
What is edematous pancreatitis like? What is acute hemorrhagic pancreatitis like? What are some etiologies of acute pancreatitis? What is the pathogenesis of acute pancreatitis (more than 1)?
- Edematous pancreatitis: reversible, polymorphonuclear leukocyte infiltrate and edema
o No necrosis or hemorrhage, well managed medically - Acute hemorrhagic pancreatitis: hemorrhage and necrosis
- Etiologies: Alcoholism (commonly in men) or chronic biliary disease (often in women)
Pathogenesis:
o Acinar cell injury and duct obstruction
o Extracellular leakage of activated digestive enzymes
o Autodigestion of pancreatic and extrapancreatic tissues
o Trypsin activation is central to the pathogenesis, trypsin does not produce cell necrosis
o Trypsin activates other pancreatic proenzymes, which cause damage
o Phospholipase A2 attacks membrane phospholipids to cause necrosis
o Elastase digests blood vessel walls, causing hemorrhage
o Pancreatic lipase contributes to fat necrosis
- Secretion against obstruction: raise intraductal pressure and exacerbate back-diffusion
- Ethanol Consumption: Injury of pancreatic acinar or duct cells
o Causing spasm or acute edema of the sphincter of Oddi
o Stimulates secretion - Other Causes: viruses (such as mumps, coxsackievirus, and cytomegalovirus), therapeutic drugs (e.g. azathioprine), blunt trauma, hyperlipidemia, hypercalcemia, scorpion stings
What is the pathology of acute pancreatitis?
C. Results in liquefactive hemorrhagic necrosis of the pancreas and fat necrosis of the peripancreatic fat (Pig. 11.1)
- Pathology: Edematous and hyperemic, friable and hemorrhagic, retroperitoneal hematoma
o Fat necrosis, firmer and chalk-like as more calcium and magnesium soaps are produced
o Microscopically with (1) acinar cell necrosis, (2) intense acute inflammation, and (3) foci of necrotic fat cells
What are some symptoms of acute pancreatitis? What symptoms point to alcohol caused? Hyperlipidemia caused? Mumps caused?
CLINICAL FEATURES
Abdominal pain, mild to severe, often radiates to the back,
Nausea, vomiting
Abdominal tenderness mild to severe.
Ecchymosis in one or both flanks (Grey Turner’s sign) or the periumbilical area (Cullen’s sign) in less than 1% of cases
Abnormal vital signs, tachypnea, dyspnea, and confusion in severe cases
Hepatomegaly, spider angiomas, and thickening of palmar sheaths favor alcoholic pancreatitis
Eruptive xanthomas and lipemia retinalis suggest hyperlipidemic pancreatitis
Parotid pain and swelling are features of mumps
o COMPLICATIONS
Shock, DIC and ARDS
Pancreatic pseudocysts with degraded blood, debris of necrotic pancreatic tissue
i. Presents as an abdominal mass with persistently elevated serum amylase
ii. Rupture is associated with release of enzymes into the abdominal cavity and hemorrhage
Pancreatic abscess
3 . Pancreatic abscess—often due to Ecoli; presents with abdominal pain, high fever, and persistently elevated amylase
What are some lab findings for acute pancreatitis? How can imaging be used to diagnose acute pancr.?
1) Elevated Amylase and Lipase at least 3 times the upper limits of normal is sensitive but not specific
2) Elevated markers of inflammation: WBC, CRP
3) Markers of organ failure: elevated creatinine, hypoxemia
4) Elevated ALT, AST, and Bilirubin may indicate gallstone pancreatitis
5) Decreased serum Calcium
Diagnostic imaging:
1) Abdominal plain films may show ileus or signs of chronic pancreatitis
2) Abdominal Ultrasonography may show gall stones or evidence of biliary obstruction
3) Abdominal CT may show pancreatic swelling, peripancreatic inflammation, pancreatic necrosis, and abdominal fluid collections.
4) MRI provides similar information regarding the severity of pancreatitis as does CT. MRI is better than CT, but equal to endoscopic ultrasound (EUS) and ERCP in detecting choledocholithiasis
How is acute pancreatitis treated?
1) Aggressive IV hydration
2) Pain control
3) Monitor and manage complications
4) Early removal of impacted gallstone
5) Early enteral nutrition
6) Surgical debridement for infected pancreatic necrosis
7) Elective cholecystectomy for gall stone pancreatitis
What is chronic pancreatitis? What are some etiologies? What are some clinical features? Complications? Pathology?
A, Fibrosis of pancreatic parenchyma, most often secondary to recurrent acute pancreatitis
1, Most commonly due to alcohol (adults) and cystic fibrosis (children); however,
many cases are idiopathic.
B. Clinical features
1 . Epigastric abdominal pain that radiates to the back
2. Pancreatic insufficiency—results in malabsorption with steatorrhea and fatsoluble vitamin deficiencies. Amylase and lipase are not useful serologic markers of chronic pancreatitis.
3 . Dystrophic calcification of pancreatic parenchyma on imaging; contrast studies reveal a ‘chain of lakes’ pattern due to dilatation of pancreatic ducts.
4, Secondary diabetes mei I it us—late complication due to destructio n of islets
5 . Increased risk for pancreatic carcinoma
7) Complications:
1) Pseudocysts
2) Pseudoaneurysms: a consequence of enzymatic and pressure digestion of the wall of a vascular structure by a pseudocyst
3) Variceal bleeding from splenic vein thrombosis
4) Bile duct or duodenal obstruction
5) Pancreatic fistulas
6) Malignancy
7) Gastro-intestinal dysmotility
- Gross examination: hard gland with dilated ducts and visible calcified concretions
- Parenchymal fibrosis, reduced number and size of acini, calcification
- Variable dilation of the pancreatic ducts, risk for a pancreatic cancer
Describe autoimmune pancreatitis.
d. Autoimmune pancreatitis: distinct form. Characterized by ↑IgG4 producing plasma cells, steroid effective. Could mimic pancreatic cancer
- Lymphoplasmacytic sclerosing pancreatitis (autoimmune pancreatitis)
o Characterized by a duct-centric mixed inflammatory infiltrate, venulitis and increased IgG4 producing plasma cells
o Clinically can mimic pancreatic cancer; responds to steroids
What are some ways in which CP is diagnosed?
5) Diagnosis: CP leads to structural and functional changes in the pancreas
a. Tests of structure:
i. MRI/MRCP (highest sensitivity)
ii. EUS
iii. ERCP
iv. CT
v. Abdominal US
vi. Plain abdominal film (Lowest sensitivity)
b. Tests of function
i. Direct hormonal testing (highest sensitivity)
ii. MRI/MRCP with secretin stimulation
* **iii. Fecal elastase and fecal fat**
iv. Serum Tripsinogen (trypsin) (Lowest sensitivity)
How is the abdominal pain of CP treated? The maldigestion?
6) Treatment:
a. Abdominal pain:
1) Analgesics
2) Cessation of alcohol and tobacco
3) Pancreatic enzymes
4) Vitamine/Antioxidants
5) Endoscopic therapy
6) Surgical therapy
7) Celiac plexus block
b. Maldigestion and steatorrhea:
1) Pancreatic enzymes
2) Replacement of fat soluble vitamins
Describe congenital pancreatic cysts. Describe pseudocysts.
- Congenital Cysts: anomalous development of pancreatic ducts
o Usually unilocular, thin-walled; range from microscopic to 5cm
o Lined by a glistening, uniform cuboidal to flattened epithelium - Pseudocysts: localized collections of necrotic-hemorrhagic material rich in pancreatic enzymes
o Usually arise after acute pancreatitis
o Morphology: usually solitary
o Composed of central necrotic-hemorrhagic material
o Rich In pancreatic enzymes surrounded by non-epithelial lined fibrous walls
Describe the pathology, prognosis, and treatment for serous cystadenoma, mucinous cystic neoplasm, intraductal papillary mucinous neoplasm, and ductal adenocarcinoma with cystic regeneration
Cystic tumors
1) Serous cystadenoma: benign
- Serous cystadenoma
o Benign cystic neoplasms composed of glycogen-rich cuboidal cells surrounding small (1-3mm) cysts containing clear, thin, straw-colored fluid
o Female: male 2:1 , 7th decade
o Almost always benign, surgical resection is curative in vast majority
2) Mucinous cystic neoplasm: risk of malignancy
- Mucinous cystic neoplasms (MCNs)
o 95% arise in women, 1/3 can be associated with invasive carcinoma
o Arise in body or tail
o Cysts filled with thick mucin, lined by columnar-mucin-producing epithelium
o Associated with a dense ovarian-like stroma
3) Intraductal Papillary Mucinous Neoplasm (IPMN): risk of malignancy
o Mucin-producing intraductal neoplasms
o More frequent in men, head of pancreas, solitary or multifocal
o Lack dense ovarian-type stroma, connect to larger pancreatic duct
4) Ductal adenocarcinoma with cystic degenration
What is pancreatic adenocarcoma? In whom is it most commonly seen? What are the major risk factors? Clinical features? Serum marker? Treatment? Prognosis?
A. Adenocarcinoma arising fro m the pancreatic ducts
i. Most commonl y seen in the elderly (average age is 70 years)
B . Majo r risk factors are smoking and chroni c pancreatitis.
C. Clinical features (usually occur late in disease)
1 , Epigastric abdominal pain and weight loss
2. Obstructive jaundic e with pale stools and palpable gallbladder; associated with tumors that arise in the head of the pancreas (most commo n location)
J. Secondary diabetes mcllitus; associated with tumors that arise in the body or tail
- Pancreatitis
5 . Migratory thrombophlebitis (Trousseau sign); presents as swelling, erythema, and tenderness in the extremities (seen in 10% of patients)
- Serum tumo r marker is CA 19-9.
D. Surgical resection involves en bloc removal of the head and neck of pancreas, proximal duodenum, and gallbladder (Whipple procedure).
E. Very poo r prognosis; 1-year survival is < 10%.
Describe acinar cell carcinoma and pancreatoblastoma.
ACINAR CELL CARCINOMA
- Acinar cell differentiation, formation of zymogen granules and production of exocrine enzymes (trypsin and lipase)
PANCREATOBASTOMA
- Rare, occur in children 1-15 years
- Squamous islands admixed with acinar cells
- Malignant, but survival better than pancreatic ductal adenocarcinomas
Describe 3 types of islet cell tumors including
ISLET CELL TUMOR
- Insulinoma/beta-cell tumor
o Produce insulin, leading to hypoglycemia, hunger, confusion, insulin coma
o Elevated insulin and C-peptide - Gastrinoma/G cell tumor
o Zollinger-Ellison syndrome
o Gastrin, leading to gastric hyperacidity and gastric ulcer
o Maybe associate with MEN-1 - Glucagonoma
o Glucagon, leading to hyperglycemia, anemia and skin rash
