Biliary and Pancreatic Disease Flashcards
Is the pancreas peritoneal or retroperitoneal?
It is retroperitoneal, except for the tip of the tail, which is peritoneal.
What are the three phases of pancreatic secretion? What happens in each?
- Cephalic phase - vagal stimulation for sight / smell of food releases some acinar juices
- Gastric phase - antral distension stimulates secretin -> cAMP-mediated water and bicarbonate secretion from ductal cells
- Intestinal phase - decrease in duodenal pH + increase in amino acids from gastric emptying leads to CCK secretion. CCK stimulates acinar cell secretion
What are the three forms of acute pancreatitis? How are they defined?
Mild = interstitial damage, with absence of organ failure or necrosis
Moderately severe = local complications and may have transient organ failure for <48 hours
Severe = necrotizing - persistent organ failure + local complications, high mortality, especially if infected
What mediates the local effects of acute pancreatitis? Describe the process of damage
Pancreatic exudate containing activated enzymes spreads through various fascial planes in retroperitoneum -> all around the organs. Leads to fat necrosis of surrounding tissues.
Fluid is protein-rich and when lost leads to hypovolemia / hypotension from third space losses
What are the mediators of the system effects of pancreatitis.
Trypsin -> activates complement, elastase, thrombin, chymotrypsin, PLA2, and kallikrein
-> widespread complement activation, damage to cell membranes, and damage to capillaries / blood vessels
Thrombin activation leads to DIC
Lipase release causes widespread fat necrosis
What are some common obstructive causes of acute pancreatitis?
Gallstones
Inspissated (thickened) secretions from alcohol
Pancreas divisum
Strictures / malignancies / other compressions
What are some metabolic causes of acute pancreatitis?
Hypertriglyceridemia (>1000), hypercalcemia (enzyme activation), ischemia / hypoperfusion, systemic inflammatory vasculitides (SLE, polyarteritis nodosa)
What causes hereditary pancreatitis and what is it associated with risk of?
Mutation in trypsin making it resistant to lysis
Autosomal dominant -> cumulative risk of pancreatic cancer is 40% (very high)
What are some medications associated with acute pancreatitis?
Azathioprine / 6-MP (think of the sponge being held in sketchy)
All sulfa drugs - furosemide, thiazides, sulfonamides
Valproic acid (sponge being held again)
Didanosine - NRTI - think of Dan holding it at the round table
What are the two distinct phases of pancreatitis which have been identified?
Early phase - within 1 week, systemic inflammatory response syndrome +/- organ failure
Late phase - after 1 week, characterized by local complications
What are the common presenting symptoms of acute pancreatitis?
Abdominal pain with radiation to the back, worsened by food and relieved by bending forwards (takes pancreas off of back)
Low grade fever, volume depletion (orthostatic changes), and jaundice if obstruction
What are some common signs of acute pancreatitis on abdominal exam?
Grey Turner’s sign - flank discoloration
Cullen’s sign - periumbilical discoloration
Paralytic ileus (absent ball sounds)
Pleural effusions, ascites, jaundice
What are the diagnostic criteria for making the diagnosis of acute pancreatitis?
Present of at least 2/3 of the following:
- Acute epigastric pain radiating to the bag
- Amylase and lipase levels elevated >3x ULN
- Characteristic imaging findings
What are the characteristic imaging modalities for acute pancreatitis?
Ultrasound - check for stones. Initial study of choice.
CT scan with contrast or abdomen MRI is more specific and can show the degree of necrosis
What are some prognostic indicators which would suggest a poor outlook for acute pancreatitis?
Severe orthostatic changes
Systemic inflammatory response syndrome
Declining kidney function
Pulmonary involvement
Old age, fat, with altered mental status
What are some common local complications of acute pancreatitis?
Necrosis, abscess, pseudocyst
Ileus
GI hemorrhage, splenic vein thrombosis (vessel damage)
What are some systemic complications of acute pancreaitis?
Organ failure - Shock, ARDS (membrane damage), renal failure
Hypocalcemia with distant fat necrosis
DIC
What is the treatment of uncomplicated acute pancreatitis?
NPO - bowel rest, feed by tube
Restoration of volume state
Remove obstructing gallstone by ERCP if need be
Other supportive treatments for complications
What are the causes of severe necrotizing pancreatitis and what is the treatment?
Cause is an infection, usually by E.coli, Klebsiella, or Enterococcus
Treatment - broad spectrum antibiotics until aspiration biopsy tells you sensitivities. Surgical debridement after infection clears.
How do pseudocysts form and how can they cause symptoms?
Form from acute local fluid collections
Can cause obstruction, severe pain, bleeding / rupture, and ascites
When should pseudocysts be treated and how is this done?
Treat if they are symptomatic
-> can treat endoscopically (via ERCP or across stomach), percutaneously under CT guidance, or surgically
What are the etiologies of chronic pancreatitis?
Think pancreatic cirrhosis:
Alcoholism CF - in children Hemochromatosis - bronze diabates Hereditary pancreatitis Hyperparathyroidism - high calcium Autoimmune
What will lab data show for autoimmune pancreatitis? Imaging?
Elevated serum gammaglobulin IgG4, with autoantibodies
Imaging shows diffuse sausage-like enlargement of pancreas with irregular narrowing of pancreatic duct, and biliary duct abnormalities
What will abdominal X-ray and ERCP show for chronic pancreatitis?
Abdominal X-ray - pancreatic calcification
ERCP - abnormal pancreatic ducts, with strictures and stones, distal narrowing of common bile duct
What causes pain in chronic pancreatitis?
Minimal enzymes are being released due to ductal stenosis and fibrosis of tissues
-> constant stimulation to contract by CCK in the presence of inflammation / fibrosis causes severe pain
What is the treatment for chronic pancreatitis?
Oral pancreatic enzyme replacement therapy -> improves maldigestion of fat, and gives negative feedback for CCK release
Analgesia, with denervation of the pancreas and Whipple procedure of needed.
When is steatorrhea normally seen in chronic pancreatitis and what is the treatment?
When 90% of normal lipase activity is lost
- > treatment is lipase replacement with acid suppression so the enzymes aren’t destroyed in the stomach
- > also hold to a low / moderate fat diet
Describe the diabetes which occurs in chronic pancreatitis and its management?
It’s a late complication since islets go last
Loss of both insulin / glucagon -> tend to be extremes of blood sugars
Minimal insulin in needed, and ketoacidosis is rare from lack of glucagon as well
What is it called when you have obstructive jaundice with a palpable, nontender gallbladder, and what is it suggestive of?
Courvoisier sign - suggestive of pancreatic adenocarcinoma
-> especially when cancer is in the head of the pancreas and blocking the emptying of the common bile duct
Other than obvious jaundice-related symptoms and Trousseau, what are a couple signs / symptoms which make you worry about pancreatic cancer?
- New onset diabetes - in the absence of pancreatitis or past history, especially late in life
- Depression - new onset depression with unclear reasoning, common in pancreatic cancer
What is biliary colic and what is it associated with?
Nausea/vomiting and dull RUQ worsened by food (CCK forces stone into cystic duct)
Associated with cholelithiasis
What are the indications for cholecystectomy?
- Symptomatic gallstones
- Persistent hemolytic anemias (sickle cell, hereditary spherocytosis)
- Gastric bypass surgery (prophylactically, since rapid weight loss is a risk factor)
- Porcelain gallbladder
- Gallbladder adenomas / polyps
What are the nonsurgical management options for gallstones?
Oral bile salt therapy (ursodeoxycholic acid)
Extracorproreal shockwave lithotripsy
What is the characteristic pain felt in acute cholecystitis?
Severe, constant RUQ pain which may radiate to the shoulder
Positive Murphy’s sign (inspiratory arrest on RUQ palpation)
What causes ascending cholangitis usually and how is it treated?
Usually an impact stone, but may also be due to biliary strictures, parasites, neoplasms, or congenital abnormalities
Treated via biliary decompression (make orifice larger) as well as antibiotics to treat the infection
What is Charcot’s triad of cholangitis?
Jaundice, fever, RUQ pain
What type of cancer is carcinoma of the extrahepatic biliary ducts and how does it present?
Adenocarcinomas - usually associated with cholelithiasis
Presentatino: Jaundice, pruritis, ascending cholangitis, and weight loss
Dismal prognosis, treatment is palliative
(think of Klatskin tumor from last Bosch lecture, that’s a type of this)
