Biliary and Pancreatic Disease Flashcards

1
Q

Is the pancreas peritoneal or retroperitoneal?

A

It is retroperitoneal, except for the tip of the tail, which is peritoneal.

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2
Q

What are the three phases of pancreatic secretion? What happens in each?

A
  1. Cephalic phase - vagal stimulation for sight / smell of food releases some acinar juices
  2. Gastric phase - antral distension stimulates secretin -> cAMP-mediated water and bicarbonate secretion from ductal cells
  3. Intestinal phase - decrease in duodenal pH + increase in amino acids from gastric emptying leads to CCK secretion. CCK stimulates acinar cell secretion
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3
Q

What are the three forms of acute pancreatitis? How are they defined?

A

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

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4
Q

What mediates the local effects of acute pancreatitis? Describe the process of damage

A

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

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5
Q

What are the mediators of the system effects of pancreatitis.

A

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

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6
Q

What are some common obstructive causes of acute pancreatitis?

A

Gallstones

Inspissated (thickened) secretions from alcohol

Pancreas divisum

Strictures / malignancies / other compressions

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7
Q

What are some metabolic causes of acute pancreatitis?

A

Hypertriglyceridemia (>1000), hypercalcemia (enzyme activation), ischemia / hypoperfusion, systemic inflammatory vasculitides (SLE, polyarteritis nodosa)

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8
Q

What causes hereditary pancreatitis and what is it associated with risk of?

A

Mutation in trypsin making it resistant to lysis

Autosomal dominant -> cumulative risk of pancreatic cancer is 40% (very high)

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9
Q

What are some medications associated with acute pancreatitis?

A

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

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10
Q

What are the two distinct phases of pancreatitis which have been identified?

A

Early phase - within 1 week, systemic inflammatory response syndrome +/- organ failure

Late phase - after 1 week, characterized by local complications

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11
Q

What are the common presenting symptoms of acute pancreatitis?

A

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

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12
Q

What are some common signs of acute pancreatitis on abdominal exam?

A

Grey Turner’s sign - flank discoloration

Cullen’s sign - periumbilical discoloration

Paralytic ileus (absent ball sounds)

Pleural effusions, ascites, jaundice

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13
Q

What are the diagnostic criteria for making the diagnosis of acute pancreatitis?

A

Present of at least 2/3 of the following:

  1. Acute epigastric pain radiating to the bag
  2. Amylase and lipase levels elevated >3x ULN
  3. Characteristic imaging findings
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14
Q

What are the characteristic imaging modalities for acute pancreatitis?

A

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

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15
Q

What are some prognostic indicators which would suggest a poor outlook for acute pancreatitis?

A

Severe orthostatic changes

Systemic inflammatory response syndrome

Declining kidney function

Pulmonary involvement

Old age, fat, with altered mental status

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16
Q

What are some common local complications of acute pancreatitis?

A

Necrosis, abscess, pseudocyst

Ileus

GI hemorrhage, splenic vein thrombosis (vessel damage)

17
Q

What are some systemic complications of acute pancreaitis?

A

Organ failure - Shock, ARDS (membrane damage), renal failure

Hypocalcemia with distant fat necrosis

DIC

18
Q

What is the treatment of uncomplicated acute pancreatitis?

A

NPO - bowel rest, feed by tube

Restoration of volume state

Remove obstructing gallstone by ERCP if need be

Other supportive treatments for complications

19
Q

What are the causes of severe necrotizing pancreatitis and what is the treatment?

A

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.

20
Q

How do pseudocysts form and how can they cause symptoms?

A

Form from acute local fluid collections

Can cause obstruction, severe pain, bleeding / rupture, and ascites

21
Q

When should pseudocysts be treated and how is this done?

A

Treat if they are symptomatic

-> can treat endoscopically (via ERCP or across stomach), percutaneously under CT guidance, or surgically

22
Q

What are the etiologies of chronic pancreatitis?

A

Think pancreatic cirrhosis:

Alcoholism
CF - in children
Hemochromatosis - bronze diabates
Hereditary pancreatitis
Hyperparathyroidism - high calcium
Autoimmune
23
Q

What will lab data show for autoimmune pancreatitis? Imaging?

A

Elevated serum gammaglobulin IgG4, with autoantibodies

Imaging shows diffuse sausage-like enlargement of pancreas with irregular narrowing of pancreatic duct, and biliary duct abnormalities

24
Q

What will abdominal X-ray and ERCP show for chronic pancreatitis?

A

Abdominal X-ray - pancreatic calcification

ERCP - abnormal pancreatic ducts, with strictures and stones, distal narrowing of common bile duct

25
Q

What causes pain in chronic pancreatitis?

A

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

26
Q

What is the treatment for chronic pancreatitis?

A

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.

27
Q

When is steatorrhea normally seen in chronic pancreatitis and what is the treatment?

A

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
28
Q

Describe the diabetes which occurs in chronic pancreatitis and its management?

A

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

29
Q

What is it called when you have obstructive jaundice with a palpable, nontender gallbladder, and what is it suggestive of?

A

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

30
Q

Other than obvious jaundice-related symptoms and Trousseau, what are a couple signs / symptoms which make you worry about pancreatic cancer?

A
  1. New onset diabetes - in the absence of pancreatitis or past history, especially late in life
  2. Depression - new onset depression with unclear reasoning, common in pancreatic cancer
31
Q

What is biliary colic and what is it associated with?

A

Nausea/vomiting and dull RUQ worsened by food (CCK forces stone into cystic duct)

Associated with cholelithiasis

32
Q

What are the indications for cholecystectomy?

A
  1. Symptomatic gallstones
  2. Persistent hemolytic anemias (sickle cell, hereditary spherocytosis)
  3. Gastric bypass surgery (prophylactically, since rapid weight loss is a risk factor)
  4. Porcelain gallbladder
  5. Gallbladder adenomas / polyps
33
Q

What are the nonsurgical management options for gallstones?

A

Oral bile salt therapy (ursodeoxycholic acid)

Extracorproreal shockwave lithotripsy

34
Q

What is the characteristic pain felt in acute cholecystitis?

A

Severe, constant RUQ pain which may radiate to the shoulder

Positive Murphy’s sign (inspiratory arrest on RUQ palpation)

35
Q

What causes ascending cholangitis usually and how is it treated?

A

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

36
Q

What is Charcot’s triad of cholangitis?

A

Jaundice, fever, RUQ pain

37
Q

What type of cancer is carcinoma of the extrahepatic biliary ducts and how does it present?

A

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)