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GI, Liver, GallBladder, Pancreas > CM- Pancreas and Hepatobiliary Diseases > Flashcards

CM- Pancreas and Hepatobiliary Diseases Flashcards

1
Q

How does the duodenum respond to the presence of HCl within the lumen?

A

endocrine S cells release secretin which stimulates biliary and pancreatic epithelial cells to secrete bicarbonate and water

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2
Q

How does the duodenum respond to the presence of fat and amino acids?

A

endocrine I cells release CCK which

  1. stimulates vagal pathways to pancreatic acinar cells to release enzymes (and proenzymes)
  2. contracts the gall bladder and relaxes the sphincter of Oddi
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3
Q

When do enzymes released from acinar cells of the pancreas become active?

A

They are released as inactive proenzymes and when they pass through the sphincter of Oddi into the duodenum trypsinogen is hydrolyzed into trypsin by enterokinase.
Trypsin then activates the other proteases

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4
Q

How do cholesterol bile stones form?

What are risk factors for this?

A

If more cholesterol is secreted into bile than can be maintained in solution, the bile is “supersaturated”. The excess can precipitate out and form stones.

  1. Female
  2. fat
  3. fertile (pregnant)
  4. Forty
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5
Q

Where do cholesterol gallstones form ?

A

ONLY in the gallbladder lumen. They cannot form freely in the bile duct (a difference from pigmented stones)

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6
Q

How do pigmented bile stones form?

A

They are composed of calium bilirubinate and form in response to anything that increased bilirubin formation (hemolysis)
Bacteria can also chemically alter bile leading to precipitation of gallstones.

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7
Q

How do bacteria cause pigmented gallstones?

A

Bacteria can chemically alter bile leading to precipitation of stones.

Ex. E. coli has glucuronidase which unconjugates bilirubin forming black stones

Ex. phospholipase produces FFA which precipitates with calcium for soft brown stones .

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8
Q

What are the major inciting factors of acute pancreatitis?

A 
Gallstones (and choledolithiasis**)
Ethanol **
Tumors
Surgery/trauma
Mumps
Autoimmune
Scorpion venom
Hyperlipidemia, hypercalcemia
Emboli/ischemia
Drugs
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9
Q

What genetic mutations lead to chronic pancreatitis?

A
  1. PRSS1 - “super trypsin” is resistant to cleavage
  2. SPINK1/PST1 - inactive trypsin inhibitor
  3. CFTR- impaired bicarb secretion
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10
Q

What does chronic pancreatitis lead to?

A
  1. loss of endocrine and exocrine cells
  2. fibrosis
  3. duct deformity
  4. fat malaborption and diabetes
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11
Q

What drives the progression to pacreatic adenocarcinoma?

A
  1. overexpression of TGFa, EGF
  2. activated oncogene K-Ras
  3. inactivated tumor suppression p53, p16
  4. overexpression of TGFB which drives fibrosis without inhibiting cellular proliferation

This leads to precursor lesions in the pancreatic duct called PanINs.

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12
Q

Why is pancreatic adenocarcinoma able to metastasize so quickly?

A

Factors derived from tumor cells drive angiogenesis, neural invasion, and mestastatic spread.

The tumor is protected from the immune system because it requires minimal vascular supply and is in a dense fibrous stroma

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13
Q

Most gallstones are asymptomatic and do not require surgical removal of stones, What are the 4 main exceptions to this rule?

A
  1. Sickle Cell Anemia (hemolysis increases bilirubin)
  2. extreme remote assignments
  3. liver transplant recipients
  4. Diabetics ( neuropathy makes it so they can’t feel the pain potentially missing sepsis)
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14
Q

What is the pathophysiology of biliary colic?

A

It is episodic abdominal pain caused by the gallbladder attempting to contract in the presence of a stone/obstruction in the cystic duct

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15
Q

A patient presents with pain in the RUQ but it is poorly localized. They say the pain started just after eating, got worse over a span of 15 minutes and then stayed bad for 4 hours.
The physical exam is normal with slight mild tenderness.
What is the likely problem?

A

Biliary colic

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16
Q

What is the main imaging modality used for diagnosis of biliary colic?
What do you do in the absence of demonstrable cholelithiasis?

A

Ultrasonography can detect gallstones in 95% of cases.

If you don’t see stones on ultrasound the next test is CCK HIDA scan.
You inject dye intravenously, and it gets excreted into the bile so you will see it fill the liver and go down the bile duct. If the dye fails to enter the gall bladder, it is fully obstructed and should be removed.
Next you give CCK which causes the gallbladder to contract. Measure the GBEF

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17
Q

If the patient seems to have biliary colic, but there is not demonstrable stones, what test would you do? What would the results tell you?

A

CCK HIDA

HIDA- shows if bile is getting into the gallbladder
CCK- contracts the gall bladder to measure GBEF.

If the patient has low GBEF and reproducible symptoms of the biliary colic, there is a biliary source of symptoms.

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18
Q

What is treatment for biliary colic?

A

laproscopic cholecystectomy because the risk of recurrent attack is 70%

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19
Q

What is the pathophysiology of acute cholecystitis?

A

when the gallbladder wall is acutely inflamed due to chemical irritation of the epithelium which eventually spreads the full thickness of the wall

20
Q

What are the major causes of acute cholecystitis?

A
  1. Gallstones (stasis of bile and chemical irritation)
  2. PAN
  3. S. typhosa
21
Q

A patient presents with RUQ pain, tenderness over the gallbladder and fever. The pain has lasted 6 hours and is localized.
The person has a positive Murphy’s sign. What are you highly suspicious of?

A

Acute cholecystitis

22
Q

What is Murphy’s sign?

What is a positive Murphy’s sign highly specific for?

A

When the patient takes a deep breath and has inspiratory arrest when the palpating hand touches the inferior of the gallbladder.
A positive sign is highly specific for acute cholecystitis.

23
Q

What lab tests are ordered if you are suspicious of acute cholecystitis?

A

US - cholelithiasis, thickened walls, pericholecystic fluid

HIDA- confirm or exclude cystic duct obstruction (hot spot on the gallbladder excludes it)

24
Q

What is treatment for acute cholecystitis?

A
  1. cholecystotomy

2. antibiotics if febrile or suspected of gangrenous or perforated gallbladder

25
Q

What is the pathophysiology of ascending cholangitis?

A

There is an obstruction of the common bile duct (choledolithiasis) leading to stagnant bile prior to the obstruction that secondarily gets infected by bacteria

26
Q

An elderly patient presents with jaundice, RUQ pain, fever. He looks very septic-looking and delerious. What are you suspicious of ?

A

Ascending cholangitis due to the presence of Reynold’s Pentad

27
Q

What labs and tests are run for ascending cholangitis?

A
  1. CBC- leukocytosis due to infection, schistocytes, left shift
  2. elevation of liver enzymes including bilirubin
  3. US- dilated common bile duct
  4. ERCP- if stabilized with fluid/antibiotics to remove stone (most likely cause of obstruction)
28
Q

What is treatment for ascending cholangitis?

A
  1. Fluids
  2. Antibiotics
  3. Decompression of the bile duct (ERCP, PTC)
29
Q

What physical exam findings and radiologic evidence support acute pancreatitis?

A

epigastric abdominal pain preceded by nausea and vomiting associated with elevated lipase and amylase.
Radiographically- edema and necrosis

30
Q

A patient has a sharp severe continuous pain that radiates through the back to the intrascapular area. There is mild relief when they are in the prone position. They have nausea and vomiting. On physical exam you note orthostatic vital signs. The abdomen is quiet and tender. What is the likely cause?

A

acute pancreatitis

31
Q

What are the Cullen and Grey-Turner sign? What disease are they associated with?

A

Cullen- blood tracking to the umbilicus

Grey-Turner- blood to the lateral ab wall

Acute pancreatitis with retroperitoneal hemorrhage

32
Q

What lab finding is most associated with acute pancreatitis?

A

elevated lipase and amylase (elevation does NOT correlate with severity of attack or prognosis)

33
Q

In addition to acute pancreatitis, what 3 other situations will raise amylase and lipase levels?

A
  1. ischemic bowel
  2. perforated vicus
  3. intestinal obstruction
34
Q

What is the best imaging modality for the pancreas itself?

A

Abdominal CT with IV and oral contrast

- stages level of necrosis(leading to immune response and systemic effects)

35
Q

What is the leading cause of mortality 2-3 weeks after symptom onset of acute pancreatitis?

A

infection

36
Q

When should multi-phasic CT be used in a person suspected of acute pancreatitis?

A
  1. diagnosis is in doubt
  2. fail to improve
  3. over 50 (maybe cancer)
  4. biliary obstruction
37
Q

When is MRCP indicated for acute pancreatitis?

A

If choledolithiasis is suspected

38
Q

What is treatment for acute pancreatitis?

A
  1. fasting the patient (rest the pancreas)
  2. fluid
  3. analgesics
  4. antiemetics
  5. monitor urine output and oxygenation

If gallstone pancreatitis, ERCP to decompress the biliary duct reducing risk of cholangitis

39
Q

What are major risk factors for pancreatic carcinoma?

A
  1. smoking
  2. chronic pancreatitis
  3. hereditary pancreatitis (PRSS1)
40
Q

A thin elderly woman presents with anorexia, nausea, weight loss, jaundice, and glucose intolerance. What do you suspect?

A

pancreatic carcinoma

41
Q

What marker is checked in pancreatic carcinoma?

A

CA19-9

If present at a level >250 with concurrent abdominal mass and absence of pancreatitis it is diagnostic

42
Q

In the absence of pancreatitis, what is the imaging modality of choice for pancreatic carcinoma?

A

EUS (endoscopic ultrasound)

43
Q

What is EUS used for? what it the limitation?

A

Diagnosis of pancreatic carcinoma.

Limitation : it has difficulty diagnosing tumors in patients with chronic pancreatitis

44
Q

Tumors larger than________ on CT are rarely cured for pancreatic carcinoma.

A

3cm diameter

45
Q

What procedure is done to remove resectable pancreatic carcinoma?

A

Whipple

GI, Liver, GallBladder, Pancreas (24 decks)

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