Abdominal Surgery: Pancreas, Liver, Bile Ducts

Question 1

Female on longterm OCP with large painful hypoechoic liver mass, elevated alk phos and GGT suggesting biliary compression, what does she likely have?

Answer 1

Hepatic Adenoma.

Question 2

A patient who recently underwent lap cholecystectomy for cholecystitis now has high fever and tender splenomegaly is concerning for…

Answer 2

splenic abscess, a rare life threatening complication of bacteremia from a distant infection (ie cholecystitis)

Question 3

Bloody ascitic fluid and elevated alpha fetoprotein should make you think of…

Answer 3

HCC hepatocellular carcinoma

Question 4

Blunt Abdominal Trauma to the liver would result in fluid in what space?

Answer 4

INTRAperitoneal space

Question 5

How might you tell the difference between something like a liver lac versus hematoma?

Answer 5

Hematomas tamponade so there wont likely be free fluid or at least this is how you will think about it

Question 6

What criteria do we use to figureout if something is an exudative vs tansudative pleural effusion?

Answer 6

Lights criteria

Question 7

What is this showing

Answer 7

Porcelain gallbladder

Question 8

This is consistent with…

Answer 8

Hepatic abscess

Question 9

Which would be responsive to rescusitation BP wise: hematoma or laceration of the liver

Answer 9

HEMATOMA because of tamponading

Question 10

Women age 20-50, well circumscribed liver lesion with central scar

Answer 10

Focal Nodular Hyperplasia

Question 11

What is the criteria for acute panreatitis?

Answer 11

At least two of the following:

Severe epigastric pain

Amylase or lipase over or equal to 3 times the upper limit of normal

Findings consistent with acute pancreatitis on imaging (CT, ultrasound, MRI)

**Note that amylase/lipase enzymes will rise within several hours of the development of symptoms whereas CT findings may not present for up to 48 hours

Question 12

Causes of acute pancreatitis

Answer 12

Question 13

When might you see the development of pancreatic pseudocysts

Answer 13

at least 4 weeks post pancreatitis onset.

Acute peripancreatic fluid collections (APFC) are free fluid associated with edematous pancreatitis. Over time, APFCs mature to become pancreatic pseudocysts (PP). PP have capsules—inflammatory and fibrotic walls that contain the fluid. This occurs over time, at least 4 weeks after pancreatitis onset.

Question 14

Why do we not want to drain pancreatic fluid collections before 6 weeks of pancreatitis onset?

Answer 14

Most FCCs require intervention—drainage—and do not self-resolve. The most success is found when there is a thick, mature capsule that will hold up under trauma (penetration by a tube or suture). This happens over time; thus, drainage of an FCC should not occur before 6 weeks from pancreatitis onset. They should be allowed to mature, so an FCC should not be drained if smaller than 6 cm, the approximate size at which they become symptomatic (early satiety, pain, screening CT). If symptomatic, get a CT. To treat, a tube is placed endoscopically between the stomach and cyst (cystogastrostomy) or duodenum and cyst (cystoduodenostomy). If that fails, surgical anastomosis is performed instead.

Question 15

In chronic pancreatitis, what will you see on CT?

Answer 15

Calcifications evidence of previous necrosis

Question 16

Chains of lakes

Answer 16

chronic pancreatitis

The best radiological test is MRCP,which will show a chain of lakes—the chains are fibrotic and stenosed pancreatic ducts, the lakes the dilated ducts of a well-functioning pancreas.

Question 16

Chronic pancreatitis increases the risk of__________________ and __________________

Answer 16

splenic vein thrombosis and pancreatic adenocarcinoma.

Question 16

What is the pathology of acute pancreatitis?

Answer 16

ZYMOGENS!

Question 17

What is the most prognostic lab test for pancreatitis?

Answer 17

BUN is the single most useful prognostic lab test for pancreatitis

Question 18

How can we tell if a pancreatiits is acute interstitial edematous pancreatitis vers necrotizing pancreatitis?

Answer 18

On CT, edema and necrosis are both grey so we have to observe on day 7 whether or not the grey is still present. If the grey resolves on day 7 then it is likely EDEMA, if it does not resolve by day 7 then it is likely NECROSIS

Question 19

What are APFC, PP, ANC, and WON?

Answer 19

APFC= acute peripancreatic fluid collection, its a complication of edematous pancreatitis

PP=pancreatic pseudocyst, its a complication of edematous pancreatitis

ANC= acute necrotic collection, its a complication of necrotizing pancreatitis

WON= walled off necrosis, its a complication of necrotizing pancreatitis

Question 20

What is the rule of 6’s for pancreatitis?

Answer 20

Its not a hard and fast rule but its a concept- 6 cm and 6 weeks, essentially its the idea that you need to wait 6 weeks to drain a pancreatic fluid collection due to the fact that it needs to wall off

Question 21

What is the atlanta criteria used for?

Answer 21

pancreatitis

Question 22

Why do we not order serum lipase for chronic pancreatitis suspicion?

Answer 22

Because it wont be elevated

Serum lipase is notoriously unreliable in the setting of chronic pancreatitis. Even if there were superimposed acute pancreatitis on chronic pancreatitis, the serum lipase might not elevate because the pancreas is so burned out. In the case of chronic pancreatitis, serum lipase cannot be made to be the correct answer.

Question 23

When assessing pancreatitis, what imaging modality is preferred?

Answer 23

Mixed
US for acute and CT for chronic

CT w/contrast, note that Abdominal ultrasound is not likely to reveal anything. It is a poor modality for looking at the pancreas. Endoscopic ultrasound is a better modality, but it is invasive. In general, an abdominal ultrasound does not work for diagnosing the pancreas.

More info:
Step 1 is Cross-sectional imaging. CT or MRI, contrast enhanced if able.

Step 2 is Endoscopic ultrasound (EUS). but without biopsy. Consensus on what constitutes a positive EUS is still being debated.

Step 3 is a secretin-stimulated MRCP (s-MRCP). It looks for chains of lakes.

Step 4 is histology, obtained by endoscopic ultrasound with biopsy, and is the gold standard.

Question 24

Rule of thumb, get a ________________ to image pancreatitis

Answer 24

contrast CT

Question 25

The CT comes back with both evidence of necrosis (necrotizing pancreatitis) and a fluid-collection complication within the pancreas. Thus, at the very least, this is an acute necrotic collection. The fever is suggestive but not diagnostic of infection. The fine-needle aspiration confirms an infected acute necrotic collection. All treatments are started (antibiotics, cultures), and the follow-up asks how to manage an acutely infected acute necrotic collection. The first thing to do is try ….

Answer 25

The first thing to do is try antibiotics alone, with a drain placed only if antibiotics fail. Thus, the right answer is to continue medical therapy.

managing an infected acute necrotic collection, treatment goes antibiotics –> antibiotics with drain –> surgery

Question 26

history of pancreatitis followed by early satiety is the classic presentation for……

Answer 26

pancreatic pseudocyst

Question 27

Why would we not place a tube to drain a pancreatic pseudocyst at 28 days?

Answer 27

Right at the 28-day cutoff, and the immature rind on CT means that successfully placing a tube to drain the pseudocyst is unlikely. Thus, more time is needed for the fluid-collection complication to resolve itself or for the rind to mature. Thus, because we need more time, the correct answer is observation, repeat CT in 2 weeks if symptoms persist.

Question 28

What is the first step in managemnt of acute pancreatitis if 2/3 criteria is met?

Answer 28

conservative measures: NPO, intravenous fluids, and pain control.

Question 29

The typical manifestation includes sudden, severe epigastric pain that radiates to the back, nausea and vomiting, and epigastric tenderness on palpation.

Answer 29

acute pancreatitis

Question 29

How do we dx acute pancreatitis?

Answer 29

Elevation of serum lipase or amylase ≥ 3× ULN and/or characteristic findings of acute pancreatitis on cross-sectional imaging (e.g., contrast-enhanced CT abdomen) confirm the diagnosis. Clinical scores (e.g., Ranson criteria, APACHE II) are used to predict the severity and prognosis of pancreatitis

Question 30

Complications of acute pancreatitis

Answer 30

Localized complications of pancreatitis include necrosis (necrotizing pancreatitis), which may become infected, pancreatic pseudocysts, and walled-off necrosis. Systemic complications include sepsis, ARDS, organ failure, and shock. Complications of pancreatitis are associated with significant morbidity and mortality.

Question 31

Most common cause of chronic pancreatitis

Answer 31

alcohol use

Question 32

How might a pt with CHRONIC pancreatitis present?

Answer 32

Affected individuals may be asymptomatic or present with abdominal pain and features of exocrine pancreatic insufficiency (e.g., steatorrhea, weight loss) or endocrine pancreatic insufficiency (e.g., prediabetes, diabetes). Diagnosis is confirmed with imaging, which typically shows pancreatic calcifications, ductal strictures, and ductal dilations.

Question 33

How do we diagnose chronic pancreatitis?

Answer 33

Diagnosis is confirmed with imaging, which typically shows pancreatic calcifications, ductal strictures, and ductal dilations. Pancreatic function tests (e.g., fecal elastase-1 measurement, 72-hour fecal fat estimation) assess the degree of enzyme deficiency.

Question 34

What happens to amylase and lipase levels in chronic pancreatitis?

Answer 34

Pancreatic enzyme levels are often normal in chronic pancreatitis and cannot be used to confirm or rule out the diagnosis. In contrast, acute pancreatitis typically causes significant enzyme elevation.

Question 35

Can support a diagnosis of steatorrhea due to exocrine pancreatic insufficiency

Answer 35

Fecal elastase-1 (FE-1), note that steatorrhea is a late manifestation of chronic pancreatitis

Question 36

Why might someone with chronic pancreatitis get gastric varices?

Answer 36

Splenic vein thrombosis, Inflammation of the splenic vein; → thrombus formation → left-sided portal hypertension → gastric varices

Question 37

Risk factors for pancreatic cancer

Answer 37

Exogenous risk factors:
Smoking (strongest risk factor)
Chronic pancreatitis (especially when present for more than 20 years)
High alcohol consumption
Type 2 diabetes mellitus

Endogenous risk factors:
Age > 50 years
Inherited genetic syndromes (10% of pancreatic cancers)
Familial atypical multiple mole melanoma (FAMMM) syndrome
Hereditary breast and ovarian cancer syndrome (BRCA1 and BRCA2 mutations)
HNPCC
Von-Hippel-Lindau syndrome
Neurofibromatosis type 1
Multiple endocrine neoplasia type 1

Question 38

What clinical features might you observe ina pt with pancreatic cancer?

Answer 38

Poor appetite, weight loss, belt shape epigastric pain, malabsoprtion, diarrheha, jaundice, Courvoisier sign: enlarged, nontender gallbladder and painless jaundice, hypercoaguability ((rousseau syndrome: superficial thrombophlebitis (in 10% of cases))

Question 39

What is double duct sign?

Answer 39

Double-duct sign: dilation of the common bile duct and pancreatic duct due to tumors of the pancreatic head blocking bile drainage.

Question 40

What tumor markers can you use in pancreatic cancer to track progress?

Answer 40

Tumor markers: not recommended for diagnosis or screening
CA 19-9
CEA (less specific)

NOTE There are no specific biomarkers for pancreatic cancer screening.

Question 41

What procedure do we do for resectable pancreatic cancers?

Answer 41

whipple

Question 42

What does a whipple entail?

Answer 42

Pancreaticoduodenectomy (Whipple procedure) involves resection of the pancreatic head, distal stomach, duodenum, gallbladder, common bile duct, lymphadenectomy, and reconstruction, most commonly by enteroenterostomy or Roux-en-Y anastomosis. It is indicated for pancreatic head carcinoma and is the most commonly performed procedure to remove pancreatic tumors.

Question 43

Causes of cirrhosis

Answer 43

Hepatitis C, alcoholic liver disease, and NASH are the most common causes of cirrhosis in the US.

excessive alcohol consumption, nonalcoholic fatty liver disease, or hepatitis C. Other causes include inflammatory or metabolic diseases, such as primary biliary cirrhosis and hemochromatosis.

Question 44

Features of cirrhosis

Answer 44

Pruritus
Jaundice
Telangiectasia: most commonly spider angiomata (a central red arteriole with numerous, thin arterial extensions, commonly manifesting on light, sun-exposed skin and the trunk)
Caput medusae
Palmar erythema
Nail clubbing
Petechiae and purpura

Question 45

How do liver chemistries differ in alcholic versus non alcoholic liver disease?

Answer 45

ALT > AST: present in most liver diseases
AST > ALT: indicative of alcoholic liver disease
Massive AST and/or ALT elevation (> 15 times ULN): Consider differential diagnoses (e.g., acetaminophen toxicity, acute viral hepatitis, autoimmune hepatitis).

Question 46

What is the Serum-ascites albumin gradient (SAAG) ?

Answer 46

Serum-ascites albumin gradient (SAAG) can be used to differentiate between ascites due to portal hypertension and non-portal hypertensive ascites.

SAAG = (albumin levels in serum) - (albumin levels in ascitic fluid)
High SAAG ascites: ≥ 1.1 g/dL, indicates portal hypertension with ∼ 97% accuracy.
Low SAAG ascites: < 1.1 g/dL, indicates non-portal hypertensive ascites.

Question 47

SAAG greater than 1.1 indicates

Answer 47

portal hypertension ascities

Question 48

What are the major causes of portal hypertension?

Answer 48

Question 49

What is chylous ascites?

Answer 49

A rare form of ascites characterized by accumulation of milky lymphatic fluid within the peritoneal cavity as a result of leakage or exudation of lymph from intraabdominal lymphatic vessels. Diagnosed by a triglyceride concentration > 200 mg/dL in ascitic fluid. The two most common causes in developed countries are intraabdominal malignancy and cirrhosis.

Question 50

What are the most common causes of chylous ascities?

Answer 50

The two most common causes in developed countries are intraabdominal malignancy and cirrhosis.

Question 51

How do we manage esophageal variceal bleeding?

Answer 51

Management of acute esophageal variceal bleeding includes fluid resuscitation, octreotide, and prophylactic antibiotics. Antibiotic prophylaxis (e.g., IV ceftriaxone for seven days) lowers mortality and reduces the risk of rebleeding and infectious complications. Further management of suspected esophageal variceal bleeding involves upper endoscopy within 12 hours of initial presentation to confirm the diagnosis and perform variceal band ligation.

Question 52

Why do we do TIPS procedures?

Answer 52

Transjugular intrahepatic portosystemic shunt; alleviates adverse effects of portal hypertension that are not well-controlled by pharmacological or endoscopic therapy. Recurrent esophageal variceal hemorrhage resulting from portal hypertension is an indication for TIPS placement.

Question 53

In a cirrhotic patient who underwent TIPS, increasing confusion, irritability, and an altered sleep-wake cycle, as well as a below-average performance in the number connection test, should raise suspicion for…………..

Answer 53

In a cirrhotic patient who underwent TIPS, increasing confusion, irritability, and an altered sleep-wake cycle, as well as a below-average performance in the number connection test, should raise suspicion for hepatic encephalopathy (HE). Constipation can be a precipitating factor for HE.

Question 54

How do we treat hepatic encephalopathy?

Answer 54

In addition to supportive care and correction of precipitating causes, the first-line treatment for acute HE consists of lactulose because of its efficacy, availability, and relatively low cost. Lactulose improves HE by decreasing the absorption of ammonia in the bowel. This effect occurs via multiple mechanisms, including a laxative effect that may help resolve constipation (a trigger for HE, as seen in this patient), reduction of the pH in the lumen of the bowel, which decreases the amount of ammonia absorbed into the plasma, and displacement of ammonia-producing bacteria. Rifaximin is used as a second-line or adjunct treatment for HE that has not improved after 48 hours on first-line therapy.

Question 55

A somatostatin analog that inhibits growth hormone secretion and causes splanchnic vasoconstriction (via decreased secretion of vasodilatory peptides such as glucagon). Used to treat acromegaly, some neuroendocrine tumors, secretory diarrhea, and acute variceal bleeding. Radiolabelled octreotide can be used to localize neuroendocrine tumors with somatostatin receptors.

Answer 55

ocretide

Question 56

jaundice and a nontender, palpable gall bladder

Answer 56

Courvoisier sign, this should raise suspicion for a pancreatic malignancy

Question 57

Which of the following confers the greatest risk for pancreatic carcinoma:
diet
alcohol use
smoking
Diabetes

Answer 57

SMOKING

Cigarette smoking significantly increases the risk of pancreatic cancer. Smoking accounts for about 25% of all cases and it is considered the most significant environmental contributing factor.

Question 58

Hepatorenal syndrome

Answer 58

Kidney injury in patients with cirrhosis. May be further differentiated into acute kidney injury (HRS-AKI) and non-acute kidney injury (HRS-NAKI). Patients with HRS have a poor prognosis and a liver transplant is the only curative treatment. seen in DECOMPENSATED LIVER CIRRHOSIS

As portal hypertension worsens in patients with decompensated cirrhosis, vasodilatory mediators are produced, leading to vasodilation of the splanchnic circulation. The altered hemodynamics result in renal hypoperfusion, which in turn causes a decrease in GFR. Patients typically present with gradual loss of kidney function, as seen in this patient who developed oliguria over a period of 1 month, an unremarkable urine sediment, and fractional excretion of sodium (FENa) < 1% and BUN/Cr ratio > 20. Treatment of this condition includes administration of albumin, octreotide, and midodrine. A liver transplant is the only curative option in advanced liver disease.

Question 59

When do we use CT and when do we use US in the assesment of pancreatitis?

Answer 59

ACUTE=US
CHRONIC=CT

Question 60

What are first line pharmacotherapy for prophylaxis in patients with nonbleeding varices?

Answer 60

Nonselective beta blockers (e.g., nadolol, propranolol) are the first-line pharmacotherapy for primary prophylaxis in patients with nonbleeding varices. These agents cause splanchnic vasoconstriction, which decreases portal blood flow and portal pressure, thereby preventing further enlargement of varices and reducing the risk of hemorrhage. Endoscopic band ligation is an alternative measure for primary prophylaxis that can be considered in individuals with medium or large varices and/or in those who do not respond well to treatment with beta blockers.

Question 61

signs of cirrhosis plus a fever should make you think of…

Answer 61

spontaneous bacterial peritonitis

Question 62

49-year-old man comes to the physician because of tender, red nodules that appeared on his chest 3 days ago. Three weeks ago, he had similar symptoms on his right lower limb and another episode on his left foot; both episodes resolved spontaneously. He also has intermittent diarrhea and has had a poor appetite for 1 month.

Answer 62

This sounds like trousseau syndrome which is the preamble to possible pancreatic or bronchial malignancy

Question 63

What are the most accurate diagnosic tests for primary sclerosing cholangitis, primary biliary cholangitis, and autoimmune hepatitis?

Answer 63

PSC: MRCP
PBC: liver bx
Autoimmune Hep: liver bx

Question 64

Answer 64

Echinococcosis

Transverse CT abdomen

A single hypodense septated cyst in the right lobe of the liver (red overlay) can be seen. The cyst is most likely due to Echinococcus granulosus. “Hyatid cyst”

Question 65

When you hear ‘cystic lesion’ or ‘liver abscess’ what differential should you start thinking about?

Answer 65

If its a cystic anechoic lesion, consider something like a hyatid cyst/eichonococcal disease, amebic liver abscess, or pyogenic liver abscess.

Something that has mixed echogenicity and is not like definitely cystic, begin to think adenoma, carcinoma…etc

Question 66

RUQ US: Whats your diff?

Answer 66

perhaps a hyatid cyst, amebic syst, or pyogenic liver abscess

Question 67

treatment of choice for acute cholangitis

Answer 67

Biliary drainage via endoscopic retrograde cholangiopancreatography (ERCP)

Question 68

What is our managment for focal nodular hyperplasia?

Answer 68

Recall FNH is likely seenin a woman age 20-50, a central hypoattenuated scar on a CT scan, which is diagnostic of focal nodular hyperplasia (FNH).

Best move is reassurance and obsercation

Question 69

Why should patients on OCPs w/ a hepatic adenoma d/c their ocp?

Answer 69

patients on OCPs with hepatic adenomas are at an increased risk of hemorrhage and, for this reason, should discontinue OCP therapy.

Question 70

An abnormal communication between the lumen of the gallbladder (cholecystoenteric) or common bile duct (choledochoenteric) and the lumen of the bowel (usually stomach or duodenum) that can lead to large gallstones entering the bowel, resulting in gallstone ileus.

Answer 70

cholecystoenteric fistula

Question 71

appear as saccular or fusiform dilations of the biliary tree or as dilated masses that communicate with the biliary tree

Answer 71

Biliary cysts

Question 72

What antibodies are sensitive/specific to primary biliary cholangitis?

Answer 72

Antimitochondrial antibodies (AMAs) are highly sensitive and specific for PBC and are found in ≥ 95% of individuals with the condition. Apart from AMAs, antinuclear antibodies (ANAs) can also be found in patients with PBC.

Question 73

What tumor marker is elevated in HCC?

Answer 73

AFP!!!!

Question 74

What is a common complication of primary biliary cholangitis?

Answer 74

Osteoporosis often accompanies PBC, dual-energy x-ray absorptiometry should be conducted to determine a baseline of bone density.