Hepatopancreaticobiliary Flashcards
What are the main risk factors for developing cholesterol gallstones?
4 “F”s: Fat Fertile Female over Fourty.
Female gender, pregnancy, oral contraceptive use (excess estrogen leads to higher cholesterol in bile and decreased gallbladder motility) as opposed to obesity (decreases bile salts), high-fat diet (increases bile cholesterol), hereditary (higher incidence in Hispanics, Pima Indians), Crohn’s disease and terminal ileal resection (loss of bile salts), and rapid weight loss after gastric surgery (impaired gallbladder emptying).
What Is the Significance of RUQ Pain Combined with Scapular Pain?
The gallbladder and the scapula share the same cutaneous dermatome from the same spinal cord levels. The scapula receives cutaneous innervation from the supraclavicular nerves. Since the same spinothalamic pathways (pain and temperature) are activated, gallbladder distention/inflammation triggers scapular pain via the phrenic nerve.
Murphy’s Sign
Patient inspiration stopping with RUQ palpation. Represents focal peritonitis of the anterior abdominal wall parietal peritoneum due to inflammation of the adjacent gallbladder.
Asymptomatic colelithiasis
Gallstones in the gallbladder. Does not require surgery.
Symptomatic colelithiasis.
Gallstones periodically block the cystic duct, causes RUQ pain especially after fatty foods. Pain dissipates after a few hours. Can be treated with elective cholecystectomy.
Acute cholecystitis
Gallstone blocked cystic duct leading to infection. Unremitting RUQ pain >6hrs assc. w/ nausea & vomiting, Murphy’s sign, fever, tachycardia, elevated WBC. Dx pericholecystic fluid, gallbladder wall thickening >0.4 cm, sonographic Murphy’s sign. Tx w/ urgent cholecystectomy.
Typical organisms in the bile assc. w/ acute cholecystitis
Escherichia coli , Bacteroides fragilis, Klebsiella, Enterobacter, Enterococcus, and Pseudomonas species
Three components of bile
Cholesterol, bile salts, lecithin
Two main types of gallstones
Cholesterol (70-80% in USA) and pigment
How do cholesterol gallstones form?
When the concentration of cholesterol in the bile exceeds its solubility, which causes precipitation of cholesterol crystals.
How to pigmented gallstones form?
Black stones are often assc. w/ hemolytic disease such as hereditary spherocytosis or sickle cell disease. Breakdown of RBCs leads to a rise in unconjugated bilirubin, leading to the formation of black stones. Black stones are most often found within the gallbladder. Brown stones , in comparison, most often form within
the bile ducts. They are larger and softer than black stones and usually are associated with bacterial infection and parasites. They are more common in Asian countries.
Choledocolethiasis
Obstruction of the common bile duct. Will see LFTs elevated, particularly Alk Phos.
What is the first diagnostic workup test for gallstones?
RUQ Ultrasound
Emphesymatous cholecystitis
Wccurs when the gallbladder becomes infected with gas-forming organisms (e.g., clostridium) and represents a clinical scenario much like a necrotizing soft tissue infection. Common in older men, often with diabetes mellitus. Can cause gallbladder perforation, intra-abdominal abscess, sepsis, and death. Tx emergency cholecystectomy.
Gallstone ileus
A large gallstone passed through a cholecystoduodenal fistula and lodged itself in the iliocecal junction, causing a SBO.
Liver panel tests ordered with any RUQ or epigastric pain
Total and direct bilirubin, aspartate (AST) and alanine (ALT) aminotransferase, alkaline phosphatase (AP), and gamma-glutamyltransferase (GGT)
HIDA scan
Radiolabeled hepatic iminodiacetic acid is given intravenously, and then imaging is performed. This compound is absorbed by hepatocytes and excreted into bile, seen within 30–60 min in the gallbladder, bile ducts, and small bowel in a normal patient. If the cystic duct is obstructed, as in acute cholecystitis, no contrast will be seen within the gallbladder, and the HIDA scan is
positive.
What antibiotics are given in cases of cholecystitis?
Second-generation cephalosporins (e.g., cefoxitin) are considered first line. An alternative would be broad-spectrum penicillin/β-lactamase inhibitors such as piperacillin/tazobactam or ampicillin/sulbactam.
Major complication of Laparoscopic Cholecystectomy, and how is it repaired?
CBD injury. If the injury involves greater than 50 % of the circumference of the bile duct, then a loop of jejunum has to be brought up and anastomosed to the proximal end of the bile duct (Roux-en-Y hepaticojejunostomy). If primary repair is attempted, it will inevitably form an ischemic stricture.
Postcholecystectomy syndrome
Recurrent RUQ/epigastric pain weeks after cholecystectomy. May be caused by obstruction due to residual gallstones in CBD or cystic duct stump, dysfunction of biliary tree, gastritis, or peptic ulcer disease.
When do you want to perform a cholecystectomy in the case of acute cholecystitis?
First 48 hours
Cholangitis
Choledocolithiasis that leads to ascending infection of the biliary tract. Will see Charcot’s triad or Reynold’s Pentad. Tx with ERCP, and follow up with cholecystectomy.
Conservative treatment for cholelithiasis
Ursodeoxycholic acid
Calcified gallbladder
Higher risk of malignancy. Perform cholecystectomy.
Choledochal cysts
Congenital dilations of the biliary tree; prone to cholangitis, risk of associated malignancy, need to excise (if intrahepatic ducts are involved (Caroli’s disease)), and may need liver transplantation
Gallbladder polyps: relate size to malignancy probability
> 1 cm suspicious for cancer; >2 cm high likelihood of cancer
Charcot’s triad
RUQ pain, jaundice, fever. Found in 40-50% of pts with cholangitis.
Reynold’s Pentad
Charcot’s triad + hypotension and altered mental status (AMS). Presents in 5% of patients with cholangitis.
Diagnostic criteria for cholangitis
Tokyo guidelines; systemic inflammation (fever and/or leukocytosis), cholestasis (jaundice and/or abnormal liver enzymes), and biliary obstruction (dilated bile ducts on ultrasound).
Pale stools
Result of prolonged biliary obstruction: will see them after a long time, not in sudden onset of cholestasis.
At what level of bilirubin is jaundice first visible?
Jaundice will be visible at total bilirubin level > 2.5 mg/dL. Normal total bilirubin level is up to 1.0 mg/dL
How do you distinguish intrahepatic from posthepatic jaundice?
Hepatic jaundice: AST and ALT can reach into the thousands, out of proportion to the ALP (indicates hepatocellular damage)
Posthepatic jaundice: A marked rise in ALP, out of proportion to the AST and ALT.
ALP is present in the cells that line the bile ducts. Since ALP levels increase with many other diseases, a concomitant and proportionate rise in GGT is helpful and more specific to liver disease.
