d. Right hepatic and gastroduodenal arteries
Rationale: The common bile duct receives its blood supply primarily from the right hepatic artery (superior portion) and the gastroduodenal artery (inferior portion). These anastomose along the duct, ensuring a dual supply.
b. Cholecystokinin (CCK)
Rationale: CCK is released from the duodenum in response to fats and proteins, stimulating gallbladder contraction and relaxation of the sphincter of Oddi, allowing bile flow into the duodenum.
d. 95%
Rationale: Bile acids are extensively reabsorbed in the ileum via active transport (Na⁺-dependent bile acid transporter), with only 5% excreted in feces—a key step in the enterohepatic circulation.
c. A primary inflammatory process with occasional bacterial contamination
Rationale: Acute cholecystitis is caused by cystic duct obstruction (usually from gallstones), leading to bile stasis, mucosal injury, and inflammation. Secondary bacterial infection may occur but is not the initiating event.
b. Adenocarcinoma
Rationale: Adenocarcinoma accounts for 85–90% of gallbladder cancers, arising from chronic inflammation (e.g., gallstones, chronic cholecystitis). It has a poor prognosis due to late diagnosis.
b. Endoscopic retrograde cholangiopancreatography (ERCP)
Rationale: ERCP is the best initial test for a suspected postoperative bile leak, as it provides both diagnostic imaging (contrast study of the bile ducts) and therapeutic options (stenting, sphincterotomy).
b. Abdominal pain
Rationale: Biliary injury postoperatively often presents with abdominal pain, bile leakage, or jaundice. Fever can develop if infection occurs, but pain is typically the earliest symptom.
d. Laparoscopic cholecystectomy with intraoperative cholangiography
c. The gallbladder concentrates the bile to reduce its volume
b. Reabsorption of bile pigments by the gallbladder mucosa
d. Ascending cholangitis
Rationale: Charcot’s triad (fever, jaundice, RUQ pain) is highly suggestive of ascending cholangitis, a life-threatening biliary infection often caused by obstruction (e.g., CBD stones), leading to bacterial overgrowth and systemic infection.
a. Ascending cholangitis
Rationale: Charcot’s triad (fever, jaundice, RUQ pain) is classic for ascending cholangitis, a biliary tract infection due to obstruction (often from choledocholithiasis).
a. 2-3 minutes
Rationale: Cholecystokinin (CCK) has a short half-life (2-3 minutes), ensuring rapid regulation of gallbladder contraction and bile secretion in response to meals.
b. In 1-3 days
Rationale: Early laparoscopic cholecystectomy (within 72 hours) is preferred for acute cholecystitis to reduce complications and shorten hospital stay. Delayed surgery increases the risk of recurrent attacks.
c. Brown pigment stones
Rationale: Choledochal (bile duct) stones are usually brown pigment stones, formed due to biliary stasis and infection, with calcium bilirubinate and bacterial debris as key components.
c. Lecithin
Rationale: Lecithin (phosphatidylcholine) is a major component of gallstones, along with cholesterol and bile salts. A deficiency in lecithin can promote gallstone formation.
b. Cholecystokinin (CCK)
Rationale: CCK is the primary hormone that stimulates gallbladder contraction, triggered by the presence of fats and proteins in the duodenum.
b. Laparoscopic cholecystectomy and intraoperative cholangiography
b. Lack of muscularis mucosae and submucosa
Rationale: Unlike the rest of the gastrointestinal tract, the gallbladder lacks a muscularis mucosae and submucosa, which makes it more prone to perforation in inflammation.
a. Porcelain gallbladder
Rationale: Porcelain gallbladder (intramural calcification) is a strong risk factor for gallbladder cancer, warranting prophylactic cholecystectomy.
a. Common channel theory
Rationale: The common channel theory explains gallstone-induced pancreatitis, where an impacted stone at the ampulla of Vater causes reflux of bile into the pancreatic duct, leading to pancreatic inflammation.
c. Acute viral infections.
🔹 Rationale: Splenectomy is not indicated for acute viral infections, as most resolve spontaneously. Common indications include:
Myeloproliferative disorders (e.g., myelofibrosis, CML)
RBC disorders (e.g., hereditary spherocytosis, sickle cell disease)
Platelet disorders (e.g., ITP, TTP)
a. Stimulates phagocytic function.
🔹 Rationale: Tuftsin is a tetrapeptide produced in the spleen that enhances phagocytosis by neutrophils and macrophages, aiding immune defense.