Gall Bladder and Pancreas MCQs

(a, b, c) Chronic pancreatitis is characterized by parenchymal fibrosis, acinar atrophy and dropout, and variable ductal dilation. (d) In acute necrotizing pancreatitis, acini, ducts, and even islets undergo necrosis. In the most severe form, hemorrhagic pancreatitis, extensive parenchymal necrosis is accompanied by intraparenchymal hemorrhage due to vascular injury. Reference: Robbins & Cotran Pathologic Basis of Diseases 10 th edition Chapter 18, pg 882

All of these are features of chronic cholecystitis.

In acute cholecystitis, the gallbladder usually is enlarged and tense, and has a bright red or blotchy, violaceous colour, the latter imparted by subserosal hemorrhages. The serosa frequently is covered by a fibrinous or, in severe cases, a fibrinopurulent exudate. In 90% of cases, stones are present, often obstructing the neck of the gallbladder or the cystic duct. The gallbladder lumen is filled with cloudy or turbid bile that may contain fibrin, blood, and pus. When the contained exudate is mostly pus, the condition is referred to as empyema of the gallbladder. In mild cases, the gallbladder wall is thickened, edematous, and hyperemic. In more severe cases, the gallbladder wall is green-black and necrotic-a condition termed gangrenous cholecystitis. Reference: Robbins Basic Pathology, 10 th ed, Pg-674

Pancreatic pseudocyst is a poorly defined cyst with a necrotic brownish wall. Histologically, the cyst lacks an epithelial lining and instead is lined by fibrin and granulation tissue, with typical changes of chronic inflammation. Signs and symptoms of pancreatic pseudocyst include abdominal pain, nausea, vomiting and bloating. Diagnosis of pancreatic pseudocyst can be based on cystic fluid analysis. Complications of pancreatic pseudocyst include infection, hemorrhage, obstruction and rupture. Pseudo cysts typically arise following a bout of acute pancreatitis, particularly one superimposed on chronic alcholic pancreatitis. Reference: Robbins Basic Pathology, 10 th edition, Pg-684

Pancreas divisum is the most common congenital anomaly of the pancreas. More than 95% of individuals are asymptomatic. The remaining 5% develop acute or chronic pancreatitis, possibly related to inadequate drainage of pancreatic secretions through the minor papilla. Reference: Robbins Basic Pathology, 10 th edition, Pg-680

The recent sequencing of the pancreatic cancer genome has confirmed that four genes are most commonly affected by somatic mutations in this neoplasm: KRAS, CDKN2A/ p16, SMAD4, and TP53: KRAS is the most frequently altered oncogene in pancreatic cancer; it is activated by a point mutation in greater than 90% of cases. Cdkn2a (chromosome 9p ) is inactivated in 30% of pancreatic cancers through point mutations or homozygous deletions Reference: Robbins Basic Pathology, 10 th edition, Pg-687

Migratory thrombophlebitis (Trousseau syndrome) occurs in about 10% of patients and is attributable to the elaboration of platelet-aggregating factors and pro-coagulants from the tumour or its necrotic products. Murphy's sign is elicited in patient with acute cholecystitis. Reference: Robbins Basic Pathology, 10 th edition, Pg-686-689

Autoimmune pancreatitis is a pathogenically distinct form of chronic pancreatitis that is associated with the presence of IgG4-secreting plasma cells in the pancreas. Autoimmune pancreatitis is one manifestation of IgG related disease, which may involve multiple tissues. It is important to recognize because it responds to steroid therapy. Reference: Robbins Basic Pathology, 10 th edition, Pg-683-84