Q6. Which of the following prevents infection in sterile necrosis of pancreas
a) Antibiotics
b) Enteral feeding
c) Ryles tube aspiration
d) Aggresive debridement
Q7. Which of the following is not true pancreatic cysts?
a) Associated with Von Hippel-Lindau Disease in 50%
b) It is associated with cysts of liver and kidney
c) Most go on to be associated with chronic pancreatitis
d) Pancraetic cysts are very rare.
Q8. Which of the following genetic modification does not ocur in Carcinoma Pancreas
a) Activation of kras oncogene
b) Mutation of p53 oncogene
c) BRCA 2 mutation
d) Under expression of EGFR receptors
Q9. Most common site for Carcinoma Pancreas is
a) Head
b) Body
c) Tail
d) Diffuse
Q10.What is false about Intrapapillary mucinous neoplasm of pancreas.
a) It is more common in the head of pancreas.
b) Diagnosis is made when mucus is seen extruding through the papillary orifice.
c) Columnar epithelium lines the walls and form papillary projections.
d) They dont follow an adenoma carcinoma sequence
Answers
6 a
Septic complications occurring after the first 10 to 14 days of the disease are the most frequent cause of death in patients with pancreatic necrosis.
When necrotic areas become infected by enteric germs, the prognosis of a patient deteriorates.
Mortality rates in infected necrosis are reported to be between 15 and 25%.
The rate of infected pancreatic necrosis correlates closely with the amount
of necrotic parenchyma in the retroperitoneum and therefore patients with
subtotal to total necrosis of the gland have the highest risk of experiencing
a fatal course.
In contrast, sterile pancreatic necrosis has a better
prognosis with lower mortality rates (between 5 and 10%).
As a consequence, the discrimination between sterile pancreatic necrosis and
infected pancreatic necrosis is one of the main staging principles of the
current treatment guidelines.
Antibiotics especially Imipenams have a role in preventing infections.
7 c
Solitary cysts of the pancreas are rare. In contrast, multiple pancreatic cysts, lined with cuboidal epithelium, are more common. They are frequently associated with polycystic disease of the liver and/or kidney, and they can be seen in up to half of patients with von Hippel-Lindau syndrome.
Pancreatic cysts only rarely become symptomatic and, in general, no treatment is indicated.
8. d
In Pancraetic cancers the following genetic abnormailities are seen
Activation of growth-promoting oncogenes like kras
Mutations that result in the inactivation of tumor suppressor genes(p53, p16, SMAD, DCC. DPC, MMR genes)
Excessive expression of growth factors and/or their receptors (EGFR,HER2, HER3, HER4)
Pancreatic cancer has been observed to be increased in families with hereditary nonpolyposis colon cancer (HNPCC), those with familial breast cancer (associated with the BRCA2 mutation), those with Peutz-Jeghers syndrome, those with ataxia-telangiectasia, and those with the familial atypical multiple mole melanoma (FAMMM) syndrome.
9. a
Ductal adenocarcinoma and its variants account for 80% to 90% of all pancreatic neoplasms and for an even greater fraction of the malignant tumors. Roughly 70% of ductal cancers arise in the pancreatic head or uncinate process.
10. d
It can be located in any or all parts of the pancreas, although involvement of the head appears to be its most common form. IPMT patients can experience pancreatitis when mucus, secreted by the tumor, transiently obstructs the orifice of the pancreatic duct. The diagnosis of IPMT can be made with near certainty if mucus is seen extruding through a large, fish-mouth orifice.
IPMT is believed to follow an adenoma-carcinoma sequence, and it can be classified according to the Pan-IN classification scheme ( that categorizes tumors as having minimal or no dysplasia (PanIN-1), moderate dysplasia (PanIN-2), or severe dysplasia/carcinoma in situ (PanIN-3) The natural history of tumors with only mild or no dysplasia is not known, but those with severe dysplasia and/or carcinoma in situ are likely to become locally invasive and metastasize if left unresected.
