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  Esophagus

 

 

Q1)All are true for CBD exploration except

a)Transcystic exploration is suited for 6-8 mm stones only

b) It is possible only when cystic duct is parallel to the CBD

c) Cystic duct needs to be diltaed to 10 mm

d) Clearance is possible in 95-98% cases

 

Q2) Regarding MRCP what is not true?

a) Hepatic vein has bright signal

b) Stones appear as enhanced signals

c) Bile duct appears as enhanced signal

d) Portal vein appears as void signal

 

Q3) In shock liver What is incorrect--

a) Liver enzymes are not elevated

b) Centrilobular necrosis is present

c) Infarction occurs after hepatic artery ligation in face of hypoperfusion

d) Asociated with hypoperfusion of liver

 

Q4)Most common cause of Budd Chiari syndrome in India is

a)      Membranous IVC obstruction

b)      Polycythemia

c)      Myeloproliferative disorders

 

Q5)What is not required for formation of cholesterol gallstones

a) Supersaturation of bile

b) Nucleation

c)Gall bladder stasis

d)Infection

 

Answers

 

1)b

All are true except b

Cystic duct needs to be at an angle to the CBD and not parallel to it for instrument insertion and manipulations.

Clearance of all common bile duct stones is achieved in 75% to 95% of patients with laparoscopic common bile duct exploration.

 

2)b

Stones in MRCP appear as a VOID SIGNAL

                          

   MRCP showing a void signal (stone) in the gall bladder and also in     Common hepatic duct

3)a

Hepatic ischemia (Shock liver) is a condition where not enough blood or oxygen gets to the liver. This shortage causes injury to liver cells.

Blood levels of liver enzymes such as AST and ALT typically rise 1-3 days after the episode of low blood pressure. Levels of another enzyme in the blood, LDH, are also usually quite high.

Patients generally recover if the underlying illness can be treated. Death from liver failure as a result of hepatic ischemia is very rare.

 

4) a

In India and asia it is membranous obstruction of the IVC and in the west myeloproliferative disorders

 

5) d

The pathogenesis of cholesterol gallstones involves three stages:

(1) cholesterol supersaturation

(2) crystal nucleation

 (3) stone growth.

The key to maintaining cholesterol in solution is the formation of both micelles, a bile salt-phospholipid-cholesterol complex, and cholesterol-phospholipid vesicles. Present theory suggests that in states of excess cholesterol production, these large vesicles may also exceed their capability to transport cholesterol, and crystal precipitation may occur. Cholesterol solubility depends on the relative concentration of cholesterol, bile salts, and phospholipid.

 

 cholesterol supersaturation results in a metastable state in which cholesterol precipitation may or may not take place and additional factors in bile must be present, therefore, to either enhance or inhibit the nucleation of cholesterol leading to the next stage in gallstone formation

Nucleation refers to the process in which solid cholesterol monohydrate crystals form and conglomerate. Several pronucleating factors including mucin glycoproteins, immunoglobulins, and transferrin accelerate the precipitation of cholesterol in bile.

Infection leads to formation of brown pigment calculi


 

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