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Gastro > Gallbladder And Bile Ducts > Flashcards

Gallbladder And Bile Ducts Flashcards

1
Q

Causative agents of emphysematous cholecystitis

A

Anaerobes
- C Welchii/ perfringens
Aerobes
- E. coli

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2
Q

Complications of cholecystitis

A

Empyema and hydrops
Gangrene and perforation
Fistula formation and gallstone ileus
Limey and porcelain GB

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3
Q

What is mirizzi syndrome

A

Gallstone becomes impacted in the cystic duct or neck of GB causing compression of CBD resulting in CBD obstruction and jaundice

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4
Q

Gallstone dissolution should be limited to:

A

Radiolucent stones smaller than 5 mm in diameter

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5
Q

Dose of UDCA for gallstone dissolution

A

10-15 mg/kg/day

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6
Q

The most specific And characteristic symptom of gallstone disease

A

Biliary colic
Pain severe intensity 30 min to 5 h
Steady

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7
Q

What are the type of gallstones detected by PFA to be radioopaque

A

10-15% cholesterol

50% pigment stones

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8
Q

Material of LOW echogenic activity that forms later in most dependent portion of GB

A

Bile sludge

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9
Q

Composition of pigment stones and where conditions where you see them

A 
Black pigment:
Calcium bilirubinate
Calcium and mucin glycoproteins
(Chronic hemolytic states, liver cirrhosis, Gilbert's, cystic fibrosis)
Brown pigment:
Calcium salts of unconjugated bilirubin
(Infection)
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10
Q

Mechanisms in the formation of lithogenic bile

A
  1. Increased biliary secretion of cholesterol
  2. Nucleation of cholesterol mono hydrate crystals
  3. Gallbladder hypomotility
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11
Q

Major factor controlling the evacuation of GB

A

Cholecystokinin

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12
Q

Total basal secretion of hepatic bile

A

500-600 ml per day

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13
Q

Major solute components of bile

By moles percent

A

Bile acids 80%
Lecithin and traces of phospholipids 16%
Unesterified cholesterol 4%

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14
Q

2 conditions assoc with cholesterol Stone or biliary sludge formation

A

Pregnancy (marked inc in cholesterol saturation of bile during 3rd trimester and sluggish GB contraction)
Rapid weight reduction through a low calorie diet

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15
Q

Primary bile acids

A

Cholic acid

Chenodeoxycholic acid

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16
Q

What is murphy’s sign

A

Subcostal palpation of RUQ produces increased pain and inspiratory arrest

17
Q

Triad of acute cholecystitis

A

RUQ tenderness
Fever
Leukocytosis

18
Q

Abnormal deposition of lipid, esp cholesteryl eaters within macrophages in the lamina propia of the GB wall

A

Cholesterolosis

19
Q

Diffuse form of Cholesterolosis

A

Strawberry GB

20
Q

Bilirubin levels where CBD stones should be suspected

A

> 5 mg/dL

If >20 mg/dL the possibility of neoplastic obstruction should be entertained

21
Q

Electrolytes that are reabsorbed through the gallbladder epithelium, thereby making bile more concentrated

A

Cl

HCO3

22
Q

Rate limiting enzyme of hepatic cholesterol synthesis

A

HMG CoA reductase

23
Q

The most impt mechanism in the formation of stone forming bile is increased biliary secretion of cholesterol. But this is not sufficient to cause stone in itself. So what else does?

A 
Nucleation of cholesterol monohydrate crystals. 
Pro nucleation 
- mucous glycoproteins S
- heat labile proteins
- immunoglobulins
- pigment particles

Anyinucleation:

  • apolipoproteins
  • lecithin vesicles
24
Q

What are the 2 abnormalities implied by a crescent layer in the most dependent portion of the gallbladder?

A

BILIARY SLUDGE

  1. Normal balance between gallbladder mucin secretion and elimination has become deranged
  2. Nucleation of biliary solutes has occurred
25
Q

Component biliary sludge

A

Cholesterol

Calcium bilirubinate

26
Q

Prophylactic cholecystectomy

A
  • large stones > 3 cm

- gallstones in congenitally anomalous GB

27
Q

Diagnosis patients presenting with biliary colic post operatively

A

Cystic duct stump syndrome
Papillary dysfunction, papillary stenosis, spasm of the sphincter of Oddi
Biliary dyskinesia

28
Q

5 criteria used to define papillary stenosis

A
  1. Upper bad pain usually RUQ
  2. Abnormal liver tests
  3. Dilatation of the CBD upon Ercp exam
  4. Delayed drainage of contrast material from the duct
  5. Increased basal pressure of the sphincter of Oddi
29
Q

Medical treatment dyskinesia of sphincter of Oddi

A

Nitrites

Anti cholinergics

30
Q

Progressive inflammatory sclerosing and obliterating process affecting extrahepatic and intrahepatic ducts

A

Primary sclerosing cholangitis

75% assoc with IBD mostly ulcerative colitis

Gastro (9 decks)

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