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Gastro > GB and Biliary Tree Diseases (Nichols/Tomb) > Flashcards

GB and Biliary Tree Diseases (Nichols/Tomb) Flashcards

1
Q

Function of bile acids in bile?

A

solubilization of cholesterol

Modulation of Intestinal motility

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2
Q

Function of phospholipid in bile?

A

Solubilization of cholesterol

Protection of bile duct epithelium

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3
Q

Function of IgA and IgM in bile?

A

bacteriostasis

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4
Q

Function of mucus in bile?

A

prevention of bacterial adhesion

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5
Q

Function of glutathione in bile?

A

induction of bile flow

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6
Q

Most frequent type of gallstones?

A

Pured and mixed cholesterol stones

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7
Q

What are pure and mixed cholesterol stones comprised of?

A
  • Monohydrate cholesterol crystals
  • Matrix of mucin glycoprotein
  • Ca salts of unconjugated bilirubin
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8
Q

What are brown pigmented stones comprised of?

A

Ca salts
deconjugated bilirubin
cytoeskeleton of bacteria

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9
Q

Brown pigmented stones most commonly occur in patients with:

A

previous srx

duodenal diverticula

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10
Q

Black pigmented stones most commonly occur in patients with:

A

liver disease, hemolysis, older age

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11
Q

What are black pigmented stones comprised of?

A
  • -Pure Ca bilirubinate
  • -calcium copper
  • -mucin glycoprotein
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12
Q

How does age cause cholesterol hypersecretion?

A

age-related decr in 7-alpha-hydroxylase

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13
Q

How does estrogen cause cholesterol hypersecretion?

A

Increased cholesterol uptake (Increased lipoprotein receptors B and E)

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14
Q

How does obesity cause cholesterol hypersecretion?

A

Incr cholesterol synthesis

increase HMG coA activity

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15
Q

How does progesterone cause cholesterol hypersecretion?

A

Increased free cholesterol

Inhibitor of AcoA CAT, Decreased conversion of cholesterol to cholesteryl ester stores

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16
Q

Bile acid Synthesis: The rate-limiting enzyme is :

A

7-alfa hydroxylase

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17
Q

How does marked weight reduction cause cholesterol hypersecretion?

A

Mobilization of tissue cholesterol

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18
Q

How does ileal disease/resection/bypass cause cholesterol hypersecretion?

A

Impaired bile acid absorption or excessive losses

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19
Q

What is “supersaturated” bile?

A

Bile that has a CSI greater than 1, which means the amt of cholesterol exceeds the max holding capacity of micelle

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20
Q

What are vesicles?

A

very large carriers of cholesterol, which do NOT contain bile salts

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21
Q

Multilamelar vesicles permit:

A

crystal formation

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22
Q

What is crystal formation?

A

Aggregation process by which a crystal particle is formed from supersaturated bile

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23
Q

How are crystals generated?

A

vesicular fusion and aggregation

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24
Q

What changes in bile composition enhance crystal formation?

A

high cholesterol saturation and an increased deoxycholate content

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25
Q

5 Factors which inhibit crystal formation:

A
  1. low total lipid conc
  2. decr cholesterol saturation
  3. biliary proteins not binding Con-A
  4. Apolipoprotein A-I and A-II
  5. Ig
26
Q

How does gallbladder emptying relate to gallstone formation?

A

delay in gallbladder emptying

= gallstone

27
Q

4 GB-related abn that are risk factors for gallstones:

A
  1. Defective acidification of gallbladder bile
  2. > pH higher ppt of Ca salts
  3. GB stasis can cause incr mucin, which interferes w/ mechanical emptying
  4. Decr response to CCK
28
Q

Cholesterol gallstone pathogenesis:

A

Hepatic chol hypersecretion causes:

  1. GB hypomotility
  2. mucin hypersecretion
  3. chol gallstone formation

Incr intestinal conversion to deoxycholate,

  1. directly causes GS formation
  2. hepatic chol hypersecretion
29
Q

Risk factors for black pigment stone formation:

A

Hemolysis
Advancing age
Long term TPN
Cirrhosis

30
Q

GB-related risk factors for black pigment stone formation

A
  1. decreases in bilirubin solubilizers
  2. GB stasis
  3. incr bilirubin secretion
31
Q

Causes of brown pigment stones?

A
  1. Bacterial infection
  2. Decreasing biliary secretory IgA
  3. High activity of B-glucuronidase
32
Q

Pathophysiology of brown pigment gallstone formation:

A
  1. bacterial degradation of biliary lipids (into free bile acids, free FA, unconj bilirubin)
  2. Ca ppt, bacterial glycoproteins, cholesterol form stones
33
Q

Cholelithiasis has a high prevalence rate in ___ countries, and a low prevalence rate in ___ countries.

A

Latin Am

Asian

34
Q

Pt risk factors associated with cholesterol gallstones?

A

Fat
Female
Forty
Fertile (hormones +pregnancy)

also: Rapid weight reduction; Gallbladder stasis; Inborn disorders of bile acid metabolism; Hyperlipidemia syndromes

35
Q

Pt risk factors associated with pigment gallstones?

A 
Asian > Western
rural > urban
Chronic hemolytic syndr
Biliary infection
GI disorders: ileal disease (e.g., Crohn disease), ileal resection or bypass, CF with pancreatic insufficiency
36
Q

Clinical Manifestation of Biliary colic:

A

abd pain

37
Q

Clinical Manifestation of Acute Cholecystitis:

A

abd pain

fever

38
Q

Clinical Manifestation of Choledocholithiasis with Cholangitis:

A

abdominal pain
fever
jaundice

39
Q

Clinical Manifestation of Biliary pancreatitis:

A

abdominal pain, increased amylase

40
Q

most sensitive test for the diagnosis of gallstone?

A

abd US

41
Q

radiologic finding highly suggestive of acute cholecystitis?

A

presence of air at the gallbladder wall

“Emphysematous cholecystitis”

42
Q

Common findings in acute cholecystitis?

A

gallbladder is usually enlarged + tense

90% of cases = stones present (obstructing neck of GB or cystic duct)

acute inflammation

43
Q

Possible findings in chronic cholecystitis?

A

GB may be contracted, normal size, or enlarged

fibrosis, mural lymphocytes

44
Q

Intrahepatic causes of Cholestasis?

Extrahepatic causes of Cholestasis?

A

PBC, drugs, malignancy, etc

Stones

45
Q

Benign causes of mechanical cholestasis?

A

Post-surgical complications

Primary sclerosing cholangitis

Infections

Chronic pancreatitis

46
Q

How do pts present w/ Post liver transplantation biliary stricture?

A

cholestatic pattern of liver enzymes (high alkaline phosphatase, GGT, etc)

47
Q

Epidemiology for Primary Sclerosing cholangitis?

A

M>F

80% of pts have IBD

48
Q

What is Primary Sclerosing cholangitis?

A

Chronic cholestatic disease of the intrahepatic and extrahepatic bile ducts

onion skin bile duct fibrosis with alternating strictures and dilation

49
Q

Patients with Primary Sclerosing cholangitis are at an incr risk for developing:

A

bile duct malignancy (cholangiocarcinoma)

50
Q

Primary Sclerosing cholangitis: Clinical presentation?

What does this resemble radiologically?

A

symptoms of chronic cholestasis (jaundice, dark urine, light stool, hepatosplenomegaly)

HIV cholangiopathy

51
Q

Trx for Primary Sclerosing cholangitis?

A

liver transplantation

52
Q

Clinical presentation of chronic pancreatitis?

A

cholestatic pattern of liver enzymes in the presence of chronic pancreatitis

53
Q

Trx of chronic pancreatitis?

A

biliary stent placement and/or surgery

54
Q

Clinical presentation of Hemobilia?

A

jaundice, melena and abdominal pain

55
Q

How does GB-related malignancy present?

A

progressive painless jaundice and weight loss

56
Q

What locations of malignancies cancause cholestasis?

A
  • Ampullary
    • Gall-bladder
    • Bile ducts
    • Pancreatic
57
Q

Epidemiology of Cholangiocarcinoma?

A

men at 50-70 years old

58
Q

Risk factors for Cholangiocarcinoma?

A

Primary sclerosing cholangitis, Hepatitis C related cirrhosis, toxin exposure, infection with liver flukes (clonorchis)

59
Q

Presentation of Cholangiocarcinoma?

A

biliary obstruction causing painless jaundice

incr total bilirubin, alk phos, 5’-nucleotidase + GGT

incr tumor marker Ca 19-9

60
Q

Presentation of pancreatic cancer w/ GB obstr?

A

progressive painless jaundice and weight loss

61
Q

MC cause of biliary obstruction by malignancy?

A

pancreatic

Gastro (25 decks)

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