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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
5 Factors which inhibit crystal formation:
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
How does gallbladder emptying relate to gallstone formation?
delay in gallbladder emptying | = gallstone
27
4 GB-related abn that are risk factors for gallstones:
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
Cholesterol gallstone pathogenesis:
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
Risk factors for black pigment stone formation:
Hemolysis Advancing age Long term TPN Cirrhosis
30
GB-related risk factors for black pigment stone formation
1. decreases in bilirubin solubilizers 2. GB stasis 4. incr bilirubin secretion
31
Causes of brown pigment stones?
1. Bacterial infection 2. Decreasing biliary secretory IgA 3. High activity of B-glucuronidase
32
Pathophysiology of brown pigment gallstone formation:
1. bacterial degradation of biliary lipids (into free bile acids, free FA, unconj bilirubin) 2. Ca ppt, bacterial glycoproteins, cholesterol form stones
33
Cholelithiasis has a high prevalence rate in ___ countries, and a low prevalence rate in ___ countries.
Latin Am Asian
34
Pt risk factors associated with cholesterol gallstones?
Fat Female Forty Fertile (hormones +pregnancy) also: Rapid weight reduction; Gallbladder stasis; Inborn disorders of bile acid metabolism; Hyperlipidemia syndromes
35
Pt risk factors associated with pigment gallstones?
``` 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
Clinical Manifestation of Biliary colic:
abd pain
37
Clinical Manifestation of Acute Cholecystitis:
abd pain | fever
38
Clinical Manifestation of Choledocholithiasis with Cholangitis:
abdominal pain fever jaundice
39
Clinical Manifestation of Biliary pancreatitis:
abdominal pain, increased amylase
40
most sensitive test for the diagnosis of gallstone?
abd US
41
radiologic finding highly suggestive of acute cholecystitis?
presence of air at the gallbladder wall | "Emphysematous cholecystitis"
42
Common findings in acute cholecystitis?
gallbladder is usually enlarged + tense 90% of cases = stones present (obstructing neck of GB or cystic duct) acute inflammation
43
Possible findings in chronic cholecystitis?
GB may be contracted, normal size, or enlarged fibrosis, mural lymphocytes
44
Intrahepatic causes of Cholestasis? Extrahepatic causes of Cholestasis?
PBC, drugs, malignancy, etc Stones
45
Benign causes of mechanical cholestasis?
Post-surgical complications Primary sclerosing cholangitis Infections Chronic pancreatitis
46
How do pts present w/ Post liver transplantation biliary stricture?
cholestatic pattern of liver enzymes (high alkaline phosphatase, GGT, etc)
47
Epidemiology for Primary Sclerosing cholangitis?
M>F | 80% of pts have IBD
48
What is Primary Sclerosing cholangitis?
Chronic cholestatic disease of the intrahepatic and extrahepatic bile ducts onion skin bile duct fibrosis with alternating strictures and dilation
49
Patients with Primary Sclerosing cholangitis are at an incr risk for developing:
bile duct malignancy (cholangiocarcinoma)
50
Primary Sclerosing cholangitis: Clinical presentation? What does this resemble radiologically?
symptoms of chronic cholestasis (jaundice, dark urine, light stool, hepatosplenomegaly) HIV cholangiopathy
51
Trx for Primary Sclerosing cholangitis?
liver transplantation
52
Clinical presentation of chronic pancreatitis?
cholestatic pattern of liver enzymes in the presence of chronic pancreatitis
53
Trx of chronic pancreatitis?
biliary stent placement and/or surgery
54
Clinical presentation of Hemobilia?
jaundice, melena and abdominal pain
55
How does GB-related malignancy present?
progressive painless jaundice and weight loss
56
What locations of malignancies cancause cholestasis?
- Ampullary - Gall-bladder - Bile ducts - Pancreatic
57
Epidemiology of Cholangiocarcinoma?
men at 50-70 years old
58
Risk factors for Cholangiocarcinoma?
Primary sclerosing cholangitis, Hepatitis C related cirrhosis, toxin exposure, infection with liver flukes (clonorchis)
59
Presentation of Cholangiocarcinoma?
biliary obstruction causing painless jaundice incr total bilirubin, alk phos, 5’-nucleotidase + GGT incr tumor marker Ca 19-9
60
Presentation of pancreatic cancer w/ GB obstr?
progressive painless jaundice and weight loss
61
MC cause of biliary obstruction by malignancy?
pancreatic

Gastro (25 decks)

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