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M2 GI > 10. Disorders of GB and Biliary Tract > Flashcards

10. Disorders of GB and Biliary Tract Flashcards

1
Q

Anatomy: what ducts feed into the common bile duct?

A

Right hepatic duct (from liver) Left hepatic duct (from liver) –> join to form the Common hepatic duct (from liver) Cystic duct (from GB)

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2
Q

what joins with the common bile duct before it ends at the duodenum?

A

the pancreatic duct

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3
Q

blood flow to the liver: what arteries supply the liver?

A

Celiac artery ->hepatic artery, which splits into R and L hepatic arteries

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4
Q

what organ receives the blood first? what does it do with that blood?

A

liver receives blood first; filters poisons, toxins and excretes them into bile. bad stuff removed from body that way

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5
Q

what is the portal triad?

A

hepatic artery, portal vein, common hepatic/bile duct

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6
Q

what are the three zones of the liver - what problems will affect them differently?

A

Zone I: portal area. affected first by viral hepatitis, toxic injury

Zone II: in between

Zone III: central vein area: affected first by ischemia, alcoholic hepatitis. Most sensitive to toxic inj.

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7
Q

describe the directions of bile flow and blood flow in the liver

A

Bile: flows from hepatic cells, then is filtered inot the bile duct (portal triad). Bile flows from Zone II/III to Zone I Blood: the other way. From Zone I to Zone III, from portal vein to central vein

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8
Q

name the 4 major components of the biliary tract

A

hepatocytes/canaliculi ductules/ducts gallbladder sphincter of Oddi

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9
Q

function of the hepatocytes/canaliculi?

A

active secretion of bile into the canaliculis

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10
Q

secretion of bile into the canaliculis depends on what (4 factors)?

A

-microvilli -cytoskeleton (has contractile features) -interaction of bile acid with secretory apparatus -permeability of bile canalicular membrane

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11
Q

describe sinusoids

A

irregular capillaries with fenestrated epithelium, no basement membrane. allows macromolecules to have full access to basal surface of hepatocytes through the space of Disse

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12
Q

what is the space of Disse?

A

like a hallway that separates teh endothelial cells of the sinusoid from the basal cells of the sinusoid. allows macromolecules to drop off things they are carrying without actually making contact with the hepatocytes.

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13
Q

what is meant by polar hepatocytes?

A

liver cells have polarity: apical side is oriented towards the canaliculus (bile flows through this) and the basal side is oriented towards the sinusoid (blood flow, space of Disse)

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14
Q

what are gap junctions and how are they impt to the liver?

A

tightly attach hepatic cells to each other; create a physical barrier between the sinusoid space and the caniculus (flow of bile)

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15
Q

what is a canaliculus?

A

canalicular surfaces of adjacent hepatocytes form the bile canaliculus; the flow of bile moves through this on the apical side of hepatocytes.

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16
Q

if hepatocytes are like shelved books in a library, which side is which?

A

the book spines are the basal side; the book opening is the apical side (faces inward and opposes the apical side of other hepatocytes)

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17
Q

list 5 components of bile

A

Bi, Bili, Pho, Cho, Ions

we need to know this

  • bile salts (drive bile flow)
  • phospholipids
  • cholesterol
  • bilirubin
  • ions, water (solvent drag)
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18
Q

what is the only mechanism the body has for cholesterol excretion?

A

loss of bile through the feces

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19
Q

bile acids serve what 2 major roles in the body?

A

-solubilize cholesterol -allow absorption of dietary fat and ADEK vits in the jejunum

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20
Q

bile acids: synthesized where? from what?

A

in liver, from cholesterol

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21
Q

what are the primary bile acids (synth from cholesterol)? what is the next step in the bile formation process?

A

-cholic acid, chenodeoxycolic acid. they are conjugated with glycine and taurine and secreted into bile as “conjugated bile acids”

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22
Q

conjugated bile acids are stored where?

A

gallbladder

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23
Q

bile is released when, in response to what?

A

in response to ingestion of food, and release of CCK

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24
Q

after being in the gut and mixing with food, what happens to the bile?

A

reabsorbed: either passively in jejunum or actively at ileum. circulated back to liver via portal vein.

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25
Q

what happens to bile that travels into the colon?

A

only a small % get this far; is turned into secondary bile acids (deconjugated, dehydroxylated). some are then reabsorbed, return to liver via portal vein

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26
Q

what happens to bile acids that are not reabsorbed at all?

A

excreted in feces. mechanism of cholesterol excretion.

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27
Q

bilirubin: pathway it takes from RBC to bile canaliculus?

A

breakdown of RBCs –> releases heme. bilirubin is a breakdown product of heme. goes through bloodstream attached to albumin. then conjugated (glucoronic acid is added) by enzyme glucoronyl transferase –> conjugated bilirubin. enters bile canaliculus in this form.

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28
Q

bile duct epithelial cells: what do they do?

A

modify the bile by adding H20 and HCO3

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29
Q

gallbladder: functions?

A

concentration, storage, controlled delivery of bile

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30
Q

sphincter of oddi: function?

A

unidirectional delivery of bile and pancreatic secretions

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31
Q

how does the gallbladder concentrate bile? what exactly is concentrated? why does it also decr the pH?

A

-active pumps: Na+ for electrolytes and water (this really does not make sense and he didn’t give explanation) -Na+ concentration is doubled, bile acid concentration x10 -lower pH prevents precipitation of CaCO3

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32
Q

some factors that increase gallstone formation?

A

high cholesterol

low bile acids

low phospholipids

low gallbladder contractility

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33
Q

how does low gallbladder contractility/emptying lead to gallstones?

A

decreased contractility -> prolonged residence of bile in GB -> precipitation of cholesterol and bile salt crystals -> gallstones

34
Q

during the fasting state, what is happening to bile flow?

A

flow is lowest, most of bile that is formed is diverted to GB for storage and concentration

35
Q

postprandial: what happens with bile?

A

ingested fat hits duodenum, CCK is released, stimulates GB contraction, sphincter relaxation, release of panc enzymes, inhibits gastric emptying

36
Q

how do bile acids aid in fat digestion and absorption?

A

they are amphipathic, and when the congregate into micelles they can emulsify lipids to be transported and absorbed.

37
Q

what is the rate limiting step in fat digestion and absorption?

A

diffusion of micelles to brush border.

38
Q

loss of ileal function (due to resection, perhaps) will result in what?

A

steatorrhea, diarrhea, nephrolithiasis, cholelithiasis

39
Q

causes of jaundice?

A
  • overproduction of bilirubin (hemolysis)
  • defective uptake of bilirubin
  • defective conjugation of bilirubin
  • defective excretion of bili

(top three are increased UNconjugated bili, last is increased conjugated)

40
Q

what is Gilbert’s syndrome?

A

hereditary dz, decr uptake of bili into liver cells.

decr activity of GT, which conjugates the bili. therefore increased indirect bili levels –> jaundice

41
Q

Crigner-Najar syndrome?

A

rare genetic condition, either no GT or very decreased GT levels

increases unconjugated bili -> jaundice

Lethal

42
Q

Dubin-Jonhson and Rotor syndromes?

A

hereditary high bilirubin due to decreased excretion from liver cells.

increased DIRECT bili. (it can be conjugated in the liver so it is direct)

43
Q

define cholestasis

A

blocked bile flow. both direct and indirect bili will increase

44
Q

reasons for intrahepatic and extrahepatic cholestasis?

A

intra: intrinsic liver disease, defect in secretion of bile across canalicular membrane
extra: obstructed bile ducts

45
Q

clinical criteria for cholestasis? (4)

A

jaundice, gray stool, dark urine, pruritis

46
Q

alkaline phosphatase is produced by what cells?

A

cholangeocytes

47
Q

labs and clinical sx associated with cholestasis?

A

labs: incr bili, incr alkaline phosphatase, incr GGT, incr cholesterol
sx: xanthomas, fat malabslrption, decr absorb of ADEK

48
Q

why might you see increased INR with cholestasis?

A

vit K has a short half life and it is critical for the clotting cascade. If it’s not absorbed (due to abnormal bile section), clotting may be impaired (increased PT/INR)

49
Q

when ALT is elevated but GGT is normal, what does that indicate?

A

problem is not the liver (ALT is present elsewhere in the body) If ALT and GGT are both elevated, then the problem is in the liver.

50
Q

4 causes of extrahepatic cholestasis? causes incr in direct or indirect bili?

A
  • gallstones
  • strictures
  • neoplasias
  • parasites

direct bili

51
Q

cholelithiasis: overall prev? what is the typical composition of gallstones?

A

Prev: 10% of adults

Gallstones: 80% are chol or mixed.

52
Q

how many cases of cholelithiasis are asymptomatic?

A

70-80%

53
Q

3 major complications of gallstones?

A

cholecystitis

choledocholithiasis

pancreatitis

54
Q

cholelithiasis: where is the pain located? what pattern does the pain follow? other sx?

A

-epigastric/RUQ pain

-crescendo-plateau-decrescendo pattern

-also nausea/vomiting

55
Q

acute cholecystitis: clinical sx? exam findings? labs? imaging? complications?

A
  • sx: ongoing RUQ epigastric pain, preceding episodes of same
  • Murphy’s sign on exam
  • Elev bili, AST, ALT
  • imaging: US normal
  • complications: empyema, gangrenous GB, perforation, peritonitis, fistula
56
Q

smaller or larger stones are more likely to be problematic?

A

the smaller the stone, the more likely it will cause probs. if he had explained why, I would have put it in this card. (Jen - smaller stones are more likely to pop in and obstruct the cystic or common bile duct, causing the problems (cholecystitis or choledocholithiasis). Larger stones are heavier and likely remains in the gall bladder)

57
Q

acute cholecystitis: changes in the GB tissue? cause?

A
  • GB distended, under pressure. acute inflammation of the GB wall, edema and wall thickening. may be hemorrhage, neutrophils, vascular congestion, mucosal ulceration
  • most often caused by obstruction of the neck or cystic duct by gallstone.
58
Q

gangrenous/necrotizing cholecystitis: definition? complications? risk factors?

A
  • coag necrosis of the gallbladder wall
  • perforation is common, 10% mortality
  • RF: male, order, heart dz, diabetes
59
Q

chronic cholecystitis: what is almost always present? what precedes it? morphology? cells present?

A
  • usually gallstones
  • prior episodes of acute cholecystitis
  • morphology variable
  • lymphos and plasma cells
  • Rokitansky-Aschoff sinus
60
Q

what are Rokitansky-Aschoff sinuses?

A

pockets of GB wall- deep crypts, may not be abnl.

61
Q

what is the difference between choledocholithiasis and cholelithiasis?

A

docho = common bile duct

cholelithiasis = biliary system in general.

62
Q

choledocholithiasis: clinical sx? exam findings? labs? imaging? complications?

A
  • sx: recurrent RUQ epigastric pain, preceding episodes of same
  • exam nonspecific
  • Elev bili, ALP, GGT (AST, ALT) may be transient
  • imaging: US normal
  • complications: choleangitis, pancreatitis, cirrhosis
63
Q

ascending cholangitis: description?

A

obstruction, leading to stasis, leading to bacterial overgrowth -> infection acute/life threatening

64
Q

ascending cholangitis: symptoms? exam findings? labs? imaging? saying?

A

sx: Charcot’s triad/Reynold’s pentad
exam: ill appearing, jaundice, tender

Labs: incr bili, ALP, GGT, AST, ALT

imaging: US (dilated CBD)

“don’t let the sun set on cholangitis!”

65
Q

Charcot’s Triad?

A

RUQ pain, jaundice, fever

66
Q

Reynold’s pentad:

A

Charcot’s Triad + Mental Status (MS) changes + shock

67
Q

Risk factors for gallstones?

A

Age

Female (preg, estrogens)

Genetics

Lifestyle (obesity, lack of exercise, diet)

Pregnancy

Diseases: diabetes, hypertrigly,

Crohn’s –> Female, Forty+, Fat, Family + Fetus

68
Q

Features of gallstones in men?

A

-increased incidence of complications over age of 65 (cholecystitis, acute pancreatitis)

69
Q

what is the second most common indication for surgery in pregnancy?

A

gallbladder disease: cholecystectomy may be required due to cholecystitis.

70
Q

gallbladder disease and pregnancy: pathophysiology?

A

increased GB residual and fasting volume, decr GB contractility and rate of emptying (maybe think of it that the duct is being squashed by baby, so the GB has to hold more bile and volume increases)

71
Q

gallbladder disease and preg: symptoms/PE? how to dx? management?

A

cannot evaluate Murphy’s with preg

labs less helpful

do US

management: ERCP for choledocholithiasis, 2nd tri is best time for cholecystectomy

72
Q

what is the most sensitive diagnostic procedure for gallstones and dilated bile ducts?

A

abdominal US

73
Q

what is ERCP? what is it most used to diagnose? risks?

A
  • Endoscopic retrograde cholangiopancreatography
  • inject contrast, see fluoroscopic images using endoscope
  • can use wire basket to grab stones
  • gold std for diagnosing choledocholithiasis
  • risks of pancreatitis (5-10%)
74
Q

what is MRCP?

A

Magnetic resonance imaging; non-invasive method for detecting CBD stones

75
Q

meds for gallstone dz?

A

ursodeoxycholic acid (oral, dissolution therapy). good for small non-calcified stones

76
Q

main treatment for symptomatic gallstones?

A

cholecystectomy

77
Q

Gallbladder carcinoma: prognosis?

A

typically a bad prognosis: usually advanced stage by the time it is discovered

78
Q

risks for gallbladder carcinoma?

A

-gallstones -chronic cholecystitis, porcelain gallbladder chronic infection -congenital anomalies

79
Q

sclerosing cholangitis: what is it?

A

Primary: chronic, fibrosing, inflammatory process of the bile ducts. may obliterate the biliary tree, cause biliary cirrhosis Secondary: chronic biliary obstruction with secondary fibrosing process. leads to biliary cirrhosis

80
Q

choledochal cysts: what are they? what is the treatment?

A

cysts in various parts of the CBD - 5 different patterns. they are typically resected due to risk for cancer.

81
Q

cholangiocarcinoma: prognosis? histo findings?

A

poor survival (5% within 5 y) histo: atypical cuboidal to columnar cells, invasive perineural and periductal growth patterns, desmoplastic stroma with thickened wall.

M2 GI (41 decks)

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