Week 5: Gallstones and ERCP Flashcards

1
Q

Risk factors for gallstones

A
  • older age
  • female 2x > male
  • native amer.> hispanics >scandinavian >white> blacks> asian
  • family hx: 4x more with 1st degree relative
  • western diet
  • obesity
  • pregnancy: increase estrogen leads to lithogenic bile, cholesterol hyper secretion and supersaturation. Progesterone decreases gallbladder mobility
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2
Q

Pathophysiology of Cholesterol gallstones

A
  • Hepatic hyper secretion of biliary cholesterol
  • supersaturated bile with cholesterol that can’t be solubilized at equilibrium by bile salts and phospholipids: hyper secretion of cholesterol and/or decrease rates of bile salt/phopholipid secretion into bile
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3
Q

Pathophysiology of pigment stones

A
  1. Black
    - chronic hemolysis: thalassemia, sickle cell, etc.
    - liver cirrhosis
    - due to increase in unconjugated bilirubin
  2. Brown
    - bile stasis associated with infection
    - dead parasites are stone “nuclei”
    - formed in gallbladder and ducts (other stones form in gallbladder and move to duct)
    - seen in Asia from roundworm infections and Clonorchis sinensis
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4
Q

Natural history of gallstones

A
  1. most are asymptomatic
  2. obstruction of cystic duct: cause intermittent biliary pain
  3. impacted in cystic duct: acute cholecystitis
  4. stone in cystic duct can compress or fistulize into bile duct: Mirizzi’s syndrome
  5. stone in distal bile duct: risk of ascending cholangitis or acute biliary pancreatitis
  6. stone can erode through gallbladder into duodenum
  7. very rare, longstanding stones can cause gallbladder carcinoma
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5
Q

Summary of presentation of gallstones and complications

A
  1. biliary pain: temporary obstruction of cystic duct. No inflammation
    - RUQ pain with nausea
  2. acute cholecystitis: inflammation of gallbladder. impacted stone in CD, acute inflammation, bacterial infection.
    - severe epigastric, RUQ pain, vomiting > 6 hours
    - fever, mild jaundice
  3. Choledocholithiasis: stone in CBD, intermittent obstruction
    - similar symptoms to biliary pain
    - jaundice possible
  4. Cholangitis: inflammation of CBD. obstruction of CBD causing bile stasis, bacteria super infection, bacteremia
    - Charcot’s Triad or Reynald’s pentad
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6
Q

Acute cholecystitis

A
  • lab findings: leukocystosis, bili 2-4 mg/dL, mild amylase and lipase elevation
  • Rx cholecystectomy. Percutaneous drainage in advanced cirrhotic patients
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7
Q

Imaging for gallstones

A
  • ultrasound: good for stones in gallbladder but not in common bile duct
  • cholescintigraphy (HIDA): most useful for cholecystitis
  • CT: good for complications -abscess, perforation
  • MRCP: MRI, non invasive, bad for CBD stones and ampulla. expensive. For pregnant patient to avoid ERCP
  • EUS
  • ERCP: but we only want to use the therapeutically, not for diagnostics because of high complications
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8
Q

Biliary pain “colic”

A
  • colic is misnomer. Pain is steady, gradual over 15min/hour, stays for an hour and resolves.
  • if pain >6 hrs, suggests cholecystitis
  • pain in epigastric >RUQ>LUQ
  • some have radiation to shoulder
  • cholecystectomy for recurring episodes
  • Rx Non surgical (uncommonly used): Ursodiol -thinning of bile by reversing supersaturation with cholesterol.
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9
Q

Cholecystitis

A
  • inflammation of the gallbladder, 90% due to obstruction of gallbladder outlet by gallstone in cystic duct
  • 3/4 patients have hx of biliary colic
  • Murphy’s sign: tenderness with inspiration
  • fever, mild jaundice
  • pain resolves in 7-10 days
  • mild AST, ALT, total Bili elevation
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10
Q

Choledocholithiasis

A
  • gallstones may pass from gallbladder into bile duct or can form de novo
  • de novo: brown stones
  • Elevated bili, alk phos
  • elevated aminotranferases
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11
Q

Cholangitis

A
  • inflammation of the common bile duct or biliary tract+ infection
  • etiology: CBD stones, malignant strictures, benign strictures, stent obstruction
  • Charcot’s triad: fever/chills, jaundice, and abdominal pain
  • 85% due to CBD stone and bile stasis
  • E. Coli and Klebsiella most common infectious agents. Bacterial ascends from duodenum or from portal vein.
  • Reynold’s pentad: charcot’s triad + altered mental status +hypotension/shock
  • labs leukocytosis, bili>2, elevated alk phos, blood culture
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12
Q

ERCP therapy

A
  • timing: best before 24-48 hours after presentation. >72 hrs associated with poor outcomes
  • risk of post ERCP pancreatitis: can be reduced in high risk patients (sphincter oddi dysfunction, prior post ERCP pancreatitis) by giving prophylactic pancreatic stents and/or rectal indomethacin
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