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
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
3
Q
Pathophysiology of pigment stones
A
- Black
- chronic hemolysis: thalassemia, sickle cell, etc.
- liver cirrhosis
- due to increase in unconjugated bilirubin - 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
4
Q
Natural history of gallstones
A
- most are asymptomatic
- obstruction of cystic duct: cause intermittent biliary pain
- impacted in cystic duct: acute cholecystitis
- stone in cystic duct can compress or fistulize into bile duct: Mirizzi’s syndrome
- stone in distal bile duct: risk of ascending cholangitis or acute biliary pancreatitis
- stone can erode through gallbladder into duodenum
- very rare, longstanding stones can cause gallbladder carcinoma
5
Q
Summary of presentation of gallstones and complications
A
- biliary pain: temporary obstruction of cystic duct. No inflammation
- RUQ pain with nausea - acute cholecystitis: inflammation of gallbladder. impacted stone in CD, acute inflammation, bacterial infection.
- severe epigastric, RUQ pain, vomiting > 6 hours
- fever, mild jaundice - Choledocholithiasis: stone in CBD, intermittent obstruction
- similar symptoms to biliary pain
- jaundice possible - Cholangitis: inflammation of CBD. obstruction of CBD causing bile stasis, bacteria super infection, bacteremia
- Charcot’s Triad or Reynald’s pentad
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
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
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.
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
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
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
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