Cholelithiasis:
- what is this?
- what makes up these?
- what colors might you see?What makes them that color?
- what is the MC type of stone?
What: formation of gallstones, supersaturation of bile with cholesterol and gallbladder hypermotility leads to the formation.
Made up of: cholesterol, Ca2+, and bilirubin
Colors:
-black stones: Ca bilirubinate associated with cirrhosis and hemolysis
-brown stones: associated with biliary tract stasis and infection.
MC stone type is Cholesterol stones 90%
Risk factors for the development of stones?
- Age
- female
- native americans, chileans
- pregnancy
- obesity
- cirrhosis
- hemolytic anemias
- hypertriglyceridemia
- Meds: ceftriaxone
- gallbladder stasis
- DM
- ** The 4 F’s ***
- Fat
- Fertile
- Female
- Forty
Cholelithiasis:
- sx and signs
- how do you differentiate between stone and polyp on US?
- Tx
- Complications
- most are asymptomatic
- biliary colic*
- steady RUQ pain radiates to back and right shoulder
- nausea
US: gallstone will have a shadow.
Tx:
- 60-80% asymptomatic - observation
- symptomatic: cholecystectomy
Complications:
-gallstone ileus: stone erodes through gallbladder wall and develops a cholecystoenteric fistula leading to obstruction of narrowest segment of bowel causing ileus.
- Gallstone pancreatitis
- Acute cholecystitis; gallbladder(GB) gangrene, GB perforation, GB emypema, emphysematous cholecystitis
- Choledocholithiasis
- cholangitis
- bile duct injuries
Cholelithiasis:
-protective factors
Protective: Statins*
- ascorbic acid
- coffee–caffeinated
- vegetable protein
Choledocholithiasis
- what is this?
- sx
- Labs
- complications
- imaging
- TX
What: gallstones within the COMMON BILE DUCT.
-may be asymptomatic, if symptomatic typically present with RUQ or epigastric pain, N/V
Labs:
-LFTs, ALT, AST, are elevated, bilirubin and ALP may be elevated
Complications:
-acute cholangitis, acute pancreatitis, hepatic abscess
Imaging:
- Transabdominal US*****
- Abd CT
- Endoscopic retrograde cholangiopancreatography (ERCP)** GOLD STANDARD
- Intraoperative cholangiography or ultrasonography
- Magnetic Resonance cholangiopancreatography (MRCP)
Tx:
- remove stone**
- lithotripsy
- laparoscopic common bile duct exploration
What is the big advantage of ERCP with choledocholithiasis?
it is the gold standard for dx of common bile duct stones AND is also therapeutic–stone retrieval and sphincterotomy
Acute Cholecystitis
- what is this?
- sx
- PE
What: gallbladder inflammation usually caused by cystic duct obstruction;
- -90% caused by impacted gallstone
- -10% caused by bile stasis or acalculus cholecystitis
Sx:
- RUQ pain, fever, leukocytosis
- anorexia
- n/v
PE:
- RUQ or epigastric pain that radiates to Right shoulder after fatty meal
- positive murphys sign (breath in and push on gallbladder = pain)
dx:
- LFTs and bilirubin = elevated
- CBC: leukocytosis w/ left shift
- CRP elevated greater than 3mg/dl
- US: stones or sludge, distended GB, thickened GB
- HIDA Scan: failure of GB filling.
* if US is non-specific you might order HIDA scan.
WHat are normal results of HIDA scan?
Normal: technetium labeled hepatic iminodiacetic acid (HIDA) is injected IV and it taken up by hepatocytes and excreted into the bile… uptake by liver, GB, CBD, duodenum within 1hr = NORMAL.
Acute Cholecystitis:
-tx
admit to hospital; supportive care, NPO, IV fluids, analgesia, close monitoring of VS and Urine output
abx: cipro or levofloxacin, and flagyl, or ceftin
* early laparoscopic cholecystectomy preferred tx… eventually will need surgery.
if failed medical management and poor surgical candidate, percutaneous cholecystostomy tube + abx
Chronic Cholecystitis
- when does this occur?
- cause
- sx
- histological signs
- tx
when: occurs after repeated episodes of mild attacks
Cause: usually d/t presence of stones
Sx:
- RUQ pain that comes and goes
- pain in right shoulder
- n/v
- trigger is ingestion of fatty foods
Histological signs:
-inflammation can lead to shrinking, scarring, thickened walls, mucosal atrophy, and fibrosis of GB wall.
Tx:
-Cholecystectomy*** via laparotomy or laparoscopy
Porcelain Gallbladder
- what is this?
- sx
- these pts have high risk of development of what?
What: extensive calcium encrustation of the gallbladder wall, blue discoloration and brittle consistency of the gallbladder wall at surgery.
Sx: usually asymptomatic and found incidentally on plain abd radiographs, sonograms, or CT.
High risk of GB adenocarcinoma
Acute Cholangitis
- what is this?
- cause
- predisposing factors for the development of this?
What: inflammation or infection of the bile duct system.
Cause: primarily by bacterial infection, organisms typically ascend from the duodenum, hematogenous spread from the portal vein is rare source of infection
Most important predisposing factor for acute cholangitis is biliary obstruction and stasis secondary to biliary calculi or benign stricture.
Acute Cholangitis
- sx
- dx
- tx
Sx:
- Charcot’s Triad
- -RUQ pain
- -Jaundice
- -fever and chills
- these can start mild and then quickly progress to sever and include sepsis and shock.
- in severe cases bacteremia and sepsis may lead to HYPOTENSION and AMS = Reynolds pentad.
Dx:
-Labs: leukocytosis, elevated LFTs, CRP, blood cultures, ABGs, if renal failure elevated BUN/Creat
-US: dilated bile duct, CBD stones
ERCP: bile duct stone or obstruction or stricture (this is also therapeutic as it can also extract the stone)
Tx:
- hospitalize, treat infection w/ IV abx
- remove stones (ERCP)
- blood cultures
- biliary drainage
Primary Sclerosing Cholangitis
- what is this?
- cause
- MC in which gender and age
- are at increased risk for development of what?
What: chronic inflammatory cholestatic dz; characterized by diffuse inflammation of biliary tract. Swelling and scaring of the bile ducts.
Cause: unknown
MC in MEN 20-40YO
Increased risk of cholangiocarcinoma, gallbladder CA, colon CA, andd if have cirrhosis.. hepatocellular carcinoma.
Primary Sclerosing Cholangitis
- presentation
- dx
- tx
Presentation:
- progressive, obstructive jaundice
- malaise, fatigue, pruritis, anorexia, dyspepsia
- 44% asymptomatic but most will develop sx over time.
- late presentation will develop sx of cirrhosis and portal HTN
Dx:
- elevated ALP, ALT, and AST
- stricturing and dilation of intrahepatic and/or extrahepatic bile ducts on ERCP
- ANCA (anti-neutrophil cytoplasmic abx)
- MRCP
Tx:
- ballooon dilation or stenting
- only liver transplant shown to improve survivaal.
Primary Biliary Cirrhosis
- what is this?
- MC in which gender?
- what aby can be found ?
- Sx
What: slowly progressive autoimmune liver dz, portal inflammation and autoimmune destruction of intrahepatic bile ducts, leads to cirrhosis and liver failure.
MC in females in 40’s
Anti-mitochondrial aby (AMA)
Sx:
- 50% asymptomatic
- fatigue and pruritis = MC
- skin hyperpigmentation d/t melanin deposition
- rheumatic sx, musculoskeletal complaints
- portal HTN, liver failure
Primary Biliary Cirrhosis:
- PE
- Dx
- Tx
PE:
- dry hyperpigmented skin, excoriations
- xanthelasmas (yellow plaques near inner canthus of eyelid)
- hepatomegaly
- jaundice, spider nevi, temporal and proximal limb muscle wasting, ascities, and edema = late sx and imply cirrhosis.
Dx:
- hyperlipidemia
- hypothyroidism, osteopenia, autoimmune dz
- positive AMA ((anti-mitochondrial aby))
- abnormal LFT; ALP and GGTP vvery high
- bx = destruction of interlobular bile ducts
Tx:
- UDCA (Ursodiol/ursodeoxycholic acid)
- -reduces bilirubin, LFTs, cholesterol, and IgM
- -delays fibrosis and varices
- -does not work in advanced dz
- reduced risk of need for liver transplantation and death over 4 years.
If significant inflamm component:
- colchicine
- methotrexate
- budesonide
End stage Liver Dz: liver transplant.
Carcinoma of the Biliary Tract; Cholangiocarcinoma:
- what is this?
- risk factors?
- dx
What: CA of bile ducts.
Risk factors:
- primary sclerosing cholangitis
- congenital liver malformations
- infection with liver flukes
- exposure to thorotrast
Dx:
- US, CT, and MRI:
- -US & CT detect actual tumor and extent to which it has spread. *Dilation of the gallbladder of bile ducts can be seen.
- -CT adds ability to detect enlarged lymph nodes thoughout abd cavity
- -MRI used to determine the involvement of bile ducts and blood vessles
Cholangiography via ERCP:
Cholangiocarcinoma:
- tx
- prognosis
Tx:
- inoperable b/c they dont present until late stage
- palliative chemotherapy w/ or w/o radiotherapy
- *considered an incurable and rapidly lethal dz unless all of its tumors can be FULLY RESECTED.
- non-resectable cases 5year surivival is 0%
- median duration of survival is less than 6 months in inoperable, untreated, otherwise healthy pts.
Gallbladder cancer
- prognosis
- greater in men and women
- risk factors
- Presentation
- MC type of CA?
Prognosis:
- highly fatal malignancy
- greater in women
Risks factors:
- gallstones
- gallbladder polyps
- chronic salmonella infection
- abnormal pancreaticobiliary duct junction
- Porcelain gallbladder*
- diabetes
- obesity
Presentation:
- non-specific; usually incidental finding on imaging or intraoperatively.
- 3 presentations:
- -GB CA discovered during or after lap/open cholecystectomy for assumed benign dz
- -GB CA suspected after diagnostic eval and found on imaging
- -GB CA in advanced stage at presentation
Most common is adenocarcinoma.
Gallbladder Cancer:
- tx
- MC site of CA
- avg age of dx
Surgical management:
- 10-30% resectable at time of dx
- -simple cholecystectomy
- -radical cholecystectomy
- -radical cholecystectomy w/ anatomic liver resection
- -radical cholecystectomy w/ whipple procedure
- Whipple = pancreaticoduodenectomy
MC site is near the ampulla of vater in duodenum.
Age at dx: 60-70YO
Tumors of Ampulla of Vater
- MC site of CA
- avg age of dx
- MC type
- sx
- imaging
- tx
- prognosis
MC site is near the ampulla of vater in duodenum.
Age at dx: 60-70YO
MC Type: adenoma and adenocarcinomas (malignant tumors)
Sx:
-weight loss, anorexia, fatigue, abd pain, GI bleeding, obstructive jaundice
Imaging:
- US* or CT
- ERCP
- Endoscopic US
- MRCP
Tx:
-surgery: whipple operation is standard approach
Prognosis:
- if unresectable; 5-9mo
- resectable is 5 years
Bilirubin physiology
unconjugated bilirubin transported to the liver bound to albumin, once at the liver albumin unbinds and becomes conjugated in hepatocytes via glucouronic acid and then secreted into bile…. in ileum and colon converted to urobilingen and reabsorbed into portal circulation, then excreted into bile or into urine via kidneys.
Causes of hyperbilirubinemia
increased production: hemolytic dz
decreased clearance:
defect in UGT1A1 gene (catalyzes the conjugation of bilirubin) So, this reduces hepatic bilirubin cleraance and increases total bilirubin levels.
