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102 Cards in this Set
- Front
- Back
Celiac trunk branches
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(1) Left gastric; (2) Splenic artery; (3) Common hepatic artery
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What does common hepatic divide into?
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The hepatic artery proper and the gastroduodenal artery
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Cantlie’s line (portal fissure)
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A line that passes from the left side of the gallbladder to the left side of the IVC, dividing the liver into right and left lobes. It is based on blood supply and is the basis of the four classic types of hepatic resection.
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Blood supply of liver
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The right and left hepatic arteries supply 50% of the liver’s oxygen. The portal vein supplies the remaining 50%. However, the liver receives 75% of its blood supply from the portal vein and only 25% from the hepatic arteries. The different degrees of oxygen saturation within the arterial and venous systems account for this fact.
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Contents of Hepatoduodenal Ligament
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(1) Common bile duct; (2) Portal vein; (3) Proper hepatic artery. Forms anterior boundary of epiploic foramen of Winslow; connects greater and lesser peritoneal cavities
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T-tube cholangiogram
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Performed after open exploration of the bile duct to rule out retained stones just before removal of the tube.
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Intraoperative cholangiogram
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Performed on the operating table via cannulation of the cystic duct to confi rm the anatomy and diagnose CBD stones.
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HIDA Scan
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Radionucleotide scan in which technetium-99m labeled iminodiacetic acid is injected by IV. A normal gallbladder would be visualized within 1 hour. In acute cholecystitis, there is no visualization of the gallbladder 2/2 obstruction of cystic duct.
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ERCP
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Involves passage of endoscope into duodenum, introduction of catheter into ampulla of Vater, and injection of contrast medium into CBD and/or pancreatic duct. Can be diagnostic (biopsy and show pancreatic cancer or choalgiocarcinoma) and threapeutic (remove stones, or stent an obstruction). 1% RISK OF PANCREATITIS FROM PROCEDURE!
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Sphincterotomy/Papillotomy
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Cut through sphincter of Oddi during ERCP to allow passage of stones from the CBD into duodenum. Often performed during ERCP but can also be performed as part of open surgery (sphincteroplasty)
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Percutaneous Transhepatic Cholangiography (PTCA)
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Involves passing needle through skin and subQ tissues into hepatic parenchyma and advancement into peripheral bile duct. When bile is aspirated, a catheter is introduced through the needle and radiopaque contrast medium is injected. VERY useful in cases with distal obstruction where ERCP is not possible or has failed
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Constituents of Bile
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(1) Cholesterol; (2) Lecithin; (3) Bile acids; (4) Bilirubin. FUNCTION: emulsify fats
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Entrohepatic circulation
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Bile acids released from liver into duodenum, reabsorbed at terminal ileum, transported back to liver via portal vein
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Cholecystokinin (CCK)
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Released by duodenal mucosal cells and stimulates gallbladder contraction
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Pre-Hepatic Causes of Jaundice
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(1) Hemolysis; (2) Gilbert's Disease; (3) Crigler-Najjar syndrome. D-bili=NORMAL, I-bili=HIGH
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Hepatic Causes of Jaundice
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(1) Alcoholic cirrhosis; (2) Acute hepatitis; (3) Primary biliary cirrhosis. D-bili=HIGH, I-bili=HIGH
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Post-Hepatic Causes of Jaundice
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(1) Gallstones; (2) Tumor. D-bili=HIGH, I-bili=NORMAL
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Signs and Symptoms of Jaundice
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(1) Yellow skin and sclera; (2) Pruritus; (3) Hepatomegaly, RUQ tenderness; (4) Dark urine; (5) Clay-colored stools, anorexia, nausea
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Obstructive Jaundice: Labs
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In obstructive jaundice, the alkaline phosphatase (ALP) level rises more quickly than the bilirubin level. Also, when the obstruction is relieved, the ALP level falls more quickly than the bilirubin level.
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Liver Trauma: what to do?
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CT to detect blood/solid organ damage. U/S as part of FAST exam. Penetrating trauma requires operative management, but blunt trauma may attempt trial of observation if patient is stable, no peritoneal signs, injury can be precisely delineated and graded by CT scan, no associated injuries, and no need for excessive hepatic related blood transfusions
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Pyogenic Hepatic Abscess
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Usually 2/2 bacterial sepsis or biliary or portal vein infection; can occur from a perforated infected gallbladder, cholangitis, diverticulitis, liver cancer, or liver mets
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Amebic Hepatic Abscess
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Usually seen in patients from Central America, homosexual men, institutionalized patients, and alcoholics
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What are the MC organisms isolated from pyogenic hepatic abscesses?
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(1) E. coli; (2) Klebsiella; (3) Proteus. Amebic abscesses are classically described as “anchovy paste” in appearance and are caused by Entamoeba histolytica, which gains access to the liver via the portal vein from intestinal amebiasis.
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Treatment of Pyogenic Hepatic Abscess
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U/S or CT-guided percutaneous drainage with IV antibiotics; operative drainage if percutaneous attempts fail or cysts are multiple or loculated
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Treatment of Amebic Hepatic Abscess
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Operative drainage is NOT indicated unless abscesses do not resolve with IV metronidazole or are superinfected with bacteria
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Hydatid Cyst
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Hepatic cyst caused by Echinococcus multilocularis or Echinococcus granulosus that is usually solitary and involves the right lobe of the liver
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Diagnosis of Hydatid Cyst
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Most are asymptomatic, but can cause hepatomegaly; often picked up incidentally on U/S or CT, which may shows calcifications outlining the cyst. Frequently see EOSINOPHILIA, positive serology
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Treatment of Hydatid Cyst
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NEVER aspirate these cysts, or they will spill their contents. Treat with albendazole/mebendazole followed by resection
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Nonparasitic Liver Cysts
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Associated with polycystic kidney disease. Most commonly involve right liver lobe, though to be congenital in origin
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Cavernous Hemangioma
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(1) Benign vascular tumor resulting from abnormal differentiation of angioblastic tissue during fetal life; usually located in right posterior segment of liver; (2) MC tumor of liver; occurs at ALL ages. (3) Usually asymptomatic; rarely presents with pain/mass/hepatomegaly
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Diagnosis of Cavernous Hemangioma
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Usually discovered incidentally; can be detected by U/S, CT, MRI; DO NO BIOPSY! Hemorrhage can occur!
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Treatment of Cavernous Hemangioma
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(1) Surgical resection if symptomatic or in danger of rupture; otherwise, observe
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Hamartoma of Liver
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Benign focal lesion of liver that consists of normal tissue that has differentiated in an abnormal fashion; Rare - often asymptomatic, but can present with RUQ pain or fullness. Diagnosis is usually discovered incidentally during imaging; may require histopathologic evaluation; TREATMENT: surgical excision
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Hepatocellular adenomas
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Mass lesion of liver characterized by a benign proliferation of hepatocytes; 95% occur in WOMEN of CHILDBEARING AGE!
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Risk factors for hepatocellular adenomas
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OCP use, long-term anabolic steroid therapy, or glycogen storage disease
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What two benign liver tumors are associated with OCP use?
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(1) Hepatic adenomas; (2) Focal Nodular Hyperplasia
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Focal Nodular Hyperplasia (FNH)
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Benign hepatic tumor, though to arise from hepatocytes and bile ducts; (2) Has a characteristic "central scar" on pathologic evaluation
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Hepatocellular carcinoma
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Malignant tumor derived from hepatocytes frequently found in association with chronic liver disease, particularly cirrhosis
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Risk Factors for Cirrhosis/HCC
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(1) HepB; (2) HepC; (3) Aflatoxins; (4) Liver flukes; (5) Hemochromatosis; (6) a1-antitrypsin deficiency; (7) Anabolic steroid use
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Diagnosis of HCC
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Increased ALP, AST, ALT, GGT, AFP; Contrast CT and U/S can visualize the tumor, guided biopsy will give definitive diagnosis
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Treatment of HCC
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(1) Surgical resection is the only cure - lobectomy or segmental resection with 1cm margin required; (2) Transplant - but high recurrence rate with HepB, HepC; (3) Local chemotherapy infusion into hepatic artery, transcatheter arterial chemoembolization (TACE), liposomal chemothreapy
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What is the MC hepatic malignancy?
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METS! Primary is usually from colon, breast, or lung, with bronchogenic carcinoma being the MC primary tumor
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Diagnosis of hepatic mets
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(1) Increased ALP, GGT, LDH, AST, ALT (nonspecific); (2) Mets will enhance on contrast CT; (3) Intraoperative ultrasound with liver palpation is the most sensitive diagnostic tool
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Treatment of hepatic mets
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(1) Resection, if possible, is treatment of choice; (2) Radiofrequency ablation is now extensively done even for multiple lesions, and the short-term results are promising
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MCC of portal hypertension
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(1) In the US: cirrhosis from alcoholism; (2) Outside US: schistosomiasis
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Portal Hypertension
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Portal pressure >10mmHg (measure with indirect hepatic vein wedge pressure)
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Causes of Portal HTN
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(1) Prehepatic: congenital atresia, cyanosis, or portal vein thrombosis; (2) Intrahepatic: cirrhosis, hepatic fibrosis from hemochromatosis, Wilson's disease, or congenital fibrosis; (3) Posthepatic: Budd-Chiari syndrome (thrombosis or hepatic veins), hypercoagulable state, lymphoreticular malignancy
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Signs and Symptoms of Portal HTN
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(1) Jaundice; (2) Splenomegaly; (3) Palmar erythema; (4) Spider angiomata; (5) Ascites; (6) Truncal obesity with wasting of extremities; (7) Asterixis; (8) Hepatic encephalopathy
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Portosystemic Collaterals and their clinical manifestations
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(1) Left gastric vein to esophageal veins - esophageal varices; (2) Umbilical vein (via falciform ligament) to epigastric veins - caput medusa; (3) Superior hemorrhoidal vein to the middle and inferior hemorrhoidal veins - hemorrhoids; (4) Veins or Retzius (posterior abdominal wall veins) to retroperitoneal lumbar veins - retroperitoneal varices.
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Hepatic Encephalopathy
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AMS 2/2 hepatic insufficiency. Toxins that are normally cleared by the liver are retained in the circulation. The exact toxin that causes CNS changes is unknown, but may be NH3, GABA, mercaptens, or SCFAs. NOTE: Serum NH3 level does NOT correlate with degree of encephalopathy
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Treatment of hepatic encephalopathy
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Lactulose to reduce intestinal formation and absorption of ammonia
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Ascites
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Excess fluid in peritoneal cavity 2/2 sodium and fluid retention by the kidney, low plasma oncotic pressure due to low albumin, and elevated hydrostatic pressure in hepatic sinusoids and portal veins allowing fluid to be lost in peritoneal cavity
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Treatment of ascites
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(1) Reduce sodium intake; (2) K+-sparing diuretic (spironolactone); (3) Abdominal paracentesis; (4) Removing too much ascitic fluid too quickly will cause intravascular fluid to be drawn into peritoneal cavity. This leads to a loss of intravascular volume and hypovolemic shock
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LeVeen shunt
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Peritoneal-jugular shunt that is used to decrease ascites; may increase hepatic encephalopathy since NH3 goes directly to systemic circulation
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Esophageal varices
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Engorged esophageal or gastric veins, usually resulting from increase portal pressure from liver disease. Asymptomatic unless rupture occurs -- GI bleeding, hematemesis, melana and/or hematochezia
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Treatment of esophageal varices
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(1) Endoscopic sclerotherapy; (2) Vasopressin/Somatostatin injection; (3) Balloon tamponade (Sengstaken-Blakemore tube); (4) Transjugular intrahepatic portocaval shunt (TIPS) - long-term management; shunts pressure away from esophageal vessels; (5) Intraoperative portocaval shunt; (6) Liver Transplant; (7) Beta-blockers to decrease portal pressure and reduce incidence of rupture
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Valves within cystic duct
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Spiral valves of Heister
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Ducts of Luschka
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Special accessory ducts that go from liver directly to gallbladder
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Cholelithiasis
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Stones in gallbladder. 85% of stones are composed of cholesterol; 15% are pigmented, Approximately 10% of US population has gallstones
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Risk factors for cholelithiasis
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(1) Female, (2) Fat, (3) Fertile, (4) Forty. Other risk factors include native american, pregnancy, OCP use, western diet, IBD, hyperlipidemia, ileal resection (loss of enterohepatic circulation), and TPN
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S&S of cholelithiasis
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Most patients are asymptomatic; symptomatic patients complain of severe RUQ pain that radiates to the back, epigastrum, or LUQ that tends to be worse after eating (esp. fatty foods) and may be associated with N/V. The symptom complex is called biliary colic and typically resolves over a few hours
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Diagnosis of cholelithiasis
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Often incidental, as most are asymptomatic; abdominal plain films pick up about 15%; U/S is procedure of choice; classic findings include an acoustic shadow ("headlight") and gravity-dependent movement of gallstones with patient repositioning
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Treatment of cholelithiasis
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Asymptomatic cholelithiasis DOES NOT require cholecystectomy unless the patient has (1) porcelain gallbladdeder - inc. risk of cancer; (2) sickle cell anemia; (3) stone > 2-3cm; (4) pediatric patient; (5) immunocompromised
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Mirizzi's syndrome
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External compression of common hepatic duct by gallstone impacted in cystic duct
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Hydrops of the gallbladder
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Complete obstruction of cystic duct by a gallstone, causing the gallbladder to fill with fluid from the gallbladder mucosa. Fluid is often milky white
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Acute cholecystitis
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Inflammation of gallbladder wall, usually 2/2 obstruction of cystic duct by gallstones
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S&S of acute cholecystitis
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(1) RUQ tenderness and guarding are present, usually for > 3 hrs; (2) fever, nausa, vomiting, anorexia; (3) Murphy's Sign = pain on deep inspiration resulting in inspiratory arrest (positive in 1/3 of patients); (4) Sonographic Murphy's = pain over RUQ when palpated with U/S probe;
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Diagnosis of acute cholecystitis
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LABS: leukocytosis w/ or w/o increased ALP, LFTs, amylase, Tbili; U/S: inflammation of gallbladder wall (>4mm), pericholecystic fluid and stones in the gallbladder. Dilation of CBD may also be seen if stone has passed; HIDA SCAN: nonfilling of gallbladder even when small bowel is visualized is characteristic of acute cholecystitis
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Treatment of acute cholecystitis
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(1) NPO; (2) IV fluids; (3) IV Abx; (4) IV analgesia; (5) Cholecystectomy within 24-48hrs
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Acalculous cholecystitis
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Acute cholecystitis w/o evidence of gallstones; thought to be due to biliary stasis; accounts for 10% of cases of acute cholecystitis
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Risk factors for acalculous cholecystitis
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Most often seen in ICU patients with multi-organ system failure, trauma (esp. after major surgery), burns, sepsis, and TPN
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Diagnosis of acalculous cholecystitis
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Biliary sludge and inflammation; HIDA scan confirms diagnosis. Often see leukocytosis, too
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Treatment of acalculous cholecystitis
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(1) Urgent lap chole; (2) Percutaneous cholecystotomy is an option in patients with high surgical risk
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Choledocholithiasis
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Stones in the common bile duct; found in 6-15% of acute calculous cholecystitis and 1-2% of acalculous cholecystitis at surgery
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S&S of choledocholithiasis
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Epigastric or RUQ pain/tenderness, jaundice, cholangitis, or recurrent attacks of acute pancreatitis w/o other risk factors
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Diagnosis of choledocholithiasis
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(1) LABS: increased ALP, LFT, T/D bili; (2) ERCP: gold standard for diagnosis - also therapeutic; (3) Endoscopic ultrasound: less sensitive than ERCP, but also less invasive; more sensitive than transabdominal ultrasound
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Treatment of choledocholithiasis
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(1) ERCP: involves endoscopic sphincterotomy with retrieval of CBD stone with basket (85-90% success rate); (2) If ERCP fails, CBD can be opened surgically and stones removed. A T-tube is placed so bile can drain externally. It is removed 2-3 weeks later on an outpatient basis
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Charcot's triad
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RUQ pain, FEVER, JAUNDICE. Sign of CHOLANGITIS
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Reynold's pentad
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RUQ pain, FEVER, JAUNDICE, CNS symptoms, SEPTIC SHOCK/HYPOTENSION. Sign of CHOLANGITIS
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Acute (Ascending) Cholangitis
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Bacterial infection of bile ducts usually associated with obstruction of CBD by stone
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S&S of acute cholangitis
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fever, chills; N/V, abdominal pain with or without AMS, septic shock
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Causes of CBD obstruction
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SINGE: Stricture; Iatrogenic [ERCP/PTC or biliary stent placement]; Neoplasm; Gallstones; Extrinsic compression (e.g., pancreatic pseudocyst, pancreatitis)
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Diagnosis of acute cholangitis
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LABS: leukocytosis with increased bilirubin, ALP, LFTs; U/S: should be initial study; dilation of common and intrahepatic bile ducts along with gallstones, and a thickened edematous gallbladder wall; ERCP/PTCA: diagnostic and therapeutic; BILE CULTURES: facilitates proper antibiotic treatment (gram-negatives and enterococci)
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Treatment of acute cholangitis
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NPO, IVF, IV Abx; If patient is in shock, decompress bile duct and remove obstruction immediately by ERCP/PTCA. If unsuccessful, intraoperative decompression with T-tube placement is indicated; If patient is stable, continue conservative management with definitive treatment later
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Primary Sclerosing Cholangitis
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Chronic, progressive inflammatory process of biliary tree of unknown etiology that results in strictures and in most cases, cirrhosis and liver failure. Associated with autoimmune disease, particularly ulcerative colitis; 2:1 male predominance, median age of onset is 40yrs
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Risk Factor for PSC
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IBD! 70% of patients with PSC have IBD, whereas just 3-7% of patients with IBD have PSC
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S&S of PSC
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Most asymptomatic at time of diagnosis; but symptoms can include fever, weight loss, fatigue, pruritus, jaundice, hepatomegaly, splenomegaly, and hyperpigmentation
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Diagnosis of PSC
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ERCP/PTC reveal a "beads on a string" appearance of the bile ducts. ALP is almost always elevated
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Treatment of PSC
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(1) Balloon dilatation with stent placement can be performed for palliative purposes, but definitive treatment varies depending on location of strictures; (2) Extrahepatic strictures: Hepatoenteric anastomosis with removal of extrahepatic ducts and T-tube placement for external drainage of bile; (3) Intrahepatic strictures: liver transplant
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Complications of PSC
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(1) Cirrhosis; (2) Cholangitis; (3) Obstructive jaundice; (4) Cholangiosarcoma
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Gallstone ileus
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Small bowel obstruction caused by a gallstone; ileocecal valve is MC site of obstruction; Most often, large stone erodes a hole through gallbladder wall to duodenum, causing a cholecystenteric fistula. A gallstone escapes through this hole into the GI tract and eventually gets stuck in ileum, causing SBO
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S&S of gallstone ileus
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Symptoms of acute cholecystitis followed by signs of SBO (nausea, vomiting, obstipation, RUQ pain). MC in women over age 70. Free air in biliary tree and "Stepladder" appearance of small bowel.
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Diagnosis of gallstone ileus
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(1) Abdominal plain films: may show pathognomonic features of pneumobilia, dilated small bowel, and a large gallstone in RLQ; (2) U/S: useful to confirm cholelithiasis; may also identify the fistula;
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Treatment of gallstone ileus
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Ex-lap, removal of gallstone, and possible small bowel reconstruction w/ or w/o cholecystectomy and fistula repair
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Carcinoma of the gallbladder
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Malignant neoplasm; most adenocarcinoma. EXTREMELY RARE (<1% of patients with cholelithiasis); incidence increases with a peak at 75 years
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Risk factors for gallbladder carcinoma
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(1) Porcelain gallbladder, gallstones, choledochal cysts, gallbladder polyps, typhoid carriers with chronic inflammation
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Courvoisier's sign
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A palpable, nontender gallbladder often associated with cancer in the head of the pancreas or the gallbladder
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Benign Tumors of the Bile Ducts
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Tumors that arise from ductal glandular epithelium most commonly found at ampulla of Vater; most are adenomas, of polypoid morphology, <2cm in size. May cause intermittend jaundice and RUQ pain
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Cholangiocarcinoma
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Uncommon tumor anywhere along intrahepatic or extrahepatic biliary tree; most commonly located at bifurcation of the right and left hepatic ducts (60-80% of cases). Nearly all are adenocarcinomas
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Klatskin tumor
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A cholangiocarcinoma that arises at the junction of the right and left hepatic ducts
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Risk factors for cholangiocarcinoma
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(1) Choledochal cyst; (2) UC; (3) PSC; (4) liver flukes; (5) toxins; (6) contrast dye (thorotrast)
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Clonorchis sinensis
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Chinese liver fluke; feed on human bile and produce inflammatory reaction, epithelial hyperplasia, and sometimes cholangiocarcinoma. More frequently cause cholangitis
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