Approach to the Jaundiced Patient. Dr. Ümit Akyüz Yeditepe University Division of Gastroenterology. Jaundice. A yellowing of the skin, sclerae ( 공막 ), and other tissues caused by excess circulating bilirubin. Bilirubin Metabolism.
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Approach to theJaundiced Patient
Dr. Ümit Akyüz
Division of Gastroenterology
The fraction of serumbilirubin which has not been conjugated with glucuronic acid in the liver cell; so called because it reacts with the Ehrlichdiazo reagent only when alcohol is added; increased levels are found in hepaticdisease and haemolyticconditions.
-Mild jaundice without dark urine : unconjugated hyperbilirubinemia caused by hemolysis or Gilbert's syndrome rather than hepatobiliary disease
-More severe jaundice or dark urine clearly indicates a liver or biliary disorder.
-Signs of portal hypertension (문맥고압증), ascites, or skin and endocrine changes usually imply a chronic rather than an acute process
-Patients often notice dark urine before skin discoloration; thus, the onset of dark urine better indicates the duration of jaundice
-Nausea and vomiting preceding jaundice most often indicate acute hepatitis or common duct obstruction by a stone; abdominal pain or rigors favor the latter
-Gilbert's syndrome: defects in the liver's uptake of plasma bilirubin (우성유전)
-Crigler-Najjar syndrome: glucuronyl transferase deficiency
-Primary shunt hyperbilirubinemia: This rare, familial benign condition is associated with overproduction of early-labeled bilirubin.
-Dubin-Johnson syndrome: Asymptomatic mild jaundice characterizes this rare autosomal recessive disorder. The basic defect involves impaired excretion of various organic anions as well as bilirubin, but bile salt excretion is unimpaired.
-Rotor's syndrome: This rare disorder is similar to Dubin-Johnson syndrome, but the liver is not pigmented and other subtle metabolic differences are present
-A clinical and biochemical syndrome that results when bile flow is impaired
-Pathophysiology : interference with microsomal hydroxylating enzymes, which leads to the formation of poorly soluble bile acids; impaired activity of Na+,K+-ATPase, which is necessary for canalicular bile flow; altered membrane lipid composition and fluidity; interference with the function of microfilaments (thought to be important for canalicular function); and enhanced ductular reabsorption of bile constituents. Because bile salts are needed for absorption of fat and vitamin K, impaired biliary excretion of bile salts can produce steatorrhea(지방변) and hypoprothrombinemia(저프로트롬빈혈증). In long-standing cholestasis (eg, primary biliary cirrhosis), concomitant Ca and vitamin D malabsorption may result in osteoporosis or osteomalacia(골연화증)
-Jaundice, dark urine, pale stools, and generalized pruritus(소양증)
-Intrahepatic and extrahepatic cholestasis must be differentiated. Intrahepatic cholestasis is suggested by symptoms of hepatitis, heavy alcohol ingestion, recent use of potentially cholestatic drugs, or signs of chronic hepatocellular disease (eg, spider nevi, splenomegaly, ascites). Extrahepatic cholestasis is suggested by biliary or pancreatic pain, rigors(오한), or a palpable gallbladder.
-In intrahepatic cholestasis, treating the underlying cause usually suffices
-Extrahepatic biliary obstruction usually requires intervention: surgery, endoscopic extraction of ductal stones, or insertion of stents and drainage catheters for strictures (often malignant) or partially obstructed areas
Plateau phase = 57 days
HCV RNADay 12
HCV AntibodyDay 70
From DL Thomas
AST < 300
Discriminant Function Formula:
DF = [4.6 x (PT – control)] + bilirubin
Consider treatment for DF > 32
CBD stones (choledocholithiasis) vs. tumor
Sex, drugs, R&R
other autoimmune dz
prior biliary surgery
family history liver dz
Left supraclavicular adenopathy (Virchow’s node)
Bilirubin – total/indirect