Approach to Patient with Jaundice Flashcards

1
Q

How is heme converted to bilirubin?

A

Heme is converted to biliverdin then bilirubin in phagocytic cells

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2
Q

How is bilirubin transported to the hepatocytes?

A

Tightly bound to serum albumin

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3
Q

What happens to bilirubin after it reaches the liver?

A

The bilirubin from the blood is in unconjugated (insoluble) from and must be conjugated before it is secreted into the bile canaliculus as part of bile and then delivered to the small intestine

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4
Q

Hepatocyte function includes all of the following except:

  1. Drug detoxification
  2. Protein synthesis
  3. Gluconeogenesis
  4. Urea formation by deamination of amino acids
  5. Breakdown of hemoglobin
A
  1. Breakdown of hemoglobin
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5
Q

Which statement about the enterohepatic circulation of bile salts is true?

  1. The bile salt pool is re-circulated only at each meal
  2. In the normal individual, 50% of the bile salt pool must
    be resynthesized and replaced daily
  3. The rate of bile salt synthesis is subject to feedback inhibition, inversely proportionate to the amount of bile salts resorbed
  4. Bile salts are stored and diluted in the gallbladder
A
  1. The rate of bile salt synthesis is subject to feedback inhibition, inversely proportionate to the amount of bile salts resorbed
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6
Q

Bilirubinuria

A

Conjugated bilirubin is detected in the urine

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7
Q

What is the most common cause of bilirubinuria?

A

Most common cause is hepatocelular disease

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8
Q

Dubin-Johnson and Rotor syndrome

A

Inability of hepatocytes to secrete conjugated bilirubin into bile

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9
Q

Neonatal Jaundice

A

-􏰀 Yellowing of the skin in a newborn

􏰀- Bilirubin level > 5mg/dL

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10
Q

What can lead to increased unconjugated bilirubin?

A
  • 􏰀Overproduction (hemolysis)
    􏰀- Impaired uptake by the liver
    􏰀- Abnormalities of bilirubin conjugation
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11
Q

What can lead to increased conjugated bilirubin?

A

-􏰀 Hepatocellular disease (viral hepatitis, cirrhosis) 􏰀
- Impaired canalicular excretion (drugs)
􏰀- Biliary obstruction (gallstones)

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12
Q

An icteric patient with sickle cell disease might be expected to have:

  1. Bilirubinuria
  2. Absence of urinary urobilinogen
  3. Cholesterol stones
  4. Unconjugated hyperbilirubinemia
A
  1. Unconjugated hyperbilirubinemia
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13
Q

Primary Biliary Cirrhosis

A

Destruction of intrahepatic bile ducts that leads to progressive cholestatic liver disease that is of autoimmune etiology

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14
Q

What Ab will be seen with Primary Biliary Cirrhosis?

A

Anti-mitochodrial Ab

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15
Q

Who most commonly gets Primary Biliary Cirrhosis?

A

Middle aged women

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16
Q

What lab value will be elevated in Primary Biliary Cirrhosis?

A

Alkaline Phosphatase

17
Q

Florrid Duct Lesion

A

Periductal inflammation with granuloma formation and duct destruction

18
Q

What is the treatment for Primary Biliary Cirrhosis?

A

Ursodeoxycholic Acid

19
Q

Primary Sclerosing Cholangitis

A

Obliterative fibrosis of intrahepatic and extrahepatic bile ducts with inflammation and dilation of preserved segments.

20
Q

What is Primary Sclerosing Cholangitis associated with?

A

Inflammatory Bowel Disease (Ulcerative Colitis and Crohn’s Disease)

21
Q

Who is affected by Primary Sclerosing Cholangitis?

A

Males are more affected

22
Q

What are the signs of Primary Biliary Cirrhosis?

A

Fatigue and pruritis

23
Q

What does ERCP of Primary Sclerosis Cholangitis show?

A

Beading with narrowing and swelling

24
Q

Jaundice

A

It describes the yellow pigmentation of skin/sclera/mucous membranes produced by increased serum bilirubin

25
Q

What are the 2 categories of jaundice?

A
  • Unconjugated hyperbilirubinemia (water insoluble)

- 􏰀Conjugated hyperbilirubinemia (watersoluble)

26
Q

A 24 yo is referred for hyperbilirubinemia. He is asymptomatic, no drug or Etoh use. Liver tests have previously been normal and he has given blood several times this year without being refused. He is on no medications, no family history of liver disease. Physical examination is normal. T. bilirubin i2 2.1 mg/dL (0-1.5 mg/dL). Direct bilirubin is 0.2 mg/dL. Liver enzymes, albumin, and INR are normal. What should the next step in management be?

􏰀 1. Liver imaging (MRI, U/S)
􏰀2. Liver biopsy
􏰀 3. Genetic testing for a hepatic transport defect 􏰀
4. Genetic testing for a hepatic metabolic defect 􏰀
5. Reassurance, no further testing.

A
  1. Reassurance, no further testing.
27
Q

Gilbert’s Syndrome

A

􏰀- Isolated elevation of total and indirect bilirubin
􏰀- Usually an incidental finding
􏰀- All other transaminases normal (ALT, AST)
􏰀- Genetic defect in the UDP-glucuronyl transferase

28
Q

What is the type of jaundice seen in Gilbert’s syndrome?

A

Unconjugated

29
Q

Courvoisier sign

A

Palpable gallbladder

30
Q

Gamma-glutamyl transpeptidase (GGT)

A

Goes up with alcohol use and is cholestasis marker

31
Q

A 20 asymptomatic male was found on a routine health exam to have the following lab results:
􏰀
Total bilirubin 4.5 mg/dL (0.2-1.2) 􏰀
Direct bilirubin 0.2 mg/dL (0-0.2) 􏰀AST normal
􏰀ALT normal
􏰀Alkaline Phosphatsase normal
Regarding this gentleman’s medical condition, which statement is correct?

  1. Bilirubin is usually undetectable in the urine
  2. Biliary dilation is commonly observed on ultrasound
  3. It is caused by a molecular defect of transport protein at the canalicular membrane
  4. Cirrhosis and hepatocellular carcinoma can develop after several decades of disease
  5. Insulin resistance plays an important role in the pathogenesis
A

1.Bilirubin is usually undetectable in the urine

32
Q

What tests allow you to determine liver function?

A

Albumin and INR determines functioning of liver to

make the normal proteins that it needs to