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Project - USMLE Step 3 > Symptom To Diagnosis - Jaundice > Flashcards

Symptom To Diagnosis - Jaundice Flashcards

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USMLE® Step 1 flashcards
1
Q

Is conjugated bilirubin REABSORBED by the intestine?

A

NO!

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2
Q

Fate of conjugated bilirubin in the intestine:

A
  1. Can be excreted unchanged in the stool.

2. Can be converted to Urobilinogen by colonic bacteria.

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3
Q

Fate of urobilinogen that is produced by colonic bacteria.

A
  1. Can be reabsorbed, entering portal circulation.
  2. Some is taken up by the liver and re-excreted into the bile.
  3. Some bypasses the liver and is excreted by the kidney, thus appearing in the urine in small amounts.
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4
Q

UCB is NOT found in the urine. Why?

A

Because it is bound to albumin.

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5
Q

1st key point in the DDx of hyperbilirubinemia is?

A

Determining which kind of bilirubin is elevated.

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6
Q

Dark, tea-colored urine means?

A

Patient has conjugated Hyperbilirubinemia.

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7
Q

Increased bilirubin production - When?

A
  1. Hemolysis.
  2. Dyserythropoiesis.
  3. Extravasation of blood into tissues.
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8
Q

Impaired hepatic bilirubin uptake - When?

A
  1. Heart failure.
  2. Sepsis.
  3. Drugs (rifampin, probenecid, chloramphenicol).
  4. Fasting.
  5. Portosystemic shunts.
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9
Q

Impaired bilirubin conjugation - When?

A 
Hereditary:
1. Gilbert syndrome.
2. Crigler-Najjar syndrome.
Acquired:
1. Neonates.
2. Hyperthyroidism.
3. Ethinyl estradiol.
4. Liver disease (causes mixed hyperbilirubinemia, usually conjugated).
5. Sepsis.
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10
Q

Most patients with UCBemia have?

A
  1. Hemolysis.
  2. Gilbert syndrome.
  3. HF.
  4. Sepsis.
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11
Q

CBemia - etiology if normal liver enzymes:

A
  1. Sepsis or systemic infection.
  2. Rotor syndrome.
  3. Dubin-Johnson syndrome.
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12
Q

CBemia - Elevated liver enzymes - Transaminases more than ALP - Hepatocellular pattern:

A
  1. Acute viral or alcoholic hep.
  2. Alcoholic or non alcoholic steatohepatitis.
  3. Chronic hel (viral, alcoholic, autoimmune).
  4. Cirrhosis of any cause.
  5. Drugs.
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13
Q

CBemia - Cholestatic pattern:

A
  1. Extrahepatic cholestasis.
  2. Intrahepatic Cholestasis (due to impaired excretion):
    - Viral hep.
    - Alcoholic hep.
    - Cirrhosis.
    - Drugs and toxins.
    - Sepsis.
    - Total Parenteral nutrition.
    - post-op jaundice.
    - Infiltrative diseases (amyloidosis, lymphoma, Sarco, TB).
    - PSC.
    - PBC.
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14
Q

AST (SGOT) - Aspect of liver assessed + Origins?

A

Hepatocyte integrity.

  1. Liver.
  2. Heart.
  3. Kidney.
  4. Skeletal muscle.
  5. Brain.
  6. RBC.
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15
Q

ALT - Aspect of liver assessed + origins:

A

Hepatocyte integrity + Liver.

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16
Q

ALP - aspect of liver assessed?

A

Cholestasis.

  1. Liver.
  2. Bone.
  3. Intestine.
  4. Placenta.
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17
Q

For bilirubin >3 Sens and spec of physical exam is?

A

Sens - 78.4%.

Spec - 68.8%.

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18
Q

For bilirubin >15, Sens of physical exam is?

A

96.4%.

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19
Q

Traube space?

A

6th rib superiorly, midaxillary line laterally, left costal margin inferiorly.

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20
Q

The 2 best historical findings in ascites are:

A
  1. Increased abdominal girth (LR+ 4.16, LR- 0.17).

2. Ankle swelling (LR+ 2.8, LR- 0.10).

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21
Q

The 2 best physical exam findings are:

A
  1. Fluid wave - LR+ 6, LR- 0.4.

2. Shifting dullness - LR+ 2.7, LR- 0.3.

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22
Q

Ultrasound can detect …mL of ascites.

A

100

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23
Q

Alcoholic liver disease encompasses a broad spectrum of abnormalities:

A

Steatosis –> Steatohepatitis –> Cirrhosis.

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24
Q

Steatosis - Textbook presentation:

A
  1. Usually asymptomatic.
  2. Normal/mildly elevated transaminases.
  3. Hepatomegaly is present in 70% of patients with biopsy proven steatosis.
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25
Q

What is the main problem with steatosis?

A
  1. Potentiates liver damage from other insults, such as viral hep or acetaminophen toxicity.
  2. Promotes obesity-related liver disease.
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26
Q

Steatosis - Reversible?

A

Yes, but… 1 study found that 18% still progressed to cirrhosis.

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27
Q

Steatosis - Cirrhosis develops in …% who continue to drink.

A

37%.

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28
Q

Alcoholic steatohepatitis - Textbook presentation.

A
  1. Fever.
  2. Malaise.
  3. Jaundice.
  4. Tender hepatomegaly.
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29
Q

Alcoholic steatohepatitis - Found in …-…% of heavy drinkers.

A

10-35%.

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30
Q

Alcoholic steatohepatitis - 3-month mortality:

A

15% –> Mild alcoholic hep.

55% –> Severe alcoholic hep.

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31
Q

Mayo End-stage Liver Disease (MELD) score - Components:

A
  1. Total bilirubin.
  2. INR.
  3. Serum creatinine.
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32
Q

MELD score >11 was found to have a sens of …% and a spec of …% for 30-day mortality.

A

86%.

82%.

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33
Q

Glasgow Alcoholic Hepatitis Score (GAHS) - Components:

A
  1. Age.
  2. WBC count.
  3. BUN.
  4. PT/INR.
  5. Total bilirubin.
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34
Q

Alcoholic steatohepatitis - Transaminases?

A

Elevated but generally <6-7 times the upper limit of normal.

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35
Q

Alcoholic steatohepatitis - GGT and ALP:

A

GGT is often elevated.

GGT/ALP is often >2.5.

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36
Q

Alcoholic steatohepatitis - AST/ALT ratio:

A

Often, but not always >2. (70-80% of cases).

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37
Q

Alcoholic cirrhosis - Prognosis:

A

5-yr survival:
90% if the patient becomes abstinent.
70% if patient continues to consume alcohol.
30-50% once complications of cirrhosis appear.

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38
Q

MC presenting complain in pancreatic cancer:

A

Abdominal pain - 80%.

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39
Q

Jaundice in pancreatic cancer - When the caner is in the body or tail?

A

Due to liver metastases.

40
Q

Rare presentation of pancreatic cancer:

A
  1. Acute pancreatitis.
  2. Malabsorption.
  3. Migratory thrombophlebitis.
  4. GI bleeding.
41
Q

CA 19-9 for pancreatic cancer:

A

37-40 –> Sens 76-90%, spec 68-98%.
100-120 –> Spec 87-100%.
>1.000 –> Spec 94-100%.

42
Q

Pancreatic cancer prognosis:

A

If resectable –> 5yr survival is still only 10-25%.

43
Q

How many pancreatic cancers are resectable?

A

15%.

44
Q

Median survival for non resectable pancreatic cancer?

A

6 months.

45
Q

When is hepatitis UNLIKELY?

A 
When:
1. Nausea.
2. Anorexia.
3. Malaise.
4. Hepatomegaly.
5. Hepatic tenderness.
are absent.
46
Q

Prevalence of hep A in the US:

A

20-40%.

47
Q

Hep A - Symptoms in adults and in children <6.

A

Symptoms develop in 70% of adults.

<30% of children under 6.

48
Q

Hep A - Incubation period:

A

25-30d average. 15-49 range.

49
Q

Course of Hep A:

A

Incubation for 25-30d –> prodromal symptoms –> Malaise, fatigue, nausea, vomiting, anorexia, fever, RUQ pain –> 1 week later –> Jaundice.

50
Q

Hep A - How many patients have jaundice and how many have hepatomegaly?

A

70% –> Jaundice.

80% –> Hepatomegaly.

51
Q

Hep A - Uncommon EXTRAHEPATIC manifestations:

A
  1. Vasculitis.
  2. Arthritis.
  3. Optic neuritis.
  4. Transverse myelitis.
  5. Thrombocytopenia.
  6. Aplastic anemia.
52
Q

Hep A - Fulminant course is more common in?

A
  1. Patients with underlying hep C.

2. 1.1% fatality rate in adults >40.

53
Q

Hep A - Recovery?

A

85% fully recover in 3 months, and nearly all by 6 months.

54
Q

Hep A - Transaminases or bilirubin normalize more rapidly?

A

Transaminases.

55
Q

Prevalence of hep B:

A

0.1-2% (low) in USA, Canada, Western Europe.
3-5% (medium) in mediterranean countries, Japan, Central Asia, Middle East, Latin and South America.
10-20% (high) in Southeast Asia, China, sub-Saharan Africa.

56
Q

Hep B - Clinical manifestations:

A

70% –> Have subclinical infection or are anicteric.

30% –> Icteric hep.

57
Q

Hep B incubation period:

A

1-4 months.

58
Q

Transmission of hep B in low prevalence areas:

A
  1. Sexual.
  2. Percutaneous inoculation.
  3. Needlestick.
  4. Tattooing.
  5. Body piercing.
  6. Contaminated blood transfusion.
59
Q

Transmission of hep B in medium prevalence areas:

A

Childhood infections occurs from contaminated household objects, via minor breaks in the skin and mucous.

60
Q

Transmission of hep B in high prevalence areas:

A

Primarily perinatal, occurring in 90% of babies born to HBeAg(+) mothers - It can be prevented by neonatal vaccination.

61
Q

Hep B - Clinical course:

A
  1. Fulminant in 0.1-0.5%.
  2. Transaminases normalize in 1-4 months if acute infection resolves.
  3. Elevation of ALT for >6months indicates progression to chronic hep.
62
Q

HBsAg:

A
  1. Appears 1-10 weeks after acute exposure.
  2. Should be present in patients with acute symptoms.
  3. Should clear in 4-6months.
  4. LR+ 27, LR- 0.2.
63
Q

HBsAb:

A
  1. Appears after disappearance of HBsAg.

2. Window period of several weeks to months between the disappearance of HBsAg and the appearance of HBsAb.

64
Q

IgM hep B core antibody (IgM anti HBc):

A

Appears shortly after HBsAg and is the only marker of acute infection detectable during the “window period”.
LR+ 45.
LR- 0.1.

65
Q

IgM anti HbC can remain detectable for?

A

2 years and titer can increase during exacerbation of chronic hep B.

66
Q

Chronic hep B - Textbook presentation:

A

Manifestation can range from Asymptomatic, to isolated fatigue, to cirrhosis with portal HTN.
Often NO history of acute hep B.

67
Q

Risk of progression from acute to chronic hep B varies depending on the host:

A
  1. <1% when the acute infection is acquired by an immunocompetent adult.
  2. 90% when the infection is acquired perinatally.
  3. 20% when the infection is acquired during childhood.
68
Q

Chronic hep B - What percentage have extrahepatic findings:

A

10-20% have extrahepatic findings (Polyarteritis nodosa, glomerular disease).

69
Q

HBsAg - Detectable or not on chronic hep B?

A

Generally detectable for life (0.5-2%/year become HBsAg).

70
Q

Risk factors for progression from chronic hep to cirrhosis:

A
  1. Alcohol intake.
  2. Concurrent hep C or HIV infection.
  3. High levels of HBV replication.
  4. HBV genotype C.
71
Q

Chronic hep B - Screening for HCC?

A

Screening with US and AFP is recommended every 6-12 months.

72
Q

True cure in chronic hep B:

A

Rare 1-5%.

73
Q

Hep C - Textbook presentation:

A

Most are ASYMPTOMATIC - Jaundice develops in less than 25%.

When symptomatic –> Similar presentation to those of other viral hep and last 2-12 weeks.

74
Q

Prevalence of hep C:

A

20% of acute hep.

1.6% prevalence of infection in the USA.

75
Q

Perinatal transmission occurs in …-…% of cases.

A

4.6-10%.

76
Q

Hep C - Average incubation period:

A

7-8 weeks.

77
Q

Hep C - Extrahepatic manifestations:

A

Found in about 75% of patients.

  1. Fatigue, Arthralgias, paresthesias, myalgias, Pruritus, sicca syndrome are found in >10%.
  2. Vasculitis 2o to Cryoglobulinemia –> 1%.
  3. Cryoglobulinemia is present in about 40%.
  4. Depression and anxiety are more common than in uninfected persons.
78
Q

Hep C - How many patients have clear the infection within 6 months?

A

15-40%.

79
Q

Percentage of patients who have detectable HCV RNA at 6 months and therefore have chronic hep C.

A

60-85%.

80
Q

Chronic hep C - Stages:

A 
5 stages:
0 - No fibrosis.
1 - Fibrous expansion of portal tracts.
2 - Periportal fibrosis.
3 - Bridging fibrosis.
4 - Cirrhosis.
81
Q

Is there a correlation between ALT levels and liver histology?

A

No correlation.

82
Q

Percentage of patients with chronic hep C that progress to at least stage 1 over 5 years?

A

27-41%.

83
Q

Cirrhosis in chronic hep C:

A

Develops in 4-24% of patients after 20 years of infection.

84
Q

Chronic hep C - Predictors to cirrhosis:

A
  1. Liver histology (best predictor).
  2. Age at infection (>40 years of age –> More progression).
  3. Duration of infection.
  4. Consumption of alcohol >50g/d.
  5. HIV and HBV Coinfection.
  6. Male sex.
  7. Higher ALT.
  8. Baseline fibrosis, and possible Steatosis.
85
Q

Prevalence of different hep C genotypes:

A
  1. 5% –> Genotype 1.
  2. 5% –> Genotype 2.
  3. 5% –> Genotype 3.
  4. 15% –> Genotype 4.
86
Q

Elevated Transaminases - Non hepatic causes:

A
  1. Celiac sprue.
  2. Inherited disorders of muscle metabolism (only AST).
  3. Acquired muscle disease (AST only).
  4. Strenuous exercise (AST only).
87
Q

Hepatic causes for elevated transaminases:

A
  1. Alcohol.
  2. Medication.
  3. Chronic hep B and C.
  4. Non alcoholic fatty liver disease.
  5. Autoimmune hep.
  6. Hemochromatosis.
  7. Wilson.
  8. Alpha-1 antitrypsin.
88
Q

NAFLD - Textbook presentation p:

A

Patients are often asymptomatic but sometimes complain of vague RUQ discomfort.
It is common to identify patients by finding hepatomegaly on exam or asymptomatic transaminase elevation.

89
Q

NAFLD - Definition:

A

A spectrum of liver abnormalities all of which include hepatic steatosis in the absence of significant alcohol use.

90
Q

NAFLD - Stages:

A
  1. Steatosis - Fatty liver.
  2. NASH.
  3. Cirrhosis.
91
Q

Prevalence of NAFLD:

A

20-30% –> in Western adults, with only 2-3% being NASH.
70% –> in diabetics.
91% in obese patients undergoing Bariatric surgery, with 37% being NASH.

92
Q

MCC of abnormal liver test results in the USA:

A

NAFLD.

93
Q

NAFLD - Clinical course:

A

Most patients with pure Steatosis are stable and do not develop progressive liver disease.
About 12-40% develop NASH with early fibrosis after 8-13 years.

94
Q

NAFLD - Blood tests:

A
  1. Transaminase elevation is usually <4 times normal. AST/ALT ratio is usually less than 1, but not if there is advanced disease.
  2. Serum ferritin is elevated in 50%.
  3. Alkaline PHOSPHATASE and GGT are often mildly elevated.
95
Q

Unconjugated bilirubin binds to?

A

Albumin.

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