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GI > Disorders of the Liver Part 2 > Flashcards

Disorders of the Liver Part 2 Flashcards

1
Q

Which hepatitis is fecal-oral?

A

Hep A

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2
Q

Which Hep is blood-borne?

A

Hep B and C and D

D is associated with B only!

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3
Q

What kind of virus is Hep A?

A

RNA

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4
Q

What is unique about having Hep A?

A

There is no chronic carrier state.

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5
Q

How does Hep A typically present?

A
  • Worse in adults
  • Distaste for smoking
  • Low grade fever
  • Malaise, arthralgia, URI, fatigued
  • Mild constant abdominal pain in RUQ aggravated by exertion/jarring
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6
Q

When does jaundice tend to occur in Hep A?

A

5-10 days after

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7
Q

What kind of stool does Hep A produce?

A

Acholic (mashed potatoes?)

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8
Q

Who should we suspect Hep A infection in?

A
  • Abrupt onset of prodromal symptoms (N, anorexia, fever, malaise, or abd pain)
  • Jaundice
  • Elevated aminotransferase levels
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9
Q

How is a Hep A diagnosis established?

A

IgM anti-HAV antibodies

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10
Q

What is the best indicator of a previous exposure, non-infectivity, and immunity of hep A?

A

IgG

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11
Q

What is the ALT/AST ratio in Hep A?

A

ALT > AST

Acute process

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12
Q

What does a blood smear look like for Hep A?

A

Atypical large lymphocytes

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13
Q

How do you treat and prevent hep A?

A
  • Treatment: rest and fluids, avoid exertion
  • Prevention: VACCINATION, washing hands, can get shot if you get exposed.
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14
Q

What are the essentials of diagnosis of Hep A?

A
  • Infection acquired via fecal-oral route and is self-limited
  • Relapsing infection and protracted cholestatic phase
  • IgM antibody test
  • IgG development leads to protection and lifelong immunity
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15
Q

What are the components of the Hep B virus?

A
  • Inner core: HBcAg and HBeAg
  • Outer surface: HBsAg

8 different genotypes as a result! 2^3

HBcAg = Hep B core antigen
HBeAg = Hep B e antigen
HBsAg = Hep B surface antigen

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16
Q

How is Hep B transmitted and prevented?

A
  • Transmission: Blood-borne and sexual intercourse
  • Prevention: VACCINATION
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17
Q

Who are the greatest risk factors for Hep B?

A
  • MSM
  • Hemodialysis center staff and pts
  • Clinical pathology and blood banks
  • STD or incarcerated
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18
Q

How long does it take Hep B to incubate?

A

6 weeks to 6 months

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19
Q

How does Hep B infection typically present?

A
  • Losing your appetite
  • Jaundice
  • Fever
  • Dark urine
  • Pale poop
  • N/V
  • RUQ pain
  • Joint pain
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20
Q

What are the serologic markers for Hep B?

A
  • HBsAg
  • Anti-HBs
  • Anti-HBc
  • HBeAg
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21
Q

What is the FIRST serologic marker to elevate in Hep B?

A

HBsAG

Past 6 months of elevation = chronic

the “Stat” antigen

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22
Q

What serologic marker changes suggest recovery from an acute Hep B infection?

A
  • Anti-HBs appearance
  • HBsAG Decrease
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23
Q

What serologic marker changes suggest Hep B immunity?

A
  • Only Anti-HBs persistence
  • No elevated HBsAG
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24
Q

When does IgM anti-HBc tend to appear in a Hep B infection?

A

1 month after HBsAG appears

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25
Q

What does IgG anti-HBc appearance suggest during a Hep B infection?

A

Persists indefinitely
* With recovery => IgG occurs with anti-HBs
* With chronic => IgG occurs with HBsAG

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26
Q

What does the appearance of HBeAG suggest?

A

Indicates viral replication and infectivity, aka most infectious time

Followed by anti-HBe as viral replication diminishes

After it penetrates the surface, the envelope is next, so its the peak

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27
Q

Appearance of what Hep B antibody suggests that the patient is a low infectious risk?

A

HBeAb

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28
Q

What is slightly more sensitive than HBeAG in terms of viral replication and infectivity?

A

HBV DNA

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29
Q

Summary graph of serologic markers of Hep B

A
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30
Q

What serologic markers characterize a previous Hep B infection?

A
  • Anti-HBs
  • IgG anti-HBc

The virus has entered both the surface and the core at one point, so there are Ab present for both. (at least thats how i think of it)

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31
Q

What serologic markers suggest Vaccination of Hep B?

A

Only anti-HBs

Vaccination = virus can’t get past the surface, so it never enters the core/envelope so no Ab get made

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32
Q

What serologic markers suggest recovery from Hep B and immunity?

A
  • Anti-HBs
  • IgG Anti-HBc
  • Potentially anti-HBe
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33
Q

What is the AST/ALT ratio in Hep B?

A

ALT > AST (more than Hep A usually)

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34
Q

What is PT prolongation associated with in terms of Hep B?

A

Fulminant Hep B

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35
Q

How do you treat Hep B?

A
  • Rest, fluids
  • antiviral therapy is not indicated in acute infection
  • 3-6 months
  • Liver manifestations = hospitalization
  • HBIG (immune globulin) must be given within 7 days to shorten duration and reduce severity
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36
Q

If an infant is born to a HBV+ mother, what do we do?

A

HBIG + vaccine series within 12 hours of birth

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37
Q

How many doses is the HBV series and who gets it?

A
  • All children
  • Healthcare workers
  • 3 series (Initial, 1 month, 6 months)
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38
Q

What chronic conditions does HBV increase the risk of?

A
  • Hepatocellular carcinoma
  • Cirrhosis
  • Liver failure
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39
Q

What patients get antiviral therapy for HBV?

A
  • Active viral replication
  • Acute on chronic (HBeAG + HBV DNA)
  • S/Sx of liver failure or cirrhosis
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40
Q

What is the antiviral therapy for HBV?

A
  1. First-line: Nucleotide and Nucleoside analogs
  2. Second-line: Interferon (BBW for infections)
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41
Q

Hep B serology interpretation

A
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42
Q

What are the essentials of diagnosis of Hep B? (Image)

A
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43
Q

How is HCV typically transmitted?

A

IVDU

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44
Q

How many major genotypes does HCV have?

A

7

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45
Q

Who are the at-risk populations for HCV?

A
  • IVDU
  • Prison inmates
  • Healthcare workers
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46
Q

What is the MC bloodborne infection in the entire US?

A

HCV

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47
Q

What other condition is often implicated with people with HCV?

A

HIV

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48
Q

What genotype spontaneously resolves in HCV?

A

CC

49
Q

What do most people with HCV go on to develop?

A

Chronic hepatitis

50
Q

What signifies an HCV infection?

A

Presence of HCV RNA

51
Q

What signifies a past HCV infection?

A

Presence of anti-HCV without HCV RNA

52
Q

Presence of what serologic marker indicates that hepatitis is due to Hep C?

A

HCV Antibodies

53
Q

What conditions does HCV increase the risk of?

A
  • Non-Hodgkin’s Lymphoma
  • GN
  • IPF
  • Thyroiditis
54
Q

Who does the CDC recommend gets screened for HCV?

A
  • Anyone over 18
  • All pregnant women
55
Q

How do you treat HCV?

A

Direct acting antiviral (DAA): Iedipasvir/sofosbuvir

Prevents chronic Hep development for acute genotype 1

56
Q

Who is highest risk for cirrhosis development secondary to HCV?

A
  • Increased risk in men
  • > 50g of alcohol daily
  • HCV after 40yo
57
Q

Drinking what slows progression of liver fibrosis?

A

Coffee

58
Q

What does an HCV protease inhibitor do and what genotypes is it for?

A
  • Inhibits replication
  • Glecaprevir/pibrentasvir
  • Genotypes 1-6
  • 8 wk tx
59
Q

What does an HCV polymerase inhibitor do and what genotypes is it for?

A
  • Inhibits viral replication
  • Sofobusvir + velpatasvir
  • Genotypes 1-6 except 3 (12 week tx)
60
Q

What are the essentials of diagnosis for HCV?

A
  • Percutaneous exposure that commonly leads to chronic infection
  • EIA for anti-HCV indicates infection or prior exposure. Can be falsely positive.
  • Presence of HCV RNA indicates active infection and takes 1-2 weeks to be detectable.
  • Liver biopsy is rarely necessary
61
Q

When does Hep D occur?

A

Hep B coinfection with presence of HBsAG

62
Q

How do you diagnose Hep D?

A

anti-HDV

63
Q

What are the essentials of diagnosis of HDV?

A
  • Infection with HDV occurs with HBV only and is detected by anti-HDV. IgM vs IgG is not useful.
  • HDV RNA is found via PCR or molecular hybridization
  • IgG positive suggests superinfection.
64
Q

What is Hep E often seen in?

A
  • Waterborne outbreaks.
  • Suspect it in anyone with acute hepatitis post trip to an endemic area.
65
Q

Where is Hep E endemic?

A
  • Asia
  • North Africa
  • Middle East
66
Q

What is the most common population for HEV?

A

Young adults, most severe among pregnant women.

67
Q

How is HEV diagnosed?

A

IgM anti-HEV

68
Q

How does HEV typically present?

A
  • Prodrome of FLS
  • Icteric phase of jaundice
  • Extrahepatic manifestations (such as GBS or peripheral neuropathy)
69
Q

How do you treat HEV?

A

3 months of PO ribavirin

70
Q

Who is HEV most severe in?

A

Pregnant women

71
Q

What are the essentials of diagnosis for HEV?

A
  • Fecal-oral route with self-limited infection
  • HEV is diagnosed via IgM anti-HEV or HEV RNA by PCR
  • HEV is most severe in pregnant women
  • No vaccine in da US :(
72
Q

What is hemochromatosis?

A
  • Autosomal recessive disorder
  • Increased iron absorption from duodenum and stored in the liver
  • Stores as hemosiderin and increased deposits everywhere
73
Q

Who is hemochromatosis MC in?

A

Northern europeans and NA caucasians

74
Q

Who is cirrhosis MC in for patients with hemochromatosis?

A
  • Alcoholics
  • Obesity
  • Advanced age
  • Diabetes
75
Q

How does hemochromatosis typically present?

A
  • Early: Fatigue, arthralgia
  • Late: symmetric arthropathy, hepatomegaly, hepatic dysfunction, bronze skin pigmentation, cardiac enlargement, DM, ED in males
76
Q

How do you diagnose hemochromatosis?

A
  • Iron studies and genetic testing
  • Low TIBC
  • HFE Mutations
77
Q

How do you treat hemochromatosis?

A
  • Low iron diet
  • Weekly phlebotomy of 1-2 units of blood for 2-3 yrs
  • Deferoxamine IV or Deferasirox PO for chelation
78
Q

What is the demographic of Wilson’s disease?

A
  • Rare autosomal recessive
  • Prior to age 40
  • Chromosome 13 defect causing increased absorption of copper and decreased excretion BY THE LIVER via low ceruloplasmin
79
Q

Where does excess copper deposit in the body?

A
  • Liver
  • Brain
80
Q

What is the pathognomic sign of Wilson’s?

A

Kayser-Fleischer Rings

81
Q

How does Wilson’s typically present?

A
  • Hepatitis
  • Hepatosplenomegaly
  • Personality changes
  • Parkinson’s like symptoms
82
Q

What labs suggest Wilson’s?

A
  • Increased urinary copper excretion
  • Low serum ceruloplasmin
  • Liver biopsy
83
Q

What is the DOC to treat Wilson’s?

A

Penicillamine PO (Indefinitely) + B6 (pyridoxine)

84
Q

What trace mineral promotes fecal excretion of copper?

A

Zinc

85
Q

Hemochromatosis vs Wilson’s image

A
86
Q

What characterizes Gilbert’s syndrome?

A
  • Mild, unconjugated bilirubinemia
  • Familial, MC in adolescents
  • Recurrent episodes of jaundice

Adolescent version of Crigler Najjar

87
Q

What enzyme has reduced activity in Gilbert’s syndrome?

A

Glucuronyl transferase

88
Q

What triggers Gilbert’s syndrome?

A
  • Dehydration
  • Fasting
  • Infection
  • Menstruation
  • Over-exertion
  • Alcohol
89
Q

How is Gilbert’s syndrome diagnosed?

A
  • Unconjugated hyperbilirubinemia
  • Normal everything else
90
Q

How is Gilbert’s syndrome treated?

A

Benign, no treatment. Self-resolving.

91
Q

What characterizes Crigler Najjar syndrome?

A
  • Glucuronyl transferase deficiency
  • Congenital, nonhemolytic jaundice
  • Rare autosomal recessive
  • Occurs in infancy
  • Rapidly severe, high levels of hyperbilirubinemia
92
Q

What are the two types of Unconjugated hyperbilirubinemia?

A
  • Type 1: 20-50 mg/dL
  • Type 2: < 20 mg/dL
  • High levels = definitive for Crigler Najjar
93
Q

How do you treat Crigler Najjar Syndrome?

A
  • Phototherapy to oxidate bilirubin
  • Plasmapheresis
  • Liver transplant
  • Type 2 is treatable with phenobarbital
94
Q

What is Dubin Johnson Syndrome?

A
  • Genetic mutation affecting transport proteins of bilirubin
  • Elevations in conjugated serum bilirubin

Crigler is unconjugated

95
Q

How does Dubin Johnson syndrome present?

A

Intermittent jaundice and fatigue

96
Q

How is Dubin Johnson Syndrome diagnosed?

A
  • Conjugated hyperbilirubinemia in the absence of any other abnormality
  • Darkly pigmented liver on inspection
97
Q

How do you treat Dubin Johnson Syndrome?

A

Benign, no tx.

Gilbert is also no tx

98
Q

What is Rotor syndrome?

A
  • Rare Genetic disorder
  • Hepatic defect in storing conjugated bilirubin
  • Presents the same as Dubin Johnson Syndrome
  • Benign treatment
99
Q

How do you differentiate between Dubin Johnson and Rotor Syndrome?

A

Injection of dye to observe the transport system of conjugated bilirubin or liver biopsy

Transport study

100
Q

What is Budd-Chiari Syndrome?

A

Hepatic venous outflow obstruction, often resulting in polycythemia vera or myeloproliferatie disorders

101
Q

How does Budd-Chiari syndrome present?

A
  • RUQ pain (tender and painful)
  • Jaundice
  • Splenomegaly
  • Ascites
  • Chronic: bleeding varices and hepatic encephalopathy
102
Q

How is Budd-Chiari syndrome diagnosed?

A

Doppler US of IVC/hepatic veins or prominent caudate lobe

103
Q

What is a good study to view the actual obstructed veins in Budd-Chiari syndrome?

A

MRI w/ con

104
Q

How do you treat Budd-Chiari syndrome?

A
  • LWMH for underlying hematologic disorder
  • TIPS placement
  • Balloon angioplasty
  • Liver transplant
  • Lifelong anticoagulation and treatment of complications (such as ascites)
105
Q

What is the prognosis of Budd-Chiari syndrome?

A

5year survival: 50-90% with treatment. (< 10% if no intervention)

106
Q

What cell type does Hepatocellular carcinoma originate from?

A

Liver parenchymal cells

107
Q

What is the majority of hepatocellular carcinoma due to?

A

Cirrhosis

108
Q

What are the risk factors for hepatocellular carcinoma?

A
  • Obesity
  • Male
  • Age > 55
  • FMHx
  • DM
  • HCV or HBV
  • Alcohol
109
Q

What is the clinical presentation of hepatocellular carcinoma?

A
  • Deterioration
  • Cachexia, severe wt loss, anorexia, weakness, muscle wasting
  • Bloody ascites
  • Tender hepatomegaly
110
Q

What biomarker is elevated in hepatocellular carcinoma?

A

Alpha fetoprotein (70%)

AFP

111
Q

What liver enzyme gets elevated in Hepatocellular carcinoma?

A

ALP

112
Q

What is the first-line imaging to identify a mass in hepatocellular carcinoma?

A

CT and MRI with contrast

113
Q

What confirms hepatocellular carcinoma?

A

Liver biopsy

DO NOT need if CT w/ con has a mass + Alpha fetoprotein is elevated

114
Q

At what T stage does vascular invasion occur?

A

T2 or higher

115
Q

At what T stage does a tumor involve a major branch of the portal or hepatic vein?

A

T3

116
Q

Invasion of what organ does not count as T4 in hepatocellular carcinoma?

A

Gallbladder

117
Q

Who gets screened for Hepatocellular carcinoma and what does screening consist of?

A
  • Cirrhosis or Chronic HBV/HCV
  • Liver US and alpha fetoprotein q 6months

CT is better but more expensive

118
Q

How do you treat hepatocellular carcinoma?

A

Resection if no vascular invasion (AKA T1 or lower)

119
Q

What MELD score suggests poor post-transplant survival rates?

MELD = Model for end-liver disease staging

A

> = 20

GI (17 decks)

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