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GI > Disorders of the Liver II - Exam 4 > Flashcards

Disorders of the Liver II - Exam 4 Flashcards

1
Q

What are the different ways viral hepatitis A-D are transmitted?

A

A: fecal-oral route

B: Bloodborne, sexually transmitted

C: Bloodborne, sexually transmitted

D: Only associated with Hepatitis B co-infection

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2
Q

What type of virus is Hep A? Where is it commonly found?

A

RNA virus

fecal-oral route and commonly seen in crowded living areas with poor sanitation and RESTURANTS

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3
Q

What is the incubation period for Hep A? How long can it be fecally excreted? Is there a chronic carrier state?

A

Incubation period averages 30 days

Can be fecally excreted for up to 2 weeks before clinical illness and up to a week after clinical illness

no chronic carrier state

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4
Q

Is Hep A more severe in adults or children? What is a weirdly sorta unique finding with Hep A and B?

A

more severe in adults

distaste for smoking

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5
Q

Hep A jaundice usually occurs after _____ days. What will their stools look like?

A

jaundice occurs after 5-10 days

stools may be acholic (very pale stools)

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6
Q

________ levels will be elevated in a pt with Hep A. **How is the dx of hep A established?

A

Elevated serum aminotransferase levels

The diagnosis is established by detection of: serum IgM anti-HAV antibodies:
Antibody to Hepatitis A (anti-HAV)

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7
Q

_____ is the best lab indicator for active hep A infection. **_____ is the best indicator of previous exposure, non-infectivity and immunity

A

IgM: active infection

IgG: previous exposure, non-infectivity, and immunity

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8
Q

What will the liver labs be doing in an acute hep A infection? What additional labs will be elevate?

A

**Striking ALT/AST elevations

elevated levels of bilirubin, WBC normal to mildly elevated

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9
Q

What is the tx for Hep A? What is the prevention? What is the prognosis?

A

tx: symptomatic: rest and fluids

prevention: wash hands and vaccination!!

Clinical recovery typically complete within 3 months (relapses may occur)

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10
Q

the diagnosis of acute hep A infection depends on the detection of _____

A

IgM anti-HAV

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11
Q

the development of an __________, which occurs subsequent to the IgM response, is protective and provides lifelong immunity

A

immunoglobin G anti-HAV (IgG anti-HAV)

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12
Q

Hep B structure is ______. What are the 2 parts that make it up?

A

partially double stranded DNA

inner core protein and outer surface coat

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13
Q

**What are the 2 components of the Hep B inner core protein? _____ makes up the outer surface coat

A

Hepatitis B core antigen (HBcAg)

Secretes Hepatitis B e antigen (HBeAg)

HBcAg secretes HBeAg
______________

Hepatitis B surface antigen (HBsAg)

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14
Q

Who are the at risk populations for hep B? What is the prevention?

A

IV drug users
Prison inmates
Healthcare workers

vaccination!

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15
Q

_____ occurs in less than 1% of Hep B infections, but if occurs, has a mortality rate of up to 60%

A

Acute liver failure

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16
Q

What is the incubation period of Hep B? What is the average incubation period?

A

6 weeks to 6 months

12-14 weeks

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17
Q

**What does HBsAG stand for? What does it indicate?

A

Hepatitis B surface antigen

Active infection (acute or chronic)

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18
Q

**What does Anti-HBs (HBsAb) stand for? What does it indicate?

A

Hepatitis B surface antibody

Immunity (from recovery or vaccination)

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19
Q

**What does HBeAg stand for? What does it indicate?

A

Hepatitis B e antigen

High infectivity and active viral replication

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20
Q

**What does Anti-HBe (HBeAb) stand for? What does it indicate?

A

Hepatitis B e antibody

Lower infectivity, less active viral replication

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21
Q

**What does Anti-HBc (HBcAb) - Total stand for? What does it indicate?

A

Current or past infection (not from vaccination)

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22
Q

**What does anti-HBc IgM stand for? What does it indicate?

A

Hepatitis B core antibody (IgM)

Acute or recent infection

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23
Q

**What is the first HBV serologic markers to elevate/first sign of infection? If it persists beyond 6 months, what does it indicate?

A

Hepatitis B surface antigen (HBsAG)

first sign of infection

indicates chronic disease

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24
Q

Appearance of ____ and decline in ____ indicates recovery of acute infection and non-infectivity.

A

anti-HBs

HBsAG

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25
Q

What markers need to be present that would indicate previous vaccination with immunity?

A

Persistence of anti-HBs without elevated HBsAG

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26
Q

____ appears one month after HBsAg is detected. What does it indicate?

A

IgM anti-HBc

indicates a diagnosis of declining acute Hepatitis B

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27
Q

_____ also appears during acute hepatitis B, but persists ____. What will show in recovery? Chronic dz?

A

IgG anti-HBc

indefinitely

With recovery → IgG occurs with Anti-HBs

With chronic ds → IgG occurs with HBsAG

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28
Q

**______ Indicates viral replication and infectivity (when patient is most infectious). When does it appear? What follows it?

A

Hepatitis B envelope antigen (HBeAG)

Appears: shortly after HBsAG in the serum in the incubation period

followed by appearance of anti-HBe

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29
Q

presence of _____ indicates the hep B acute phase is over and the chance of infectivity is low

A

Hepatitis B e-antibody (HBeAb)

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30
Q

______ parallels the presence of HBeAg. ** What is important to note about it?

A

HBV DNA

precise marker of viral replication and infectivity

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31
Q

_______ and _____ makes the diagnosis of acute Hep B infection

A

IgM anti-HBc with combo of HBsAG

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32
Q

What is the tx for ACUTE hep B?

A
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33
Q

What is the prophylaxis Hep B tx after exposure? **What is the associated timeframe?

A

Hepatitis B immune globulin (HBIG) then initiation of the vaccine series

Must give within 7 days of exposure

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34
Q

What is the tx for an infant born to a Hep B positive mother?

A

Hepatitis B immune globulin (HBIG)

Indicated in newborns with HBV + mothers: HBIG and initiation of vaccine series within 12 hours of birth to infant

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35
Q

What is the prevention for Hep B?

A

universal precautions
safe sex education
do NOT share needles
VACCINATION

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36
Q

What lab values would make you think chronic Hep B? 40% of chronic hep B will develop _____

A

Elevated ALT/AST for > than 6 months and presence of HBsAg

cirrhosis

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37
Q

**What is the tx for CHRONIC hep B?

A

1st line: Nucleoside and nucleotide analog (first line)
Entecavir (Baraclude) or Tenofovir (Vemlidy)

2nd line: Interferon

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38
Q

________ MOA incorporates into viral DNA and inhibits reverse transcriptase = mutations of virus rendering ineffective

A

Nucleoside and nucleotide analog (first line)

Entecavir (Baraclude) or Tenofovir (Vemlidy)

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39
Q

____ MOA inhibits viral replication. What is the BBW?

A

interferon

BBW: for infections

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40
Q

What is the interpretation?

A

prior infection (inactive)

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41
Q

What is the interpretation?

A

immune due to Hep B vaccination

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42
Q

What is the interpretation?

A

acutely infected

43
Q

What is the interpretation?

A

chronically infected

44
Q

The diagnosis of Hep B relies on the presence of _____ in the serum

A

HBsAg

45
Q

Which antibody shows immunity?

A

anti-HBs

46
Q

What is the structure of Hep C? **50% of cases are transmitted via _____

A

single stranded RNA

IV drug use

47
Q

What is the risk of Hep C maternal-neonate transmission?

A

Risk of maternal-neonatal and sexual transmission low in Hep C

higher transmission rate for Hep B

48
Q

______ is the most common bloodborne infection in the United States, with an estimated 2.4 million people harboring an active infection. Approximately 21% of ____ pts also have Hep C

A

Hep C

HIV

49
Q

What is the incubation period of Hep C? High incidence develop _____ (up to 85%)

A

Average 6-7 week incubation period

with waxing and waning jaundice

chronic hepatitis

50
Q

**diagnosis of Hep C is based on ______. What does the presence of HCV RNA tell you?

A

HCV antibodies = presence of Anti-HCV

HCV RNA: Presence indicates current infection

51
Q

**What does the presence of Anti-HCV without HCV RNA indicate?

A

prior Hep C exposure with recovery.

52
Q

What hep has the highest incidence of becoming chronic? What does Hep C increase your risks for?

A

Hep C

Non-Hodgkin’s lymphoma
Glomerulonephritis
idiopathic pulmonary fibrosis
thyroiditis

53
Q

What is the prevention for Hep C?

A

NO VACCINE!!!

NOT spread sexually or during childbirth

really just spread from dirty needles associated with IV drug use

54
Q

What is the older tx method for Hep C?

A

Interferon x 6-24 weeks and can add Ribavirin if no improvement

55
Q

**What is the newer tx options for Hep C?

A

A 6 week course of ledipasvir/sofosbuvir (Harvoni)

56
Q

What are 3 risk factors that would add to the progression of chronic hep C to cirrhosis?

A

Increased risk in men
Those who drink more than 50g alcohol daily
Those who acquire HCV infection after age 40 years

57
Q

_____, _____ and _______ promotes progression of Hep C to fibrosis. What can slow progression?

A

Tobacco
cannabis smoking
hepatic steatosis

coffee can slow progression

58
Q

antiviral cure about _____ of hep C infections

A

95%

59
Q

**What is Hep D associated with? What pt population? How is it dx? What is the tx?

A

Only associated with Hepatitis B - coinfection

mainly among IV drug users

detection of serum antibodies: anti-HDV

tx: self care, supportive and avoiding alcohol

60
Q

Where is Hep E commonly found? What is the structure?

A

Central and Southeast Asia, the Middle East, and North Africa, where it is responsible for WATERBORNE hepatitis outbreaks

RNA virus

not common in the US, need to ask travel history

61
Q

**What is the MC pt population associated with Hep E? In developed countries, how is it commonly spread?

A

pregnant women

swine, and consuming undercooked organ meats

62
Q

What is the incubation period for Hep E? How is the dx made?

A

2-10 weeks

The diagnosis is made most readily by testing for IgM anti-HEV in serum

63
Q

“flu-like symptoms” followed by “icteric phase” of frank jaundice

What am I?
What are some extrahepatic manifestations?
What labs will be elevated?

A

Hep E

arthritis; pancreatitis; thrombocytopenia; and a variety of neurologic complications, including Guillain-Barré syndrome and peripheral neuropathy

elevated aminotransaminase and bilirubin levels

64
Q

What is the tx for Hep E? **What is the important take away regarding Hep E?

A

A 3-month course of treatment with oral ribavirin

can be very severe in preg women!! mortality rate can reach 15-25%

no vaccine approved in the US, but there is a promising one in China

65
Q

What is hemochomatosis? How is it inherited? What is the associated gene?

A

Increased iron absorption from duodenum and stored in liver

autosomal recessive

HFE gene mutation

66
Q

How is iron stored?

A

stored in the liver as hemosiderin

67
Q

When does hemochromatosis typically present? What are some late findings?

A

usually around 50

symmetric arthropathy
hepatomegaly
hepatic dysfunction
bronze skin pigmentation (melanin deposition), cardiac enlargement (can progress to heart failure)
DM

68
Q

What will the iron lab values show of a pt with hemochromatosis?

A

Elevated serum iron levels and serum ferritin
LOW TIBC: total iron binding capacity

69
Q

____ can be used to confirm hemochromatosis dx and ____ to determine the extent of liver damage

A

genetic testing

liver bx

70
Q

What is the tx for hemochromatosis? What are the chelating agents?

A

low iron diet
decrease alcohol
weekly phlebotomy until iron stores are depleted then PRN

Deferoxamine IV or Deferasirox po

71
Q

What is Wilson Dz? How is it inherited?

A

genetic defect on chromosome 13 that affects the copper transporting enzyme and leads to excessive absorption of copper form intestines, and decreased excretion by the liver

rare autosomal recessive disorder

72
Q

What does Wilson disease lead to ? When does it commonly present?

A

deposition of copper in liver and brain

childhood or young adult

73
Q

What are the 2 organs systems affected the most by Wilson disease?

A

liver and brain: can present with parkinsonian like symptoms, ataxia, dysphagia, incoordination

elevated LFTs and cirrhosis

can also have psych features

74
Q

**What is the pathognomic sign for Wilson disease?

A

Kayser-Fleischer ring
copper deposits in cornea

75
Q

What are some common lab findings on a pt with Wilson disease?

A

Increased urinary copper excretion

Low serum ceruloplasmin levels

Liver biopsy to assess chronic hepatitis and cirrhosis

76
Q

What is the tx for Wilson Disease?

A

restriction of dietary copper: shellfish, nuts, mushrooms, chocolate

**oral penicillamine: chelating agents with vit B6

oral zince to promote fecal excretion of copper

77
Q

What is Gilbert syndrome? What enzyme?

A

Characterized by MILD unconjugated bilirubinemia

Reduced activity of glucuronyl transferase

78
Q

What is the role of glucuronyl transferase?

A

Liver enzyme that gives glucuronic acid and changes bilirubin into a form that can be removed from body in bil

79
Q

**Recurrent episodes of jaundice that are triggered dehydration, fasting, infection, menstruation, over-exertion, alcohol

What am I?
What lab finding?
What is the tx?

A

Gilbert Syndrome

Unconjugated hyperbilirubinemia ( < 3mg/dL)
and NORMAL everything else!

benign, no tx is necessary

80
Q

What is Crigler Najjar Syndrome? What is it caused by?

A

Congenital nonhemolytic jaundice

Rapidly severe, High levels of unconjugated hyperbilirubinemia

Rare autosomal recessive disorder that is either a complete or partial Glucuronyl transferase deficiency

81
Q

When does Crigler Najjar Syndrome present? What can it lead to?

A

Occur in infancy

High levels of bilirubin can lead to neurological damage.
“Kernicterus”

82
Q

**What are the different levels of Crigler Najjar Syndrome?

A

Type I levels 20-50 mg/dL
Type II levels < 20mg/dL
High levels definitive for diagnosis

83
Q

What is the tx for Crigler Najjar Syndrome? What is the tx for Type II?

A

Phototherapy!!

phenobarbital which will also induce the enzyme

84
Q

Why does phototherapy work well for Crigler Najjar Syndrome? ______ is curative

A

Lowers bilirubin levels through photo-oxidation

Adds oxygen to the bilirubin so it easily dissolves

Body can excrete through urine/feces

liver transplant is curative

85
Q

What is Dubin Johnson Syndrome? What is the key word here? What does it result in?

A

Genetic mutation affecting transport proteins of bilirubin

Elevations in Conjugated serum bilirubin

86
Q

Intermittent Jaundice, fatigue
May see darkly pigmented liver on gross inspection
Conjugated hyperbilirubinemia in the absence of other abnormalities

What am I?
What is the tx?
What can exacerbate the condition?

A

Dubin Johnson Syndrome

benign condition: no tx needed

illness, OCP and pregnancy

87
Q

What is the Rotor Syndrome? What are the 2 key words?

A

Rare genetic disorder
Hepatic defect in storage of conjugated bilirubin
Leaks back into bloodstream

88
Q

How can you tell Rotor Syndrome apart from Dubin Johnson?

A

Can inject dye and do “transport study” to determine if Rotor or Dubin Johnson

liver bx: Rotor will have a norma looking liver and Dubin Johnson will have dark liver

89
Q

What is the tx for Rotor Syndrome?

A

benign condition: no tx needed

90
Q

What is Budd-Chiari Syndrome? What is the usually underlying cause?

A

Hepatic venous outflow obstruction

Hereditary and acquired hypercoagulable states can be defined in 75% of patients

91
Q

tender, painful hepatic enlargement (RUQ pain)
Jaundice
Splenomegaly
Ascites
chronic: bleeding varices and hepatic encephalopathy may be evident

What am I?
**What is the imaging of choice? What will it show?

A

Budd-Chiari Syndrome

Doppler ultrasonography: occlusion/absence blood flow in hepatic veins/IVC
May see “spider web” pattern of occluded hepatic veins

92
Q

In Budd-Chiari Syndrome, the doppler ultrasonography may show prominate _______ since its venous drainage may be occluded

A

caudate lobe: venous drainage may be occluded since it is supplied by L/R hepatic veins

93
Q

_______ allows visualization of the obstructed veins and collateral vessels in _______

A

MRI with contrast

Budd-Chiari Syndrome

94
Q

What is the tx for Budd-Chiari Syndrome?

A
95
Q

Hepatocellular Carcinoma arise from liver _______ cells and 80% are due to ________

A

parenchymal cells

d/t Cirrhosis

96
Q

What are the hepatocellular carcinoma risk factors for patients with cirrhosis?

A

Obesity
Male gender
Age > 55
Family History
DM
HCV or HBV infection
Alcohol

97
Q

**What are the 2 lab findings associated with hepatocellular carcinoma?

A

Spike in ALP
Alpha fetoprotein in 70% of patients

98
Q

**What are the first line imaging for hepatocellular carcinoma? What confirms?

A

CT and MRI are first line imaging to identify masses

liver bx confirms

99
Q

**When can a liver bx be deferred in Hepatocellular Carcinoma?

A

Can be deferred if mass on CT and + alpha fetoprotein

100
Q

What are the staging classifications for Hepatocellular Carcinoma?

A
101
Q

What is the screening for hepatocellular carcinoma?

A
102
Q

What is the tx for Hepatocellular Carcinoma? What MELD score?

A
103
Q
A

GI (12 decks)

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