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GI Boards > Liver Disease and Transplantation > Flashcards

Liver Disease and Transplantation Flashcards

1
Q

Rates of fulminant hepatic failures in HAV, acute HBV, and HBV and HDV coinfection

A

HAV = 0.1%
Acute HBV = 1%
HBV and HDV Confection = 20%

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2
Q

Percent of individuals who develop chronic HBV when exposed perinatally? When exposed in childhood? When exposed in adulthood?

How about chronicity in patients exposed to HCV?

A

Chronicity is 90% when exposed perinatally, 50% if exposed during childhood, and 5% in adulthood.

HCV becomes chronic in 60-85% of patients exposed regardless of age.

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3
Q

When to screen HBV carriers without cirrhosis for HCC?

A

Africans >20, Asian males >40, asian females >50, family history of HCC

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4
Q

2 extrahepatic complications of chronic HCV? How to improve symptoms?

A

Essential mixed cryoglobulinemia, membranoproliferazive glomerulonephritis (MPGN).

Can improve renal function and proteinuria with eradication of HCV RNA.

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5
Q

Extrahepatic manifestation of chronic hepatitis B infection? How to improve symptoms?

A

Polyarteritis nodosa (positive for HBsAg).

Can improve symptoms with antivirals, as well as mortality.

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6
Q

HBV genotype that is most responsive to peginterferon? Least responsive

A

Most responsive is genotype A with high ALT or low HBV DNA.

Least responsive is genotype D.

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7
Q

Symptoms of chronic HBV spontaneous seroconversion

A

Where HBeAg is suppressed by immune system, HBV DNA is lost, and HBeAb appears. Can cause elevations in AST/ALT and sometimes acute liver failure. These patients can still get HCC, but not cirrhosis

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8
Q

Risk of fulminant liver failure from HEV?

A

Very low, less than 1% but as high as 15-25% in pregnant women

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9
Q

HCV genotype most likely to progress to cirrhosis?

A

Genotype 3

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10
Q

Most challenging HCV genotype to treat? How to treat more effectively?

A

Genotype 3 is the most challenging to treat. Can treat most effectively by increasing therapy to 24 weeks.

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11
Q

What is the risk of recurrent HCV after transplant?

A

25-33% of recurrent HCV patients after transplant can develop fibrosis or cirrhosis again.

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12
Q

What are the features and lab tests for Type II AIH?

A

Autoimmune hepatitis which is rapid onset usually seen in children under 14. Test for Anti-LKM

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13
Q

Most common cause of drug-induced autoimmune hepatitis? How to treat?

A

Nitrofurantoin and minocycline
Cause interface hepatitis and abundance of plasma cells
Stop drug, sometimes will need acute course of steroids

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14
Q

Which beta blocker is best for variceal ppl during pregnancy?

A

Propranolol

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15
Q

Management of HEV in solid organ transplant?

A

Reduction of immunosuppression, if that doesn’t work, then ribavirin

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16
Q

Ribavirin major side effect

A

Hemolytic anemia (dose dependent)

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17
Q

Treatment options for HCV in patients without cirrhosis

A

Glecaprivir/pibrentasvir for 8 weeks (Mavyret)

Sofosbuvir/velpatasvir for 12 weeks (Epclusa)

Ledipasvir/Sofosbuvir for 12 weeks (Harvoni)

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18
Q

Difference between treating HCV in patients with compensated cirrhosis and without cirrhosis?

A

None, can still use Glecaprevir/pibrentasvir for 8 weeks, though need to increase to 12 weeks if connected with HIV.

Can still use sofosbuvir/velpatasvir for 12 weeks.

Can still use ledipasvir/sofosbuvir for 12 weeks.

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19
Q

Critical lab test to check before starting HCV therapy? Why?

A

HBV serologies because risk of HBV reactivation increases with DAA therapy, even for patients who are core positive.

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20
Q

How to treat HCV in patients with decompensated cirrhosis?

A

Need to increase duration of treatment in most cases, consider addition of ribavirin, and start transplant eval because may be beneficial to transplant before tx

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21
Q

Do you need to dose-reduce DAAs for HCV in patients with CKD

A

No

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22
Q

Should you treat acute HCV?

A

Monitor HCV q4-8 weeks for up to 12 months to determine if spontaneous clearance occurs.

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23
Q

How to treat chronic hepatitis D infection?

A

PEG-IFN alpha for 12 months, can also add Bulevirtide

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24
Q

How to prevent HBV infection in transplant recipients?

A

All HBsAg positive patients undergoing transplant should receive entecavir, TDF, or TAF, with or without HBIG

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25
Q

How to treat HBsAg negative patients who receive HBsAg negative, HBcAb positive donor livers?

A

Long term prophylactic antivirals with entecavir TDF or TAF

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26
Q

How to diagnose CMV hepatitis?

A

Biopsy is needed

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27
Q

Which patients are most susceptible to HSV hepatitis?

A

Immunosuppressed patients or pregnant patients in 2nd or 3rd trimester

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28
Q

How to treat HSV hepatitis

A

IV acyclovir is preferred, start before diagnosis is confirmed because delay can be catastrophic

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29
Q

Which drugs require prophylaxis for HBV reactivation?

A

Very high risk: Rituximab and stem cell transplant
All others just require monitoring with HBV DNA.

High risk: >20mg pred, cytokine inhibitors
Moderate risk: Chemotherapy, antiTNF, anti rejection meds
Low risk: Azathioprine, methotrexate

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30
Q

3 groups for which to treat chronic HBV

A
  1. Cirrhosis and low viremia (<2000)
    2.HBeAg+ immune-active if HBV DNA >20,000 and ALT >2x ULN
  2. HBeAg- Immune-active if HBV DNA >2000 and ALT > 2x ULN
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31
Q

Why is TAF superior to TDF

A

Decreased chance of bone and renal abnormalities

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32
Q

When to stop oral meds for chronic HBV with HBeAg+

A

12 months after seroconversion from HBeAg to HBeAb

Lifelong if no seroconversion

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33
Q

When to stop oral meds for chronic HBV with HBeAg-?

A

With 3 years of viral load suppression if they can be monitored closely

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34
Q

Microvesicular steatosis vs Macrovesicular steatosis

A

Microvesicular steatosis seen in rare conditions (Reye syndrome, mitochondrial disorders, drug toxicity [tamoxifen, amiodarone, methotrexate])

Macrovesicular steatosis seen with NAFLD and alcoholic steatosis

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35
Q

Features of alcoholic hepatitis on pathology

A

Ballooning degeneration, apoptosis, giant mitochondria, mallory bodies (not specific).

Damage most prominent in perivenular region

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36
Q

Presentation and treatment for acute Wilsonian hepatitis

A

Elevated LFTs, jaundice, hemolysis due to copper

Transplant

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37
Q

How to diagnose hemochromatosis?

A

Ferritin, transferrin saturation, hemochromatosis genetics.

BUT ultimately liver biopsy IS necessary

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38
Q

Features of metabolic syndrome

A

High visceral fat, dyslipidemia, insulin resistance, hypertension

Waist circumference
Fasting triglycerides >150
HDL <40
BP>130/85
Fasting BG >110

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39
Q

Likely cause of elevated ALT if no obvious cause

A

75% of these patients will have NASH

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40
Q

Acute Fatty Liver of Pregnancy presentation, cause, and treatment

A

Rapidly progressive rise in AST/ALT, diffuse micro vesicular steatosis. Can cause liver failure. Caused by toxic intermediates of fatty acid oxidation. Need immediate termination of pregnancy and sometimes transplant

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41
Q

Difference between Dubin-Johnson and Rotor Syndrome

A

Both cause conjugated hyperbilirubinemia, liver turns black in Dubin-Johnson syndrome

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42
Q

PFIC

A

Progressive familial intrahepatic cholestasis can cause cirrhosis in infancy. Likely will need transplant

43
Q

BRIC

A

Benign recurrent intrahepatic cholestasis. Intermittent, non progressive, normal liver function

44
Q

CF associated liver disease, and treatment to delay progression

A

Causes progressive cholestasis due to thick bile, can give patients ursodiol, can progress to biliary cirrhosis

45
Q

Hereditary Tyrosinemia Type 1 and treatment

A

Enzyme missing leading to toxic intermediates in pathway of phenylalanine and tyrosine metabolism. Causes childhood fibrosis and cirrhosis. NTBC inhibits early step in pathway and can be used for treatment. Some patients may need transplant.

46
Q

Glycogen storage diseases and hepatic consequences

A

Type 1 (Von Girke)
Type 3 (Cori)

Changes in G6P (type 1) and debranching enzyme (type 3)

Causes hepatic adenomas and HCC

Some can have ALF and require transplant

47
Q

Gaucher Disease

A

Lipid storage disease (glucocerebrosidase deficiency). Most common deficiency in jews

Causes hepatosplenomegaly, bone fractures, anemia, thrombocytopenia

Some patients can develop progressive fibrosis and portal hypertension

48
Q

Role of hepcidin

A

Hepcidin regulates iron release from macrophages and intestinal absorption by binding to ferroportin in enterocytes

49
Q

What manifestations of hemochromatosis usually don’t improve with chelation of phlebotomy

A

Testicular atrophy and arthropathy

Risk of HCC does not improve either

50
Q

What does ATP7B do?

A

Secretes copper into bile for excretion. Mutation causes Wilson disease

51
Q

How to diagnose Wilson disease?

A

Check ceruloplasmin, if low, eye exam and 24h copper extretion

52
Q

How to treat Wilson disease

A

Copper chelation with Trientine and prevent absorption with oral zinc.

Can also use d-penacillamine but has side effects

53
Q

Treatment for ALF due to wilson’s

A

Transplant, if normal ATP7B in graft then chelation is not needed

54
Q

A1AT Alleles

A

M is normal
S is modest deficiency
Z is severe deficiency

MM normal
ZZ is severe deficiency, SZ also relatively severe

55
Q

Diseases that often accompany PBC?

A

Sjogrens Syndrome, CREST.

Inflammatory destruction of small bile ducts causing cholestasis and biliary cirrhosis.

56
Q

PBC presentation

A

Elevated AP, pruritis, fatigue, xanthomas/xanthelasmas, fat soluble vitamin deficiencies

57
Q

Treatment of PBC

A

13-15mg/kg ursodiol or OBCA for ursononresponders

58
Q

Histology of PBC

A

Florid duct lesion

59
Q

How to diagnose AIH?

A

Serologies are helpful but need to biopsy to confirm

60
Q

AIH histology

A

Plasma cell infiltration, interface hepatitis

61
Q

How to treat AIH

A

40-60mg pred, transition to 1.5-2mg/kg azathioprine

can also use mycophenolate or tacrolimus

62
Q

Which treatment for AIH cannot be used in pregnancy?

A

Mycophenalate

63
Q

Presentation of acute cellular rejection

A

Elevations in transaminases and alc phos weeks to months after transplant

64
Q

What condition has hepatocyte injury, ductulitis, venular Endothelitis?

A

Acute cellular rejection

65
Q

How to treat ACR?

A

Mild: Conservative
Severe: IV steroids and anti-lymphocyte globulin

66
Q

What condition usually follows ACR?

A

Chronic ductopenic rejection – marked by progressive loss of bile ducts

67
Q

Schistosomiasis causes…

A

isolated pre-sinusoidal portal hypertension

68
Q

ABCB11

A

Gene implicated in BRIC PFIC and intrahepatic cholestasis of pregnancy

69
Q

Jaundice and transaminase elevation in the setting of chemotherapy or bone marrow transplant?

A

Hepatic sinusoidal obstruction syndrome

70
Q

Cholestasis with hilar biliary structures in a patient with a history of shock

A

Ischemic cholangiopathy

71
Q

An insulin sensitizing peptide secreted by adipose tissue whose levels decline as fat accumulates, low levels characterize metabolic syndrome

A

Adiponectin

72
Q

A phospholipase enzyme associated with the propensity to hepatic steatosis and fibrosis in both NASH and alcoholic liver disease

A

Adiponutrin

73
Q

A circulating signalling peptide that participates in the up regulation of hepcidin production

A

Bone morphogenic protein 1

74
Q

Hepatic co-receptor for bone morphogenic protein 1

A

Hemojuvelin

75
Q

What is the antibody against the lipoid antibody moiety of the pyruvate dehydrogenase complex in bile duct epithelial cells

A

Anti-mitochondrial antibody

76
Q

What is the antibody against hepatic enzyme cytochrome P450 2E6

A

Anti liver kidney microsomal antibody (AIH type 2)

77
Q

How to calculate HVPG? What is considered elevated

A

Hepatic wedge pressure - free hepatic pressure. More than 5 is elevated, varies tend to happen over 10

78
Q

Paradigm for primary prevention of varices

A

Look at liver stiffness and platelet count. If PLT >150,000 or liver stiffness <20, no need for primary prevention.

If LS>20 and platelet <150K, or LS>25 then start NSBB.

If not tolerated, do EGD. If no varices, EGD q2y. If large varices, band.

79
Q

Important treatment of variceal hemorrhage

A

CTX 1g/day for up to 5 days
Octreotide

PPI is not important if variceal bleed

80
Q

GOV1 vs GOV2 vs IGV1 vs IGV2?

A

GOV1 extend along lesser curve
GOV 2 extend from esophagus to the fundus
IGV1 are isolated in the fundus
IGV2 are in the antrum

81
Q

Which patients benefit from early tips and variceal bleeding?

A

CP C after hemorrhage or CP B with active hemorrhage

82
Q

How to treat portal hypertensive gastropathy

A

Iron and beta blocker

83
Q

Two different types of high SAAG (>1.1) ascites?

A

Portal hypertension (low ascites albumin <2.5)

Cardiac ascites (higher ascites albumin >2.5)

84
Q

Who should be on SBP ppx? What to use

A

Those who have ever had SBP – use cipro

85
Q

What causes persistent encephalopathy in patients that are otherwise compensated?

A

Splenorenal or other shunt

86
Q

How to diagnose hepatic sarcoid

A

Biopsy

87
Q

Hepatopulmonary syndrome cause, presentation, treatment

A

Caused by dilated pulmonary capillaries and shunting causing hypoxemia. Presentation is platypnea and orthodeoxia.

Tx with transplant

88
Q

Portopulmonary hypertension

A

Pulmonary vasoconstriction due to unprocessed mediators from splanchnics causes severe pulmonary hypertension

89
Q

Typical imaging features of HCC?

A

Arterial hypervascularity and early washout in venous/portal/delayed phase

90
Q

How to treat early stage HCC in healthy patient?

A

Resection if single mass <5cm is curative

Otherwise will need RFA +/- TACE or TARE

91
Q

Milan criteria

A

Patients can be transplanted for HCC if they have 3 or fewer tumors <3cm, or 1 tumor <5cm provided no vascular invasion or extra hepatic disease

92
Q

What must be included in transplant workup for HCC patients?

A

CT chest and bone scan

93
Q

How to treat advanced stage HCC in Childs A or B patients?

A

Atezolizumab/bevacizumab&raquo_space;> sorafenib

94
Q

How to treat advance stage HCC in Childs C patients?

A

Supportive care, median survival is 3 months

95
Q

What is the MELD to consider TXP?

A

15, but patient should be referred to txp center after their first decompensation

96
Q

Does AIH recur post transplant?

A

Yes – do not taper steroids completely

97
Q

What are the signs of primary liver graft nonfunction?

A

No bile production, liver failure, renal failure

98
Q

What causes hepatic venous outflow obstruction after transplant?

A

Stenosis of the anastomosis of the hepatic vein and the IVC

99
Q

What is the baseline IS regimen after liver transplant?

A

A CNI (tac/cyclo), immunomodulator (MMF, everolimus, azathioprine), and steroids

100
Q

What is long term IS regimen after liver transplant?

A

Tacrolimus

101
Q

Why is an immunomodulator added to the baseline IS regimen?

A

To reduce doses of the calcineurin inhibitor (tac/cyclo) and prevent nephrotoxicity

102
Q

What is the colonoscopy interval for post liver transplant patient with UC/PSC

A

Every year

103
Q

Should you treat HBV with cirrhosis?

A

Yes Always treat

104
Q
A

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