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80 Cards in this Set
- Front
- Back
What is considered a high HCV load?
Baylor uses IU/mL |
> 800,000 IU/mL (Baylor uses IU/mL)
or >2 millions copies/mL. High viral load is associated with less chance of response to therapy. Patients with baseline viral leves < 800,000 IU/mL are most likely to have a RVR |
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What are treatment options for HCV patients with cryoglobulinemia, vasculitis, and HCV-associated glomerulonephritis?
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Interferon or Rituxan. Interferon may improve cutaneous vasculitis, reduce cryoglobulins and rheumatoid factor.
Response is more likely if HCV-RNA levels are suppressed during therapy |
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What is RVR, EVR, and SVR?
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RVR- undetectable at 4 weeks
EVR- partial EVR- 2 log drop, complete EVR- undetectable SVR- undetectable 6 months after the end of therapy |
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When should patients with Hepatitis C be treated?
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Stage 3- Bridging fibrosis
Consider treatment in stage 2- periportal expansion |
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When whould ferridex be given during a liver MRI
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If FNH or an adenoma is suspected.
All normal reticuloendothelial cells take up ferridex, so the FNH and adenomas will be bright. HCC and hemagiomas won't take up ferridex so surrounding liver will be bright |
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When does Intrahepatic Cholestasis of Pregnancy (ICP) occur? Treatment
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Manifests with pruritis in the 3rd trimester. Diagnosis- elevated bile acids. Treatment- Urso. There is an increased risk of bleeding at delivery- give Vitamin K
ICP usually recurs in subsequent pregnancies and runs in families |
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This disorder is associated with pre-eclampsia, jaundice, elevated transaminases (usually < 1000 U/L) and an AST:ALT ration > 1
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Acute Fatty Liver of Pregnancy- usually occurs in 3rd trimester (but may even occur post-partum). A defect in hepatic lipid metabolism is the etiology, and it results in microvesicular steatosis
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Hepatic infarction and rupture is associated with what liver disorder?
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HELLP syndrome
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When do patients die of tylenol toxicity?
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Stage 3- 72-96 hours after ingestion.
Recovery begins in stage 4 (after 96 hours) |
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What stage of hepatic encephalopathy is asterixis?
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Stage 2
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What liver diseases cause steatorhea, vitamin D deficiency, osteoporosis?
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All of the chronic cholestatic liver disorders, specifically primary biliary cirrhosis. Steatorhea is due to lack of bile acids
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What is the starting dose of aldactone and lasix?
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Aldactone- 100 mg
Lasix- 40 mg |
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What is the specific pressure definition of portal hypertension
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HVPG > 6 mm Hg
This is mostly a research definition. pts with HVPG < 10 do the best |
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What is the risk of adenocarcinoma in a calcified gallbladder?
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20-30%
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What is the most responsive type of Hepatitis B? What are other predictors of response?
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Genotype A- most common in African Americans- very rare in Asians. There are 8 genotypes- A-H
The response only relates to interferon therapy (not oral antivirals). Other predictors of good response are low HBV DNA (<20,000 IU/mL) and high ALT |
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What is the most common associated autoimmune systemic manifestation of PBC
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1) Sicca syndrome present in 50%.
2) RTA Others: (20% of patients with PBC will have a coexsistent autoimmune disorder- thyroiditis, glomerulonephritis, RA, scleroderma, Sjogrens |
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What are the histologic findings of cholestasis?
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Bile duct proliferation, Bile lakes, bilirubin stasis
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What is the serology of PBC
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95% positive AMA,
ANA positive in 20% (especially in those negative for AMA) |
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What PBC patients benefit from Urso?
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Those that have a decline in alk phos with Urso
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What is the relationship between PSC and IBD?
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80% have UC, 5-10% Crohns
< 5% of patients with IBD develop PSC. PSC is unrelated to severity of IBD- it may develop years after colectomy for UC |
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Are there screening tests for cholangiocarcinoma?
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CA 19-9 and CEA
Cholangiocarcinoma is highly likely when CA 19-9 + 40(CEA) > 400 |
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Are statins needed to treat the increased cholesterol of PBC?
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No- because it is mostly HDL.
Xanthelasmas are common |
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What is characteristic of ascites associated with CHF vs cirrhosis
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High protein (>2.5) They both have high SAAG (>1.1)
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What is the incubation period for Hepatitis A? Is post-exposure prophylaxis recomended?
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Incubation period: 2-6 weeks (HAV in stool is highest during incubation period)
Yes, vaccine (preferable) or IgG for family contacts. Jaundice is age dependent- the older you are with acute Hep A, the more likely you are to get jaundice |
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Who develops relapsing Hepatitis A? Any specific symptoms?
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Pregnant women. During relapse- high incidence of extrahepatic manifestations- arthritis, vasculitis, cryoglobulinemia
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What are the causes of death in patients with acute liver failure?
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Cerebral edema- 40%
Hepatic failure- 30% |
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What is the incidence of cholangiocarcinoma in PSC?
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10% (range 6-13%)
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A patient with chronic liver disease presents with Hyperchloremic (non-gap) metabolic acidosis and akaline urine pH. What liver conditions are possible
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Renal Tubular Acidosis (Type 2- Proximal)
Wilsons (copper) PBC (copper) Any cholestatic liver disorder. Copper interferes with the kidneys ability to reabsorb HCO3 The most common cause of a non-gap metabolic acidosis is diarrhea |
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What is the most common Hepatitis B mutant?
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The precore mutant which causes failure of expression of HBeAg. HBeAg is a marker of active replication of the virus.
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What is the window period of acute hepatitis B infection?
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The "window" between when HBsAg disappears and HBsAb appears- usually weeks to months.
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What percent of patients with acute icteric HBV develop chronic hepatitis B?
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Less than 10%.
Chronic hepatitis B is more likely to develop in those with asymptomatic infection |
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How long are oral HBV agents (lamuvidine, adefovir, tenofovir, entacavir) continued?
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Until seroconversion (ie. loss of HBeAg, and appearance of HBeAb). Some advocate continueing for 6 months after seroconversion.
All patients with HBV cirrhosis should be on oral agents, even if they are HBeAg negative and have low viral DNA |
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In any patient presenting with acute hepatic failure with Coombs-negativeintravascular hemolysis, modest elevations in serumaminotransferases, or low serum alkaline phosphatase, what should be considered? |
Wilson's disease |
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What role does urine copper play in the diagnosis of Wilsons.
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Urine copper increases.
If someone has KF rings, low ceruloplasmin, and elevated urine copper a biopsy is not needed. This is the only scenario in which hepatic copper concentration and/or genetic testing is not required. AASLD 2008 |
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Why does urine copper increase in Wilsons?
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When hepatic copper maximally accumulates, copper is released or spilled into the bloodstream.
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What happens to Kayser-Fleischer rings and sunflower cataracts with treatment?
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They gradually disappear
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In addition to chelation therapy with D-penicillamine ortrientine, what is recommended for Wilson's disease patients? |
1) Low-copper diet: avoid mushrooms, nuts, chocolate, dried fruit, liver, and shellfish. 2) Avoid water with high concentrations of copper AASLD 2008 |
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In patients with acute liver failure or decompensated cirrhosis due to Wilson's disease, what should be done? |
Referral for liver transplantation AASLD 2008 |
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What is the interval and target ferritin for phlebotomy in hereditary hemochromatosis?
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Stop frequent (weekly) phlebotomy when Ferritin is <50. Check ferritin every 10-12 phlebotomies. H/H prior to each phlebotomy. Phlebotomy weekly or biweekly. Hct should not be allowed to fall by more than 20%
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What is the risk of HCV transmission at the time of
delivery? |
Low: 1-5%
C-section is not recomended. Some pediatricians recomend against fetal scalp monitors and for delivery within 6 hours of rupture of membranes. |
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Can HCV positive mothers breastfeed?
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Yes
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When should PSC patients undergo a ERCP?
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1) increases in serum bilirubin
2) worsening pruritus 3) progressive bile duct dilatation on imaging studies 4) cholangitis The purpose of ERCP in this setting is to exclude a dominant stricture (2010 AASLD guidelines) |
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Does endoscopic balloon dilation increase survival in PSC?
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Yes
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Should IGG4 levels be measured in patients suspected of having PSC?
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Yes, in order to exclude IgG4-associated sclerosing cholangitis
(2010 AASLD guidelines) |
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Is UDCA recomended in PSC?
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No. Particularly high dose (30 mg/kg) has been associated with increased mortality and need for liver transplantation
The Lindor trial using 15 mg/kg only showed decreased LFTs |
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The most frequent site of hydatid cysts?
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The most common site is the liver. The cysts usualy have a mother/daughter component and can occasionally spontaneously rupture causing anaphylaxis.
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How are echinococcal cysts treated
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The cysts can be treated with albenedazole, then percutaneous drainage
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Where is echinococcosis endemic?
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Echinococcus granulosa is endemic in large sheep raising areas in Europe, Asia, the Mediterranean, South America, and northern Kenya
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If there is signficant bleeding after a liver biopsy, what should be done?
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Angiography and embolization or surgical exploration
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What is the most important risk factor for hepatorenal syndrome?
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Ascites, particularly tense ascites.
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What are the two types of hepatorenal?
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Type 1- rapid progression of renal failure, high mortality median survival of approximately 2 weeks
Type 2- slower progression and a better prognosis and is associated with ascites that is refractory to diuretics |
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How is hepatorenal syndrome diagnosed?
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Diagnosis of exclusion- discontinuing diuretics, expanding intravascular volume with albumin
Urine Na <10, Low FeNA <1% |
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What are the two types of AIH
based on serological markers? |
Type 1- ANA, SMA (80% of cases)
Type 2- anti-LKM 1, or anti-LC1 (usually in children) |
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Does AIH type 3 exist?
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It has been abandoned, as its serologic marker (anti-SLA) is also found in type 1 and in type 2
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Should Anti-LKM1 antibodies be routinely investigated?
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Yes, to to avoid overlooking type 2 AIH
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What is the histology of AIH?
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Interface hepatitis of moderate or severe activity with or without lobular hepatitis or central portal bridging necrosis
Without biliary lesions or well defined granulomas or other prominent changes suggestive of a different etiology |
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If a liver mass is >2 cm, AFP >400 and it arterially enhances on MR or CT, what is the diagnosis? Is biopsy required
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HCC. Biopsy is not required
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When is biopsy indicated for HCC?
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When the nodule is < 2cm, as imaging techniques do not have sufficient accuracy.
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Does aflatoxin intake have a role in the genesis of HCC?
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Only in patients who have pre-existing chronic hepatitis B
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What is aflatoxin? What is the source
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A mycotoxin produced by aspergillus,they contaminate grains before harvest or during storage.
Virtually all sources of commercial peanut butter in the United States contain minute quantities of aflatoxin |
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How long does it take for UDCA to work in PBC? What is the success rate?
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Improvement LFTS in 2-3 weeks
90% of the improvement usually occurs within 6-9 months. 20% of patients will have normalization of LFTs after 2 years and a further 15% or 35% of the total will have normalization by 5 years. |
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In addition to LFTs, what does UDCA improve in PBC?
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1) reduces LDL,
2) reduces risk of developing varices 3) slower histologic progression |
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What does UDCA not improve in PBC patients?
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UDCA therapy does not improve fatigue, pruritus, associated bone disease, or autoimmune features
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In women with cirrhosis who become pregnant, what are the recomendations?
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1) check for varices in the second trimester when the mother’s blood volume increases
2) short second stage of labor is optimal as the Valsalva maneuver may precipitate variceal hemorrhage |
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What are the side effects of tenofovir? Should it be renally dosed?
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Small risk of nephrotoxicity ranging from decrease renal clearance to renal tubular defects, including Fanconi anemia. Renal dose if CrCl <50
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Prior to initiation of chemotherapy or immunosuppressive therapy, what should be tested in those high risk for HBV.
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Theoretically, even those that are HBsAg negative and core positive may reactivate, therefore check DNA |
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Who are at high risk of HBV
infection? |
Anyone from a country with high HBsAg prevalence >8% such as Africa and Southeast asia or intermediate prevalance- 2-7%
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Resolved CHB infection is defined by? |
Clearance of HBsAg with acquisition of antibody to HBsAb |
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Clearance of HBsAg, whether spontaneous or after antiviral therapy, reduces risk of ? |
hepatic decompensation and improves survival. |
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What % of person with inactive CHB will clear HBsAg yearly? |
Approximately 0.5% of persons with inactive CHB will clear HBsAg yearly; most will develop antibody to HBsAg (anti-HBs). |
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What is the best predictor of sustained remissionoff-treatment |
Loss of HBsAg loss |
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What percentage of patients lose HBsAg on Tenofovir and Entacavir at 3 years? |
Tenofovir- 8 % Entacavir- 4-5 % (at 2 years) |
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This form of noncirrhotic portal hypertension can be caused by chronic use of medications such as Azathioprine |
Nodular regenerative hyperplasia (NRH) |
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What is the pathophysiology of NRH? |
NRH is thought to be a regenerative response to vascular injury. The injury may represent a small vessel vasculitis that injures the small portal veins. |
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How is NRH diagnosed- 2 criteria? |
The diagnosis is made by liver biopsy, which shows: 1) absence of significant fibrosis (normal trichrome) 2) presence of nodularity usually best defined by reticulin staining. On superficial review, the liver biopsy may appear normal. |
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In additional to medications, what are other causes of NRH? |
NRH has been reported to occur in association with other systemic diseases including: 1) Rheumatologic disorders (PAN, RA) 2) Vascular disorders 3) Myeloproliferative disorders |
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Hydrophobic bile acids in bile, the major biliary organic solutes, may play a crucial role in the initiation of this inflammatory bile duct disease |
Primary biliary cholangitis (formerly cirrhosis) |
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In early acute hepatitis B, what is the first serologic marker? |
Hepatitis B surface Ag ** this can sometimes be transient (up to 18 days) after vaccination |
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How long does HBcIgM stay positive? |
Six months |
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What is the serologic pattern of acute hepatitis B |
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