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123 Cards in this Set
- Front
- Back
What is the function of the liver? |
Temporary nutrient storage Removes toxins from the blood Removes old damages red blood cells Regulates nutrients and metabolite levels in the blood (carb, amino acids, lipids) Secretes bile |
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What is Jaundice? |
Yellow discoloration of sclera, skin, mucous membrane due to deposition of bile pigment |
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How is jaundice clinically detected? |
With serum bilirubin 2-2.5 mg/dL or increase of 2x ULN |
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What is bilirubin |
The breakdown product of Hgb from injured RBCs and other heme containing proteins |
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What produces bilirubin? |
Reticuloendothelial system |
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True or False Bilirubin is released to plasma bound to albumin. |
True |
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What conjugates and excretes bilirubin through bile channels into the small intestine? |
Hepatocytes |
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What cause increased bilirubin? |
Overproduction by reticuloendothelial system Failure of hepatocyte uptake Failure to conjugate or excrete Obstruction of biliary excretion into intestine |
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What does elevation of indirect unconjugated bilirubin indicate? |
Production exceeds the ability of the liver to conjugate |
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What are examples of disorders that can cause an elevation of indirect unconjugated bilirubin? |
Hemolytic anemias Hemoglobinopathies Transfusion reaction |
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What does elevation of direct water soluble conjugated bilirubin indicate? |
Liver can product not cannot excrete as bilirubin is conjugated in the liver |
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What is an example of a disorder than can cause an increase in conjugated bilirubin? |
Intra/extra hepatic obstruction |
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What liver biochemical tests are increased in hepatocellular jaundice? |
Increased direct and indirect bilirubin Increase urine bilirubin Decreased Serum albumin Increased Alk Phos 1x ulna Prolonged PT-INR but does not respond to Vit K Increased ALT AST in hepatocellular damage |
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What liver biochemical tests are increased in uncomplicated/obstructive jaundice? |
Increased direct and indirect bilirubin Increase urine bilirubin Unchanged Serum albumin Increased Alk Phos 3x ulna Prolonged PT-INRand respond to Vit K Minimal increase in ALT AST |
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How is Hep A transmitted? |
Fecal-Oral route |
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How is Hep A spread? |
Spread is favored by crowding and poor sanitation |
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What are the sources of outbreak for Hep A? |
Food Water Inadequately cooked shellfish |
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What is the incubation for Hep A? |
Incubation averages 30 days |
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HAV is excreted in feces for how long before clinical illness symptoms occur? |
2 weeks |
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What are the clinical findings of a pt with HAV? |
Onset of symptoms may be 5-10 days after exposure Anorexia, N/V, Malaise, Fever Hepatomegaly RUQ abdominal tenderness Jaundice Clay colored stool Lymphadenopathy |
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What are the laboratory findings of a patient with HAV? |
IgM HAV IgG HAV CBC with diff Complete Metabolic profile Proteinuria |
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When does peak titers of IgM anti HAV occur? |
During the 1st week of clinical disease and disappear 3-6 months |
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When does titers of IgG anti HAV rise? |
After 1 month of disease and may persist for years in asymptomatic patient |
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What is the treatment for HAV? |
Supportive care Post exposure prophylaxis with a single dose of HAV vaccine or immunoglobulin Prevention (hand washing and vaccination) Precaution |
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How is Hep B trasmitted? |
Transmitted by inoculation of infected blood, blood products, or sexual contact |
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Which bodily fluids can carry HBV virus? |
Saliva, Semen, Vaginal secretions |
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Can HBV be transmitted vertically by HBsAg positive mothers to baby specifically at birth? |
Yes |
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Which population is at risk for contracting HBV? |
Sexually active Healthcare workers H/O incarcerations H/O sexually transmitted disease Illicit drug use Non-sterile tattoos |
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What is the incubation period of HBV? |
6 weeks to 6 months |
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What is the clinical course of HBV? |
10% of adults who are infected do NOT clear the virus and develop what is called Chronic HBV infection. |
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What are complications of Chronic HBV? |
Cirrhosis Hepatocellular carcinoma HCC |
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What are the clinical findings of a patient with Acute Hep B? |
Onset will be more insidious than Hep A Anorexia, N/V, Malaise, Fever Hepatomegaly RUQ abdominal tenderness Jaundice Clay Colored Stool Lymphadenopathy |
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What are the laboratory findings of a patient with Acute Hep B? |
CBC with diff Complete metabolic profile (Aminotranferase levels are higher then in Hep A) Proteinuria Hep B serologies |
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What can be seen to determine chronic Hep B? |
Persistent elevated LFT > 6 months HBeAg and active viral replication Anti-HBe and low viral replication |
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What is the treatment for Acute Hep B? |
Supportive Care Post exposure hep B immunoglobulin (large doses, within 7 days of exposure, followed by HBV vaccine series) Prevention (use condom, H/C workers gloves,no recapping, appropriate disposal of sharp, lifestyle changes, vaccination) |
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What is the treatment is recommended for individuals who have replicative disease (HBeAg positive) Chronic Hep B? |
Interferon treatment |
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What % of individuals will lost serum HBeAg after 16 weeks of treatment with interferon alpha? |
40% |
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What is correlated with loss of HBeAg? |
An improved prognosis |
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Who should not be treated with interferon alpha except in the setting of an approved clinical study? |
Patients with severe decompensated liver disease (encephalopathy, ascites, very high serum bilirubin prolonged Prothrombin time) |
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What is the recommended dose if interferon alpha-2b for treatment of chronic hep b? |
5,000,000 units daily SC or IM injection for 16 weeks but pt must be monitored during tx period for SE of flu like symptoms, depression, rashes, other rxn, and abnormal blood count |
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What other Treatments for chronic hep B is there? |
Nucleoside analogues Lamivudine orally 100 mg/day Adevofir dipivoxil 10 mg/day |
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Which Hep virus is the most common chronic blood borne viral infection in North America? |
Hep C |
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True or False Hep B is a major cause of chronic hepatitis. |
False Hep C is a major cause of chronic hepatitis |
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Hep ___ causes progressive hepatic fibrosis which leads to cirrhosis and an increased risk of hepatocellular carcinoma. |
C |
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What is the most common reason for liver transplantation in the US? |
HCV liver disease |
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How many know genotypes and subtypes of HCV is there |
6 and 50 |
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What are the most common genotypes of HCV in the US? |
Type 1 75% Type 2 10% Type 3 10% |
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What contributes to the chronic infection of HCV occurrence? |
Lack of a robust T lymphocyte response to and a high rate of mutations within the genotypes, thus allowing HCV to elude the immune system mediated clearance and so produce the chronic infection |
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How many ppl in the USA is infected with the HCV and how many ppl have chronic infection? |
4 million and 2.7 million |
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How many new cases of HCV each year is there? |
35,000 |
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How many deaths per yr from HCV related chronic liver disease is there? |
8,000-10,000 |
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What is the estimated prevalence of HCV in the population? |
1.8% |
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There is a ___________ fold increase in the number of persons diagnosed with chronic HCV projected from 1990-2015. |
fourfold |
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Persons between _____ and ____ years have the highest seroprevalence |
40-59 years |
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How is HCV transmitted? |
Before 1992 Blood tranfusion Injection drug use Solid organ transplantation from infected donor Occupational exposure to infected blood Infected mother to child during birth High risk sexual practices Intranasal cocaine use Body piercing |
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What is the incubation period for HCV? |
Up to 8 weeks |
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What percentage of HCV become persistent infection? |
> 85% |
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Which population have a slower progression of HCV? |
Young age at time and female gender |
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What can contribute to rapid progression of HCV? |
Co infection with HIV or HVB and alcohol use |
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What is the clinical presentation of a patient with HCV? |
Majority of infections are asymptomatic Prodrome of anorexia, N/V, myalgia, malaise, diarrhea or constipation, low grade fever and abdominal pain (tender hepatomegaly) Icteric phase-jaundice may occur 5-10 days Convalescent phase Acute illness may be mild and subsides in 2-3 weeks (Fulminant infection are rare) |
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What are the laboratory findings of a patient with HCV? |
|
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Chronic inflammation of the liver with persistence of HCV RNA of how long will lead to chronic infection and risk of progression? |
> 6 months |
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What does chronic infection and risk of progression sequelae include? |
Progressive liver fibrosis, cirrhosis, End stage liver disease, and hepatocellular carcinoma |
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Risk of progression of HCV is increased by what? |
Older age at time of infection, male gender, immunosuppression, HBV, HIV, EtOH |
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What other factors may also increase progression of HCV? |
Iron overload, nonalcoholic fatty liver disease, hepatotoxic medication, and environmental contaminants |
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What are Extra hepatic manifestations of Chronic HCV? |
Rheumatoid symptoms Keratoconjunctivitis sicca Lichen planus Glomerulonephritis Lymphoma Essential mixed cryoglobulinemia Porphgyria cutanea tarda Psychological disorders Leukocytoclastic vasculitis |
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How is laboratory diagnosis done to conclude diagnosis of HCV? |
|
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How is liver biopsy useful in HCV? |
Provides useful information about the degree of fibrosis in HCV infected pts. Important in management decision
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How is liver biopsy NOT useful in HCV? |
Not useful for diagnosis of HCV infection |
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True of False Liver biopsy in HCV is used for assessment of severity of inflammation, presence of fibrosis, evaluate possible concomitant disease processes, assess therapeutic intervention. |
True |
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What is the treatment for Chronic HCV with progression? |
Gold standard pegylated interferon (PEG-INF) combined with ribavirin (Associated with SE) |
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What are contraindications to using combo therapy of pegylated interferon (PEG-INF) combined with ribavirin? |
Hypersensitivity to drugs Pregnant women Men whose partner are pregnant Hepatic decompensation Neonoates and children Autoimmune hepatitis Hemoglobinopathies |
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What adjunctive therapy is there for Chronic HCV? |
Hep B vaccine series if non immune Hep A vaccine series Contraception during therapy for 6 months after Counseling-avoid EtOH and drugs and use condoms to prevent transmission and STD Support group |
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What is Cirrhosis characterized by? |
Formation of fibrous tissue, nodules, and scarring, which interfere with liver cell function and blood circulation |
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What are the two most common cause of cirrhosis in the US? |
EtOH liver disease and HCV which together account for almost 1/2 of those undergoing transplantation |
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True or False It is estimated that the development of cirrhosis requires on average the ingestion of 80 g of EtOH daily for 10 to 20 yrs |
True This is one L of wine, 8 beers, 1/2 pint of hard liquor each day |
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What is the pathophysiology of cirrhosis? |
Irreversible chronic injury of the hepatic parenchyma Extensive fibrosis-distortion of hepatic architecture Formation of regenerative nodules |
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What are the clinical manifestations of cirrhosis? |
Spider angiomas Palmar erythema Nail changes (Muehrcke's and Terry's nails) Gynecomastia Testicular atrophy |
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What is the most common measured laboratory tests for a patient with cirrhosis? |
Serum aminotransferases, Alk Phos, GGT, serum bilirubin |
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What tests of synthetic function is done for someone with cirrhosis? |
Serum albumin concentration and PT/INR time |
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True or False Radiologic modalities cannot suggest the presence of cirrhosis. |
False it can occasionally suggest the presence of cirrhosis, they are not adequately sensitive or specific for use as a primary diagnostic modality |
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How is usually radiologic modalities useful in cirrhosis? |
Useful in it's ability to detect complications of cirrhosis |
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What is the sensitivity of a liver biopsy for cirrhosis? |
In the range of 80 to 100% depending upon method used and size and number of specimens obtained |
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What are complications of cirrhosis? |
Ascites Spontaneous Bacterial Peritonitis Hepatorenal syndrome Variceal hemorrhage Hepatopulmonary syndrome Other Pulm syndrome (hepatic hydrothorax, portopulmonary HTN) Hepatic encephalopathy Hepatocellular carcinoma |
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What is ascites? |
Accumulation of fluid within the peritoneal cavity
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What is the most common complication of cirrhosis? |
Ascites |
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What is the 2 yr survival rate of patient with ascites? |
Approx. 50% |
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On the assessment of ascites what is Grade 1? |
Mild, detectable only by US |
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On the assessment of ascites what is Grade 2? |
Moderate, moderate symmetrical distention of the abdomen |
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On the assessment of ascites what is Grade 3? |
Large or gross ascites with marked abdominal distention |
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What imaging studies can be done to confirm ascites? |
US is probably most cost effective modality |
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What routine tests are ordered on ascitic fluid? |
Cell count and differential Albumin concentration Total protein concentration Culture in blood culture bottles |
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How do you treat cirrhotic ascites? |
Treatment is aimed at the underlying cause of the hepatic disease and at the ascitic fluid itself Dietary sodium restriction (limiting to 88 mEq/day) Most effective therapeutic regimen is combo of single morning oral dose of Spironolactone 100mg and Furosemide 40 mg |
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What are the two major concerns with diuretic therapy for cirrhotic ascites? |
Overly rapid removal of fluid Progressive electrolyte imbalance |
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What is spontaneous bacterial peritonitis? |
Infection of the ascitic fluid |
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When can a patient get spontaneous bacterial peritonitis? |
Almost always seems in the setting of end-stage liver disease |
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How do you diagnose a patient with spontaneous bacterial peritonitis? |
Diagnosis established by: A positive ascitic fluid Elevated ascitic fluid absolute polymorphonuclear leukocyte (PMN) count > 250 cells/mm3 |
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What are clinical manifestations of patient with spontaneous bacterial peritonitis? |
Fever Abdominal pain Abdominal tenderness Altered mental status |
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What is the treatment for spontaneous bacterial peritonitis?? |
Cefotaxime 2gm IV q8-12 h X 5 d Ceftriaxone 1gm IV QD X 5d Amoxicillin-clauvulanate 875 mg IV q 12h X 5 d Ofloxacin 400 mg IV X 5 d followed by Ciprofloxacin 500 mg 1 tab po bid X 5 day |
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What is hepatorenal syndrome? |
Acute renal failure couple with advanced hepatic disease (due to cirrhosis or less often metastatic tumor or severe alcoholic hepatitis |
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What is characterized by hepatorenal syndrome? |
Oliguria Benign urine sediment Very low progressive rate of sodium excretion Progressive rise in the plasma creatinine concentration |
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What is the treatment of choice for hepatorenal syndrome?? |
Liver transplantation |
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In what percentage of patient's with cirrhosis does esophageal varices occur in? |
25 to 40% |
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True or False There is no need for prophylatic measures to be taken in pt with cirrhosis and concern for esophageal varices. |
False-should take prophylactic measures |
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True or False Screening EGD recommended for all cirrhotic patients. |
True |
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When is hepatopulmonary syndrome considered? |
When pt has Pulmonary restriction Atelectasis Triad (chronic liver disease, increased alveolar arterial gradient on room air, intrapulmonary vascular dilation)
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Clinically what does the patient with hepatopulmonary syndrome present with? |
Short of breath when sitting up |
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What is Portopulmonary HTN? |
Refers to the presence of pulmonary hypertension in the coexistence of portal hypertension |
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What is the prevalence of Portopulmonary HTN in cirrhotic patients? |
Approx 2 percent |
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How is Portopulmonary HTN diagnosed? |
Suggested by ECG Confirmed by right heart catherization |
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In which cirrhotic coexisting disease is Liver transplantation contraindicated? |
Portopulmonary HTN |
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What is hepatic encephalopathy? |
Spectrum of potentially reversible neuropsychiatric abornomalities seen in pts with liver dysfunction |
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What is the treatment for hepatic encephalopathy |
Dietary restriction of protein Give lactulose Metronidiazole 250 mg PO TID Rifaximin 550 mg PO BID Avoid OPIOIDS |
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True or False Patients with cirrhosis have a markedly increase risk of developing hepatocellular carcinoma. |
True |
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Whos is at highest risk for hepatocellular carcinoma? |
Cirrhosis from Hep B Cirrhosis from Hep C Hemochromatosis |
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What is the prognostic tool for end stage liver? |
MELD (model for end-stage liver disease). Identify patients whose predicted survival post procedure would be three months or less |
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How to calculated MELD? |
3.8 serum bilirubin + 11.2 INR + 9.6 serum creatinine + 64 |
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What is the Child-Turcotte Pugh CTP score? |
Initially designed to stratify the risk of portacaval shunt surgery in cirrhotic patients. Good predictor of outcome with complications of portal hypertension. |
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What parameters is the CTP score based on? |
Serum bilirubin Serum Albumin PT Ascites Enceophalopathy |
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What are the treatment option major goals for Cirrhotic patients? |
Slowing or reversing the progression of liver disease Preventing superimposed insults to the liver Preventing and treating the complications Determining the appropriateness and optimal timing for liver transplantation |
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What is the definitive treatment for patients with decompensated cirrhosis? |
Liver transplantation |
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What does liver transplantation depend on for patients with decompensated cirrhosis? |
The severity of disease, quality of life and absence of contraindications |
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What are contraindications for liver transplantation in patients with decompensated cirrhosis? |
Malignancy Advanced cardiopulmonary disease Sepsis |