Hepatic Cirrhosis


Article Author:
Bashar Sharma


Article Editor:
Savio John


Editors In Chief:
Hela KCHIR
Joseph Lee
Savio John


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Trevor Nezwek
Radia Jamil
Patrick Le
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Hassam Zulfiqar
Hussain Sajjad
Steve Bhimji
Muhammad Hashmi
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Sarosh Vaqar
Mark Pellegrini
James Hughes
Beata Beatty
Beenish Sohail
Nazia Sadiq
Hajira Basit
Phillip Hynes


Updated:
6/3/2019 5:58:12 PM

Introduction

Cirrhosis is characterized by fibrosis and nodule formation of the liver, secondary to a chronic injury, which leads to alteration of the normal lobular organization of the liver. Various insults can injure the liver, including viral infections, toxins, hereditary conditions, or autoimmune processes. With each injury, the liver forms scar tissue (fibrosis), initially without losing its function. After a long-standing injury, most of the liver tissue gets fibrosed, leading to loss of function and the development of cirrhosis.

Etiology

Chronic liver diseases usually progress to cirrhosis. In the developed world, the most common causes of cirrhosis are hepatitis C virus (HCV), alcoholic liver disease, and nonalcoholic steatohepatitis (NASH) [1], while hepatitis B virus (HBV) and HCV are the most common causes in the developing world. Other causes of cirrhosis include autoimmune hepatitis, primary biliary cholangitis, primary sclerosing cholangitis, hemochromatosis, Wilson disease, alpha-1 antitrypsin deficiency, Budd-Chiari syndrome, drug-induced liver cirrhosis, and chronic right-sided heart failure. Cryptogenic cirrhosis is defined as cirrhosis of unclear etiology.

Epidemiology

The worldwide prevalence of cirrhosis is unknown; however, in the United States, it has been estimated to be between 0.15% and 0.27% [2][3].

Pathophysiology

Multiple cells play a role in liver cirrhosis including hepatocytes and sinusoidal lining cells such as hepatic stellate cells (HSCs), sinusoidal endothelial cells (SECs) and Kupffer cells (KCs). HSCs form a part of the wall of the liver sinusoids, and their function is to store vitamin A. When these cells are exposed to inflammatory cytokines, they get activated, transform into myofibroblasts, and start depositing collagen which results in fibrosis. SECs form the endothelial lining and are characterized by the fenestrations they make in the wall that allow the exchange of fluid and nutrients between the sinusoids and the hepatocytes [4]. Defenestration of the sinusoidal wall can happen secondary to chronic alcohol use and can promote perisinusoidal fibrosis [5]. KCs are satellite macrophages that line the wall of the sinusoids as well. Studies mainly from animal models have shown that they play a role in liver fibrosis by releasing harmful mediators when exposed to injurious agents and acting as antigen presenting cells for viruses [6]. Hepatocytes also are involved in the pathogenesis of cirrhosis, as damaged hepatocytes release reactive oxygen species and inflammatory mediators that can promote activating HSCs and liver fibrosis [7].

The major cause of morbidity and mortality in cirrhotic patients is the development of portal hypertension and hyperdynamic circulation. Portal hypertension develops secondary to fibrosis and vasoregulatory changes, both intrahepatically and systematically, leading to collateral circulation formation and hyperdynamic circulation [8].

Intrahepatically, SECs synthesize both nitric oxide (NO) and endothelin-1 (ET-1) which act on HSCs, causing relaxation or contraction of the sinusoids, respectively, and controlling sinusoidal blood flow. In patients with cirrhosis, there is an increase in ET-1 production as well as an increase in the sensitivity of its receptors with a decrease in NO production. This leads to increased intrahepatic vasoconstriction and resistance, initiating portal hypertension. Vascular remodeling mediated by the contractile effects of HSCs in the sinusoids augments the increase in vascular resistance. To compensate for this increase in intrahepatic pressure, collateral circulation is formed [8].

In systemic and splanchnic circulation, the opposite effect happens, with an increase in the production of NO leading to systemic and splanchnic vasodilation and decreased systemic vascular resistance. This promotes the activation of the renin-angiotensin-aldosterone system (RAAS), leading to sodium and water retention and resulting in a hyperdynamic circulation. Thus, in cirrhosis with portal hypertension, there is depletion of vasodilators (predominantly NO) intrahepatically but an excess of NO extrahepatically in the splanchnic and systemic circulation, which lead to sinusoidal vasoconstriction and splanchnic (systemic) vasodilation. The collaterals also contribute to the hyperdynamic circulation by increasing the venous return to the heart [8][9].

Histopathology

Cirrhosis is classified based on morphology or etiology. 

Morphology Classification

Morphologically, cirrhosis is (1) micronodular, (2) macronodular, or (3) mixed. This classification is not as clinically useful as etiologic classification.

  • Micronodular cirrhosis (uniform nodules less than 3 mm in diameter): Cirrhosis due to alcohol, hemochromatosis, hepatic venous outflow obstruction, chronic biliary obstruction, jejunoileal bypass, and Indian childhood cirrhosis.
  • Macronodular cirrhosis (irregular nodules with a variation greater than 3 mm in diameter): Cirrhosis due to hepatitis B and C, alpha-1 antitrypsin deficiency, and primary biliary cholangitis.
  • Mixed cirrhosis (when features of both micronodular and macronodular cirrhosis are present): Usually micronodular cirrhosis progresses into macronodular cirrhosis over time.

Etiology Classification

Based on the cause of cirrhosis which is sub-classified as follows:

  • Viral - hepatitis B, C, and D
  • Toxins - alcohol, drugs 
  • Autoimmune - autoimmune hepatitis
  • Cholestatic - primary biliary cholangitis, primary sclerosing cholangitis 
  • Vascular - Budd-Chiari syndrome, sinusoidal obstruction syndrome, cardiac cirrhosis
  • Metabolic - hemochromatosis, NASH, Wilson disease, alpha-1 antitrypsin deficiency, cryptogenic cirrhosis.  

History and Physical

Patients with cirrhosis can be asymptomatic or symptomatic, depending on whether their cirrhosis is clinically compensated or decompensated. In compensated cirrhosis, patients are usually asymptomatic, and their disease is detected incidentally by labs, physical exam, or imaging. One of the common findings is mild to moderate elevation in aminotransferases or gamma glutamyl transpeptidase with possible enlarged liver or spleen on exam. On the other hand, patients with decompensated cirrhosis usually present with a wide range of signs and symptoms arising from a combination of liver dysfunction and portal hypertension. The diagnosis of ascites, jaundice, hepatic encephalopathy, variceal bleeding, or hepatocellular carcinoma in a patient with cirrhosis signifies the transition from a compensated to a decompensated phase of cirrhosis. Other complications of cirrhosis include spontaneous bacterial peritonitis and a hepatorenal syndrome which occur in patients who have ascites.

Multiple Organs Affected

Gastrointestinal:

Portal hypertension can cause ascites, hepatosplenomegaly and prominence of the periumbilical abdominal veins resulting in caput medusa. Esophageal varices are another complication of cirrhosis secondary to increased blood flow in the collateral circulation, with a mortality rate of at least 20% at six weeks after a bleeding episode [10]. Patients with alcoholic cirrhosis are at increased risk of small bowel bacterial overgrowth and chronic pancreatitis [11], and patients with chronic liver disease have a higher rate of gallstones formation [12].

Hematologic:

Anemia can occur due to folate deficiency, hemolytic anemia (spur cell anemia in severe alcoholic liver disease), and hypersplenism. There can be pancytopenia due to hypersplenism in portal hypertension, impaired coagulation, disseminated intravascular coagulation, and hemosiderosis in patients with cirrhosis due to different causes.

Renal:

Patients with cirrhosis are prone to develop hepatorenal syndrome secondary to systemic hypotension and renal vasoconstriction, causing the underfilling phenomenon. Splanchnic vasodilation in cirrhosis leads to decreased effective blood flow to the kidneys, which activates the RAAS system, leading to retention of sodium and water and renal vascular constriction [13]. However, this effect is not enough to overcome the systemic vasodilation caused by cirrhosis, leading to renal hypoperfusion and worsened by renal vasoconstriction with the end point of renal failure [14].

Pulmonary:

Manifestations of cirrhosis include hepatopulmonary syndrome, portopulmonary hypertension, hepatic hydrothorax, decreased oxygen saturation, ventilation-perfusion mismatch, reduced pulmonary diffusion capacity, and hyperventilation.

Skin:

Spider nevi (central arterioles surrounded by multiple smaller vessels that look like a spider, hence the name) are seen in patients with cirrhosis secondary to hyperestrogenemia. Liver dysfunction leads to a sex hormone imbalance, causing increased estrogen to free testosterone ratio and the formation of spider nevi [15]. Palmer erythema is another skin finding that is seen in cirrhosis and is also secondary to hyperestrogenemia. Jaundice is a yellowish discoloration of the skin and mucous membranes that is seen when the serum bilirubin is greater than 3 mg/dL and in decompensated cirrhosis.

Endocrine:

Patients with alcoholic liver cirrhosis can develop hypogonadism and gynecomastia. The pathophysiology is multifactorial, mainly due to hypersensitivity of estrogen and androgen receptors seen in cirrhotic patients. Hypothalamic pituitary dysfunction has also been implicated in the development of these conditions [16]. Hypogonadism can lead to decreased libido and impotence in males with loss of secondary sexual characteristics and feminization. Women can develop amenorrhea and irregular menstrual bleeding as well as infertility.

Nail changes:

Clubbing, hypertrophic osteoarthropathy, and the Dupuytren contracture are seen. Other nail changes include azure lunules (Wilson disease), Terry nails and Muercke nails.

Others:

Fetor hepaticus (sweet musty breath smell due to high levels of dimethyl sulfide and ketones in the blood) [17] and asterixis (flapping tremor when the arms are extended and the hands are dorsiflexed) are both features of hepatic encephalopathy that can be seen in cirrhosis. Cirrhosis can lead to a hyperdynamic circulation, reduction in lean muscle mass, muscle cramps, and umbilical herniation. 

Physical examination in patients with cirrhosis may reveal stigmata of chronic liver disease (spider telangiectasias, palmar erythema, Dupuytren's contractures, gynecomastia, testicular atrophy), signs of portal hypertension (ascites, splenomegaly, caput medusae, Cruveilhier-Baumgarten murmur- epigastric venous hum), signs of hepatic encephalopathy (confusion, asterixis and fetor hepaticus), and other features such as jaundice, bilateral parotid enlargement, and scant chest/axillary hair. 

Evaluation

Lab Findings

Aminotransferases are usually mildly to moderately elevated with aspartate aminotransferase (AST) greater than alanine aminotransferase (ALT); however, normal levels do not exclude cirrhosis [18]. In most forms of chronic hepatitis (except alcoholic hepatitis), the AST/ALT ratio is less than one. As chronic hepatitis progresses to cirrhosis, there is a reversal of this AST/ALT ratio. Alkaline phosphatase (ALP), 5'- nucleotidase, and gamma glutamyl transferase (GGT) are elevated in cholestatic disorders. Prothrombin time (PT) is elevated due to coagulation factor defects as well as bilirubin, while albumin is low as it is synthesized by the liver and the liver's functional capacity goes down. Thus serum albumin and PT are true indicators of synthetic hepatic function. Normochromic anemia is seen; however, macrocytic anemia can be seen in alcoholic liver cirrhosis. Leukopenia and thrombocytopenia are also seen secondary to sequestration by the enlarged spleen as well as alcohol suppression effect on the bone marrow [19]. Immunoglobulins, especially the gamma fraction, are usually elevated due to impaired clearance by the liver [20].

Specific Labs to Investigate Newly Diagnosed Cirrhosis

Serology and PCR techniques for viral hepatitis and autoimmune antibodies (anti-nuclear antibodies [ANA], anti-smooth muscle antibodies (ASMA), anti-liver-kidney microsomal antibodies type 1 (ALKM-1) and serum IgG immunoglobulins) for autoimmune hepatitis and anti-mitochondrial antibody for primary biliary cholangitis may be ordered. Ferritin and transferrin saturation for hemochromatosis, ceruloplasmin and urinary copper for Wilson disease, Alpha 1-antitrypsin level and protease inhibitor phenotype for Alpha 1-antitrypsin deficiency, and serum alpha fetoprotein for hepatocellular carcinoma (HCC) are other useful tests.

Imaging and Liver Biopsy

A number of imaging modalities are used alongside with labs to help in the diagnosis of cirrhosis. These include ultrasound, CT, MRI, and transient elastography (fibroscan).

Ultrasonography is a cheap, noninvasive, and available modality for the evaluation of cirrhosis. It can detect nodularity and increased echogenicity of the liver, which are seen in cirrhosis; however, it is nonspecific as these findings can be seen in fatty liver as well [21]. It can also determine the ratio of the caudate lobe width to right lobe width which usually increases in cirrhosis [22]. Moreover, it is a useful screening tool for HCC in cirrhotic patients. Duplex Doppler ultrasonography helps to assess the patency of hepatic, portal, and mesenteric veins.

CT and MRI with contrast can be used to detect HCC and vascular lesions, with MRI being superior to CT [23]. MRI also can be used to detect the level of iron and fat deposition in the liver for hemochromatosis and steatosis, and biliary obstruction if an MRC (magnetic resonance cholangiography) is obtained [24][25]. MRI, however, is expensive and not readily available.

Transient elastography (fibroscan) is a noninvasive method that uses high velocity ultrasound waves to measure liver stiffness which correlates with fibrosis. In cirrhosis, a colloid liver spleen scan using technetium-99m sulfur colloid may show increased uptake of colloid in the bone marrow and spleen when compared to the liver. Presence of varices in the esophagus or stomach on esophagogastroduodenoscopy (EGD) suggests portal hypertension.

Liver biopsy is the gold standard for diagnosing cirrhosis as well as assessing the degree of inflammation (grade) and fibrosis (stage) of the disease. Nevertheless, it can miss the diagnosis at times due to sampling errors [26]. The diagnosis of cirrhosis by biopsy requires the presence of fibrosis and nodules. The nodular pattern can be micronodular, macronodular, or mixed with the micronodular pattern representing an independent risk factor of elevated hepatic venous pressure gradient (HVPG) and a more severe disease [26].

Noninvasive tests using direct and indirect serum markers are being used to detect patients with significant fibrosis/cirrhosis from patients with no/mild fibrosis. Examples are AST to platelet ratio index (APRI), Fibrosis-4 (FIB-4), FibroTest-ActiTest, and Fibrosure [27][28][29].

Treatment / Management

Damage to the liver is permanent. Nevertheless, further injury to the liver should be avoided to halt the progression of the disease. General management to prevent chronic liver disease includes avoidance of alcohol, vaccination for HBV and HCV, good nutrition with a balanced diet, weight reduction, and early treatment of precipitating factors like dehydration, hypotension, and infections. This is achieved by routine monitoring of volume status, kidney function, varices development, and progression to HCC.

Specific therapy usually targets the etiology including antiviral medications in viral hepatitis, steroids and immunosuppressant agents in autoimmune hepatitis, ursodeoxycholic acid and obeticholic acid in primary biliary cholangitis, copper chelation in Wilson disease, and iron chelation and phlebotomy in hemochromatosis. Weight loss of at least 7% is beneficial in NASH [30], and alcohol abstinence is crucial in alcoholic cirrhosis. 

Prognosis

Predictive models for the prognosis of cirrhosis estimate the ten-year survival in patients with compensated cirrhosis at 47%, but this drops to 16% once a decompensating event occurs. The Child-Turcotte-Pugh (CTP) scoring or classification uses serum albumin, bilirubin, PT, ascites, and hepatic encephalopathy to classify patients with cirrhosis into classes A, B, and C. One- and two-year survival rates for these classes are 100% and 85% (A),  80% and 60% (B), and 45% and 35% (C). The model for end-stage liver disease (MELD) score is another model used to predict the short-term mortality of patients with cirrhosis. It uses serum bilirubin, creatinine, and INR to predict the mortality within the next three months [31]. Based on the MELD score (more recently the MELDNa score), the priority of organ allocation for liver transplantation for patients with cirrhosis is adjudicated in the US [31].

Liver transplantation is indicated in decompensated cirrhosis that does not respond to medical treatment. The one-year and five-year survival rates after liver transplantation are approximately 85% and 72%, respectively. Recurrence of the underlying liver disease can occur after a transplant [32]. Long-term side effects of immunosuppressant drugs is another cause of morbidity in transplant patients.

Pearls and Other Issues

Hepatocellular Carcinoma

HCC is the most common primary cancer in the liver, and its incidence is increasing [33]. Cirrhosis secondary to HBV and HCV are the most common risk factors [33]. Routine monitoring of cirrhotic patients for development of HCC is recommended, with at least six monthly screenings using abdominal ultrasonography [2].

Enhancing Healthcare Team Outcomes

Treatment and Prevention liver cirrhosis is best done by a multidisciplinary team that includes a hepatologist, gastroenterologist, liver surgeon, pathologist infectious disease specialist, nurse practitioner, primary care provider and the internist. All healthcare workers should follow patients with liver dysfunction from any cause because it can quickly become irreversible. Liver cirrhosis is associated with many systemic complications that can cause death. Liver transplant is not always an option because of the shortage of donors. 


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Hepatic Cirrhosis - Questions

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How will the liver surface feel in most 59-year-old patients with alcoholic cirrhosis?



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In chronic liver failure, there is a marked decrease in the level of what component in blood?



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A patient with cirrhosis is found to have anemia. Which of the following is not a plausible explanation for anemia in this setting?



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One would expect to see Gamna Gandy bodies in a patient with which of the following conditions?



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What is the most common cause of liver cirrhosis in North America?



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In a patient with severe pruritus after developing liver cirrhosis, which of the following is the best treatment?



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Which of the following is not a manifestation of liver cirrhosis?



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An elderly man with a history of ethanol abuse and a small, scarred liver is agitated, confused, and diaphoretic. Vital signs: blood pressure 140/85 mmHg, heart rate 130 beats per minute, respiratory rate 24 breaths per minute, temperature 37.0 C. Which of the following should be considered for initial treatment of this patient?



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A patient has cirrhosis of the liver and is receiving neomycin. What is the purpose of this medication?



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On an abdominal exam, which of the following is not always evident?



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What is the number one cause of hepatic cirrhosis in North America?



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The Cruveilhier Baumgarten (CB) bruit is most likely to be heard in a patient with which condition?



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An elevated level of antidiuretic hormone (ADH) in a cirrhotic patient with ascites reveals which of the following electrolyte imbalances?



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Which of the following would confirm a diagnosis of cirrhosis in an alcoholic patient?



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What happens to urinary sodium in patients with hepatic cirrhosis?



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What happens to hemoglobin levels in patients with cirrhosis?



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Ascites due to hepatic cirrhosis is treated with which of the following drugs?



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What type of diet is recommended for patients with hepatic cirrhosis?



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A patient with hepatic cirrhosis is retaining a great deal of fluid. Which of the following is measured to best assess fluid retention?



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What is the recommended diet for a patient with liver cirrhosis?



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A 42-year-old male has a protuberant abdomen, thin extremities, yellow skin, gynecomastia, spider angiomas, testicular atrophy, and confusion. What is the most likely diagnosis?



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What is the most common cause of hepatic cirrhosis in the United States?



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What is the most common cause of cirrhosis in the United States?



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What antiarrhythmic drug is contraindicated for patient with hepatic cirrhosis?



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Biopsy of a cirrhotic liver shows an increase of which tissue?



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Which is least likely to be found in a patient with hepatic cirrhosis?



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In a patient with hepatic cirrhosis and ascites, which abnormality is most likely?



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What is the life expectancy for untreated macronodular cirrhosis?



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Which of the following is not proper reporting of cirrhotic nodules?



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Select the true statement about regenerative nodules in cirrhosis.



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Select the true statement about dysplastic nodules in cirrhosis.



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The regenerative, dysplastic, hepatocellular carcinoma (HCC) nodule spectrum explains the following which of the following?



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Which of the following cells is involved in the pathophysiology of cirrhosis?



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Which of the following is false about the pathophysiology of cirrhosis?



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Abnormal level of which of the following markers do not indicate abnormal hepatic function in cirrhosis?



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Which of the following is true about the diagnosis of cirrhosis?



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A nurse is studying with some fellow students and reviewing cirrhosis of the liver for a test. What are essential characteristics or manifestations of this disease for the study group to go over during the test review? Select all that apply.



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A nurse is working in triage when presented with a male patient that is confused, jaundiced, has palmar erythema, and a flapping tremor when his hands are raised. Other features include the presence of spider angiomas and a sweet, musty odor to his breath. Edema of the legs and marked ascites are present. Vitals are a respiratory rate of 42 and labored, pulse oximetry 90% on room air, heart rate 122 beats/ min, blood pressure 100/50 mmHg, and he is afebrile. He is confused to date, time, and events. He denies pain but is uncomfortable with the increasing size of his abdomen and struggling to breathe. How should the nurse proceed in the management of care for this patient? Select all that apply.



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A 65-year-old man who has never seen a medical provider presents complaining of abdominal distention. The patient drank about 5 to 6 shots a day for the last 20 years. His vitals are stable. On examination, his abdomen is distended with engorged paraumbilical veins. His palms appear red, and multiple spider nevi are present. Which of the following structures is expected to have an increased pressure?



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Someone brings a 39-year-old male with a history of hepatitis C to the hospital due to abdominal distention. He cannot answer basic questions and does not know where he is. They report him to be a heavy alcohol drinker. The physical examination shows gynecomastia, palmar erythema, and multiple spider nevi. The abdomen is distended with dilated periumbilical veins noted. The patient demonstrates asterixis, and the splenic tip is palpable with the dipping method of palpation. Which of the following findings best correlates with the cause of his gynecomastia?



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A 65-year-old female patient with history of compensated cirrhosis secondary to non-alcoholic fatty liver disease was seen at the clinic for a follow-up. She was diagnosed with cirrhosis incidentally one year ago after she was found to have a nodular appearing liver on imaging. Her METAVIR fibrosis score is F4. She denied having any symptoms. When should he be screened for hepatocellular carcinoma (HCC)?



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A 56-year-old male with a history of cirrhosis secondary to alcohol use and a history of esophageal variceal bleeding presents to the clinic with abdominal pain and distention. He noticed that his abdomen has been increasing in size over the past two weeks and he started developing abdominal pain and fevers for the past two days. Which of the following is the next best step in the management of this patient?



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A 48-year-old male with a history of liver cirrhosis secondary to alcohol use presents to the office for a follow-up. His last endoscopy showed grade II esophageal varices. His labs were significant for a WBC count of 6000/microL with less than 1% eosinophils and a platelet count of 52,000/microL. His abdominal ultrasound from 2 months ago showed nodular appearing liver and splenomegaly. He has a history of travel to southeast Asia 1 month ago where he spent a 2-week vacation. He does not have any family history of splenomegaly. He denies having any fevers, chills, abdominal pain or bleeding. Which of the following is the most likely etiology of splenomegaly in this patient?



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A 40-year-old male who was recently diagnosed with cirrhosis secondary to chronic hepatitis C infection presents to the clinic for a regular visit. He has no history of jaundice, esophageal bleeding, ascites or hepatic encephalopathy. He is well-nourished and asymptomatic. What serological test is most likely to be abnormal in this patient?



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A 65-year-old male with a history of decompensated cirrhosis secondary to alcoholic liver disease presented to the emergency department with acute encephalopathy that started two days ago. His family noticed that he has been lethargic and difficult to arouse and brought him to the hospital. His labs were significant for an elevated ammonia level, and he was started on lactulose. He was also found to have thrombocytopenia with a platelet count of 48,000 cells per microliter. His hemoglobin was 11 g/dL. Peripheral smear was negative for schistocytes. Kidney function was normal. Which of the following is the likely explanation for his thrombocytopenia?



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A 66-year-old female with a history of cirrhosis of unknown etiology presents for a follow-up. She has a history of bleeding esophageal varices that were banded 6 months ago. Labs were significant for a serum hemoglobin 10.3 g/dL and platelet count of 74/microliter. She has moderate ascites on exam. Which of the following electrolyte imbalances is most likely to be present in this patient?



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A 68-year-old female with a history of decompensated cirrhosis and ascites presents to the hospital with a decreased urine output for the past three days. She currently takes furosemide and spironolactone. Labs are significant for serum creatinine of 3.5 mg/dL and BUN 50 mg/dL. Her blood pressure was noted to be 96/65 mmHg. Her diuretics were held, and she was started on IV fluids. 2 days later, her serum creatinine did not improve, and serum potassium was noted to be 4.2 mEq/L. A renal ultrasound did not show any evidence of hydronephrosis. Which of the following is the next best step in the management of this patient?



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Hepatic Cirrhosis - References

References

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Alcohol-induced sinusoidal endothelial cell dysfunction in the mouse is associated with exacerbated liver apoptosis and can be reversed by caspase inhibition., Deaciuc IV IV,D'Souza NB,Fortunato F,Hill DB,Sarphie TG,McClain CJ,, Hepatology research : the official journal of the Japan Society of Hepatology, 2001 Jan 1     [PubMed]
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[Epidemiology and natural history of cirrhosis]., Naveau S,Perlemuter G,Balian A,, La Revue du praticien, 2005 Sep 30     [PubMed]
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Kim MY,Baik SK,Lee SS, Hemodynamic alterations in cirrhosis and portal hypertension. The Korean journal of hepatology. 2010 Dec;     [PubMed]
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Garcia-Tsao G,Sanyal AJ,Grace ND,Carey W, Prevention and management of gastroesophageal varices and variceal hemorrhage in cirrhosis. Hepatology (Baltimore, Md.). 2007 Sep;     [PubMed]
Casafont Morencos F,de las Heras Castaño G,Martín Ramos L,López Arias MJ,Ledesma F,Pons Romero F, Small bowel bacterial overgrowth in patients with alcoholic cirrhosis. Digestive diseases and sciences. 1996 Mar;     [PubMed]
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Green GR, Mechanism of hypogonadism in cirrhotic males. Gut. 1977 Oct;     [PubMed]
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Tanaka S,Okamoto Y,Yamazaki M,Mitani N,Nakqjima Y,Fukui H, Significance of hyperglobulinemia in severe chronic liver diseases--with special reference to the correlation between serum globulin/IgG level and ICG clearance. Hepato-gastroenterology. 2007 Dec;     [PubMed]
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Tchelepi H,Ralls PW,Radin R,Grant E, Sonography of diffuse liver disease. Journal of ultrasound in medicine : official journal of the American Institute of Ultrasound in Medicine. 2002 Sep;     [PubMed]
Giorgio A,Amoroso P,Lettieri G,Fico P,de Stefano G,Finelli L,Scala V,Tarantino L,Pierri P,Pesce G, Cirrhosis: value of caudate to right lobe ratio in diagnosis with US. Radiology. 1986 Nov;     [PubMed]
Burrel M,Llovet JM,Ayuso C,Iglesias C,Sala M,Miquel R,Caralt T,Ayuso JR,Solé M,Sanchez M,Brú C,Bruix J, MRI angiography is superior to helical CT for detection of HCC prior to liver transplantation: an explant correlation. Hepatology (Baltimore, Md.). 2003 Oct;     [PubMed]
Bonkovsky HL,Rubin RB,Cable EE,Davidoff A,Rijcken TH,Stark DD, Hepatic iron concentration: noninvasive estimation by means of MR imaging techniques. Radiology. 1999 Jul;     [PubMed]
Qayyum A,Goh JS,Kakar S,Yeh BM,Merriman RB,Coakley FV, Accuracy of liver fat quantification at MR imaging: comparison of out-of-phase gradient-echo and fat-saturated fast spin-echo techniques--initial experience. Radiology. 2005 Nov;     [PubMed]
Regev A,Berho M,Jeffers LJ,Milikowski C,Molina EG,Pyrsopoulos NT,Feng ZZ,Reddy KR,Schiff ER, Sampling error and intraobserver variation in liver biopsy in patients with chronic HCV infection. The American journal of gastroenterology. 2002 Oct;     [PubMed]
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Myers RP,Tainturier MH,Ratziu V,Piton A,Thibault V,Imbert-Bismut F,Messous D,Charlotte F,Di Martino V,Benhamou Y,Poynard T, Prediction of liver histological lesions with biochemical markers in patients with chronic hepatitis B. Journal of hepatology. 2003 Aug;     [PubMed]
Zeremski M,Dimova RB,Benjamin S,Makeyeva J,Yantiss RK,Gambarin-Gelwan M,Talal AH, FibroSURE as a noninvasive marker of liver fibrosis and inflammation in chronic hepatitis B. BMC gastroenterology. 2014 Jul 3;     [PubMed]
Promrat K,Kleiner DE,Niemeier HM,Jackvony E,Kearns M,Wands JR,Fava JL,Wing RR, Randomized controlled trial testing the effects of weight loss on nonalcoholic steatohepatitis. Hepatology (Baltimore, Md.). 2010 Jan;     [PubMed]
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