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Liver Disease

Liver Disease. Brenda Beckett, PA-C. Liver. Large, 4 lobes Highly vascularized Nutrient-rich blood from GI tract with products of digestion via portal vein Oxygen-rich blood via hepatic artery Metabolism, detoxification, storage, excretion Ability to regenerate. Mechanisms of disease.

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Liver Disease

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  1. Liver Disease Brenda Beckett, PA-C

  2. Liver • Large, 4 lobes • Highly vascularized • Nutrient-rich blood from GI tract with products of digestion via portal vein • Oxygen-rich blood via hepatic artery • Metabolism, detoxification, storage, excretion • Ability to regenerate

  3. Mechanisms of disease • Hepatocyte damage • Biliary tract obstruction • Metabolic disorders • Metallic deposition • Fibrotic changes • Neoplasms

  4. Symptoms of Liver Disease • May be asymptomatic until advanced • RUQ abdominal pain • Pruritis – bile salts deposited below skin • Fatigue • Weakness • Decreased libido • Nausea • Bleeding

  5. Signs of Liver Disease Gynecomastia Diabetes Testicular atrophy Ataxia / Asterixis Xanthomas, xanthelasmas Jaundice (icterus) Spider angiomata Palmar erythema Hepatosplenomegaly Ascities / anasarca Encephalopathy Fetor hepaticus Caput medusa

  6. Asterixis

  7. Assessing for Liver Disease • Typical patterns in lab tests • Many patients with abnormal labs are asymptomatic (need for screening) • Tests for hepatocellular damage • Tests for liver function

  8. Hepatocellular Damage • Aminotransferases – AST, ALT • Present in hepatocytes. AST also in cardiac muscle. Released with necrosis • Alkaline phosphatase • Isoenzymes in liver, bone, gut • GGT • Enzyme present in multiple tissues • Nonspecific. Will help to locate liver source

  9. Tests for Liver Function • Prothrombin time - measures synthesis of factors II and VII • Albumin – plasma protein. Maintains oncotic pressure • Cholesterol – Not specific, many variables. May be decreased in end-stage disease

  10. Bilirubin • Hemoglobin heme biliverdin unconjugated bilirubin. • Combines with albumin to liver. • Conjugated and excreted as bile to intestines • Elevated in liver disease and hemolysis

  11. Jaundice • Prehepatic - excess production • Hepatic - impaired function (uptake or conjugation) • Posthepatic - obstruction

  12. Jaundice Unconjugated - (pre and hepatic) • Excess production • Hemolytic anemia, hemolysis • Hepatic • Causes • Hepatocellular disease, Gilbert’s, neonatal jaundice

  13. Jaundice Conjugated (posthepatic) • Causes • Obstruction • Hepatocellular disease • Drugs • Sepsis • Post surgical

  14. Jaundice Evaluation • History • Drugs – prescribed, otc, vit., herbs, etc • Transfusions, IVs, tattoos, IV rec drugs, sexual activity • Recent travel, exposure to jaundiced, alcohol intake • Duration, constitutional symptoms, fever, weight loss, RUQ pain

  15. Jaundice Evaluation • Physical • Nutrition, signs of chronic liver disease • JV distention, liver and spleen enlargement, • Ascites, tender RUQ • Labs • Bilirubin, Conj and Unconj. Liver enzymes

  16. Other diagnostic tools

  17. Ultrasound • Obstruction: • Biliary tract stones • Intrahepatic biliary dilation • Texture of liver (fatty vs. cirrhosis) • Cystic/solid tumors

  18. CT Scan • Characterize/quantify lesions • Enhancement with contrast • Smallest detectable lesion is 1cm • Obstruction

  19. MRI • Best for: • Cystic lesions • Hemangiomas • Iron overload

  20. PET Scan • Positron emission tomography • FDG (Fluorodeoxyglucose) taken up by active tissue and cancer cells • Whole body scan • Especially to rule out extrahepatic disease in colon cancer patients

  21. Percutaneous Biopsy • Can be safely done • Use US or CT guidance • Allows tissue diagnosis

  22. Alcohol Related Liver Disease • Chronic alcohol intake can lead to fatty liver, hepatitis and finally, cirrhosis • Fatty liver and hepatitis (inflammation) are reversible, but are precursors to cirrhosis • Exact mechanism unknown, but partially due to toxicity and partially due to nutritional deficits

  23. Alcohol Related Liver Disease • Mechanism not well understood • mechanisms • Direct toxicity to hepatocytes • Malnutrition • Immune reactivity after cell damage • Inc risk of Hepatocellular Carcinoma (HCC)

  24. Alcohol Induced Hepatotoxicity • Alcohol Dehydrogenase primary metabolic pathway • Present in gastric mucosa and liver • Women with less in stomach so more reaches liver • Fatty acid & triglyceride deposition 1st response • Fatty Liver or Steatohepatitis in 80%+ EtOH abusers • Usually reversible - may be due to obesity • EtOH metabolism products toxic to hepatocytes • Pathologic changes cause hepatitis • Infiltrative PMNs • Inflammatory product cell changes • Fibrotic changes and cirrhosis • Partially reversible

  25. Alcohol Related Liver Disease • Risk for EtOH disease fxn of quantity and duration of abuse • No correlation to type of beverage • Women develop ARLD with less intake EtOH • 1 beer, 4 oz wine, 1 ounce whiskey has about 12 g of EtOH • Inc risk with intake of >60-80 g EtOH daily for 10 years by men, >20-40 g daily by women

  26. Alcohol Abuse • Patient may not admit to over-consumption • First clue may be liver failure/disease • Use transaminase levels for clue, then biopsy to definitively diagnose • R/O other causes and comorbidities • HBV, HCV, etc.

  27. Cirrhosis • Inflammation activates lipocytes • Lose Vit A and form collagen • Fibrotic bands form and replace normal cellular architecture • Lose compliance  firm liver • Results in  liver function and Portal Hypertension • Treatment possible early in process • Treat cause: EtOH, metals, infection, etc.

  28. Causes of Cirrhosis • Alcohol • Viral hepatitis • Biliary obstruction • Veno-occlusive disease • Hemochromatosis • Wilson disease • Autoimmune • Drugs and toxins • Metabolic diseases • Idiopathic

  29. Cirrhosis Manifestations - determined by pathology • Scarring and disruption of architecture distorts vascular bed • Inadequate blood flow and ongoing damage disturbs hepatocyte function • Initially: fatty infiltration

  30. Alcohol Related Liver Disease • Signs and symptoms: • Often asymptomatic until late. • Hepatomegaly • Anorexia, nausea • Jaundice • Abdominal pain, RUQ tenderness, splenomegaly, ascites, fever, encephalopathy

  31. Dx: ARLD • Typical blood abnormalities: Incr GGT, AST, ALT (AST>ALT), ALP, Bilirubin. Decr Albumin. Anemia. Prolonged PT • Liver biopsy to confirm • Large fatty droplets in fatty liver • Inflammatory changes in hepatitis • Fibrosis with nodular formation, Mallory bodies, destruction of liver architecture in cirrhosis

  32. DDX: ARLD • US and other imaging to r/o obstruction • Hepatitis screening • NAFLD can be diagnosed AST/ALT ratio, BMI, MCV and gender

  33. Trt: ARLD • Abstain from alcohol! • Maintain adequate coloric intake • Thiamine and folate supplements • Cirrhosis: often hospitalization • Low protein diet, monitor lytes, remove ascites, give clotting factors, lactulose to decrease nitrogen absorption from gut

  34. Complications of Cirrhosis Chronic Liver Failure • Portal hypertension. Causes: • Esophageal varices • Ascites • Encephalopathy • Hepatorenal syndrome • Hepatopulmonary syndrome

  35. Ascites - fluid in abdomen • Total body water and sodium excess • Cause unknown but 3 theories: • Portal HTN causes sequestration fluid in splanchnic bed  dec circulating blood volume • Primary renal process causing retention H2O, Na+ • Portal HTN causes release NO  arterial vasodilatation • All cause RAA system activation, worsening problem • Dec albumin levels dec oncotic pressure to hold fluid in vascular space

  36. Ascites • Anasarca less common form of same pathophys • Inc abdominal girth, weight • Dyspnea as fluid restricts diaphragmatic excursion • Shifting dullness and US to confirm diagnosis • Treat the root cause: fix the liver • Na+ restrict 1500 mg/d • Spironolactone initially, add furosemide prn • Paracentesis (up to 4-6L) • Beware of spontaneous bacterial peritonitis

  37. Other Complications • Hepatorenal syndrome: cause unknown • Azotemia, hypernatremia, oliguria in presence of histologically normal kidneys • No urinary sediment indicating nephritis • Dx by failure to resolve with hydration • No known treatment • Hepatopulmonary syndrome causes hypoxemia • Pulmonary hypertension and R-to-L intrapulmonary shunts • Confused with co-morbid COPD

  38. Hepatic Encephalopathy • Change in mental status in presence of liver disease • Spectrum from subtle personality changes to confusion to coma • EEG changes noted • Can cause coma and death • Usually follows precipitating event: • GI bleed, sepsis, electrolyte disturbance, shock, sudden inc dietary protein intake

  39. Hepatic Encephalopathy • Pathophysiology unknown • Theory: hepatocellular damage and cirrhosis cause extrahepatic shunting of venous portal blood • Toxic substances not removed from blood • Increased serum ammonia level • Treat with lactulose up to qid to cause diarrhea (decr nitrogen absorption)

  40. Portal Hypertension Classified as: • Sinusoidal: Alcoholic cirrhosis • Presinusoidal: Splenic/portalvein thrombosis, hepatitis, hepatic fibrosis • Postsinusoidal: Vascular outflow problem - Budd-Chiari syndrome: Thrombosis of hepatic veins

  41. Portal Hypertension • Signs: • Ascites • Caput medusa • Splenomegaly • Variceal bleeding • Encephalopathy

  42. Management of Portal HTN • Medical: Ascities, encephalopathy, coagulopathy • Surgical: TIPS (Transjugular Intrahepatic Portosystemic Shunt), other shunting procedures

  43. Acute Liver Failure • Acute massive loss of hepatocyte function • No pre-existing liver disease or portal HTN • Acetaminophen overdose, viral hepatitis, drug toxicity, herbal and dietary supplements

  44. Acute Liver Failure • Extremely elevated transaminases • Bilirubin may be normal • Coagulopathies • Increased ammonia • Acetaminophen overdose: treat with acetylcysteine

  45. Acute Liver Failure • Can progress to fulminant hepatic failure with encephalopathy • Sepsis • Cerebral edema • High mortality rate • May need transplantation • No long term sequelae in survivors • Uncommon

  46. Benign Solid Liver Tumors Hepatic Adenoma - Reproductive age females on OCPs - Sheets of hepatocytes with no parenchymal cells - Risk of rupture and malignant transformation

  47. Hepatic Adenoma DX: Difficult to distinguish from FNH (Focal Nodular Hyperplasia) - CT/MRI: to differentiate Can rupture and bleed

  48. Hepatic Adenoma Management: <4cm: cessation of OCPs, can regress >4cm, no regression; resection

  49. Malignant Tumors of Liver Hepatocellular Carcinoma (HCC) - Associated with cirrhosis, hepB, C - Weight loss, weakness, abdominal pain, hepatomegaly, mass DX: CT scan, perc. biopsy - Will have elevated Alk Phos, AFP

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