Liver Disorders
Liver Disorders
Introduction
Presented by: Jessica Cheuk
Contact: cheukyyj@hku.hk
Learning Outcomes
After this lecture, students should be able to:
Describe the location and functions of the liver.
Explain the liver function tests in relation to pathophysiologic alterations of the liver.
Identify the clinical manifestations of liver disorders & cirrhosis.
Describe the complications associated with cirrhosis.
Describe the nursing care for patients undergoing liver biopsy and abdominal paracentesis.
Describe nursing and interprofessional management strategies for patients with liver disorders & cirrhosis.
Functions of the Liver
Metabolic Functions
Blood Clotting: Synthesis of prothrombin (factor I), fibrinogen (factor II), and factors V, VII, IX, and X.
Carbohydrate Metabolism: Involves:
Glycogenesis: Conversion of glucose to glycogen.
Glycogenolysis: Breakdown of glycogen to glucose.
Gluconeogenesis: Formation of glucose from amino acids and fatty acids.
Detoxification: Inactivation of drugs and harmful substances and excretion of their breakdown products.
Fat Metabolism:
Synthesis of lipoproteins.
Breakdown of triglycerides into fatty acids and glycerol.
Formation of ketone bodies.
Synthesis of fatty acids from amino acids and glucose.
Synthesis and breakdown of cholesterol.
Protein Metabolism:
Synthesis of nonessential amino acids and plasma proteins (excluding gamma globulin).
Synthesis of clotting factors.
Deamination of amino acids in the colon to form ammonia (NH3), which is then converted to urea (NH4).
Metabolism of Steroid Hormones: Such as aldosterone, estrogen, and testosterone.
Secretory Functions
Bile Production: Formation of bile, which contains bile salts, bile pigments (predominantly bilirubin), and cholesterol.
Bilirubin Management: Conjugation and secretion of bilirubin.
Vascular Functions
Blood Filtration: Breakdown of old red blood cells (RBCs), white blood cells (WBCs), bacteria, and other particles.
Blood Reservoir: Temporary storage of blood within circulation.
Storage Functions
Nutrient Storage:
Stores glucose as glycogen.
Stores vitamins:
Fat-soluble: A, D, E, K.
Water-soluble: B1, B2, cobalamin, folic acid.
Stores fatty acids, minerals (iron, copper), and amino acids in the form of albumin and β-globulins.
Common Liver Disorders
Hepatitis
Non-alcoholic Fatty Liver Disease (NAFLD)
Cirrhosis
Hepatitis
Types of Hepatitis:
Infectious:
Viral, Bacterial, Fungal, Parasites.
Non-infectious:
Alcohol, Drugs, Autoimmune, Chemicals, Herbs.
Definition: Widespread inflammation of liver cells.
Viral Hepatitis
Categories of Viruses:
Hepatitis A virus (HAV)
Hepatitis B virus (HBV)
Hepatitis C virus (HCV)
Hepatitis D virus (HDV)
Hepatitis E virus (HEV)
Hepatitis A Virus (HAV)
Characteristics:
Ribonucleic acid (RNA) virus of enterovirus family.
Resistant to detergents and acids but susceptible to chlorine (bleach) and extremely high temperatures.
Symptoms similar to flu-like infection.
Transmitted via fecal-oral route (contaminated water and food).
Serological Markers:
Hepatitis A IgM indicates acute infection.
Hepatitis A IgG without anti-HAV IgM indicates past infection.
Prevention: Vaccination and thorough hand washing.
Hepatitis B Virus (HBV)
Characteristics:
Double-shelled particle containing DNA (HBcAg, HBsAg, HBeAg).
Modes of Transmission:
Perinatal from infected mothers to infants.
Percutaneous (in contact with infectious blood or body fluids).
Sexual transmission.
Serological Markers:
Presence of anti-HBs indicates immunity (from vaccine or past infection).
Presence of HBsAg indicates chronic HBV infection.
Blood Test for Hepatitis B
HBsAg (Hepatitis B Surface Antigen): Marker of infectivity, indicating acute or chronic infection.
Anti-HBs (Hepatitis B Surface Antibody): Indicates previous infection or vaccination.
HBeAg (Hepatitis B E Antigen): Indicates high infectivity; used for clinical management.
Anti-HBe (Hepatitis B E Antibody): Indicates low infectivity in chronic HBV.
Anti-HBc IgM: Indicates acute infection.
Anti-HBc IgG: Indicates previous or ongoing infection.
Hepatitis C Virus (HCV)
Characteristics:
RNA virus and blood-borne.
Common Transmission Modes:
Sharing contaminated needles among drug users.
High-risk sexual behavior and sharp exposures.
Major cause of liver failure and cancer.
Serological Marker:
Presence of anti-HCV indicates Hepatitis C infection.
Preventive Measures for Viral Hepatitis
General Measures:
Hand washing, avoid sharing personal items.
HBIG administration for one-time exposure (e.g., needle stick).
Active immunization: HBV vaccine.
Percutaneous Transmission:
Blood screening for donors:
HBV: HBsAg.
HCV: Anti-HCV.
Use disposable needles and syringes.
Sexual Transmission Precautions:
Acute exposure: HBIG to partners of HBsAg-positive persons.
HBV vaccine for uninfected sexual partners; condoms usage is recommended.
Considerations for Health Care Personnel:
Use standard infection control precautions.
Minimize contact with potentially infectious blood.
Drug Therapy for Hepatitis
Acute Hepatitis:
No specific therapies for HAV infection.
Treatment for severe HBV cases only.
Monitoring for spontaneous clearance in acute HCV cases, with direct-acting antivirals (DAAs) when necessary.
Chronic Hepatitis B:
Drug therapy aims to reduce viral load and liver enzyme levels, preventing complications like cirrhosis and liver cancer.
Drug Classes Used
Immune Modulators:
Example: Pegylated interferon.
Mechanism: Antiviral, antiproliferative, immune-regulating.
Indication: Chronic hepatitis B and C.
Nucleoside and Nucleotide Analogs:
Examples: Entecavir, Lamivudine, Telbivudine, Tenofovir.
Mechanism: Inhibit HBV DNA polymerase, prevent viral replication for chronic HBV treatment.
Non-alcoholic Fatty Liver Disease (NAFLD)
Definition: Condition characterized by fat accumulation in the liver not attributed to significant alcohol consumption.
Progression: Can advance to non-alcoholic steatohepatitis (NASH), leading to cirrhosis and liver cancer.
Diagnosis:
Ultrasound, CT scan, MRI, and liver biopsy.
Cirrhosis
Pathophysiology: Progressive destruction of functional liver tissue replaced by fibrous scar tissue:
Hepatocytes and liver lobules destroyed.
Lost metabolic functions and disrupted blood/bile flow, leading to portal hypertension.
Irreversible Disease Process
Mechanism of Cirrhosis Development
Toxin or Disease →
Inflammation
Degeneration and destruction of hepatocytes →
Tissue becomes nodular (excess fibrous tissue) blocking normal flow →
Impaired hepatic function → development of metabolic abnormalities.
Common Causes of Cirrhosis
Alcoholic liver disease.
Viral hepatitis.
Autoimmune hepatitis.
Steatohepatitis (from fatty liver).
Drug and chemical toxins.
Gallbladder disease (e.g., primary sclerosing cholangitis).
Metabolic/genetic causes.
Pathophysiology of Liver Disorders
Disruption in Function:
Decreased protein metabolism → lower albumin, clotting factors.
Glucose storage and metabolism impairment.
Reduced bile production.
Impaired steroid hormone metabolism.
Bilirubin conversion issues leading to jaundice.
Portal hypertension from disrupted blood flow.
Clinical Manifestations of Liver Dysfunction
Jaundice Types:
Pre-hepatic/Hemolytic Jaundice: Excessive RBC destruction → increased unconjugated bilirubin.
Intra-hepatic/Hepatic Jaundice: Impaired function → raised conjugated and unconjugated bilirubin.
Obstructive Jaundice: Impaired bilirubin excretion → increased conjugated bilirubin.
Portal Hypertension
Definition: Impaired blood flow increases pressure in the portal venous system, leading to:
Esophageal/gastric varices, hemorrhoids, splenomegaly, ascites, portal systemic encephalopathy.
Complications Arising from Portal Hypertension
Esophageal/gastric varices leading to potential massive hemorrhage.
Splenomegaly leading to anemia, leukopenia, and thrombocytopenia.
Ascites
Definition: Accumulation of plasma-rich fluid in the abdominal cavity.
Mechanism: Due to decreased serum colloidal oncotic pressure and various hormonal imbalances.
Hepatic Encephalopathy
Description: Result of increased ammonia levels in the blood due to liver dysfunction, leading to:
Clinical Presentations: Confusion, agitation, impaired consciousness, asterixis (
"liver flap"), and other neurological signs.
Factors Contributing: Cerebral depressants, dehydration, and infections.
Hepatorenal Syndrome (HRS)
Description: A form of functional renal failure associated with liver failure, indicating poor prognosis.
Symptoms: Sudden decrease in urinary flow, elevated blood urea nitrogen, and creatinine.
Treatment Options: Exclusion of reversible conditions, renal replacement therapy, liver transplant.
Assessment of Liver Function and Diagnostic Tests
Patient Medical History
Evaluation of:
Viral hepatitis history.
Alcohol consumption habits.
Medication and occupational history.
Family medical background.
Signs of Liver Disease
Clinical indicators observed during assessment.
Laboratory Tests
Complete Blood Count (CBC): Examining RBC, Hb, WBC, and platelets.
Coagulation Profile: Evaluating prothrombin time (PT).
Liver Function Tests (LFT) including:
Total protein, albumin, serum ammonia.
Viral antigens.
Serum liver enzyme levels, which may only show abnormalities after significant liver cell damage.
Laboratory Test Results Snapshot (Example)
Date: 26/9/2017
Parameters:
Sodium: 139 mmol/l
Potassium: 4.1 mmol/l
Creatinine: 80 mmol/l
Total Bilirubin: 46 μmol/l (abnormal)
ALT: 65 U/L (elevated).
Liver Function Test (LFT) Ranges
Total Bilirubin: 4-23 μmol/L
Abnormality indicates jaundice severity.
AST/SGOT: 14-38 U/L
Elevated levels indicate hepatocellular disease.
Alkaline Phosphate (ALP): 32-93 U/L
Significant elevation may indicate cholestasis or hepatic infiltration.
ALT: 7-36 U/L
Evaluates hepatocyte damage.
Albumin: 39-50 g/L
Indicators of hepatic synthetic function.
Nursing and Interprofessional Management for Cirrhosis
Overall Management Strategies
Nutrition Therapy:
High-carb, moderate-fat, and high-protein diet (if no contraindications).
Changes necessary for elevated serum ammonia or encephalopathy symptoms.
Sodium and vitamin restrictions/supplements.
Incorporate family in dietary counseling.
Medications:
Diuretics: Furosemide, spironolactone for managing fluid retention.
Laxatives: Lactulose to decrease ammonia production.
Anti-infective agents: Neomycin, Metronidazole, Rifaximin to manage gut bacteria.
Others: Beta-blockers to manage portal hypertension; vitamin K for bleeding risks, Antacids for gastritis.
Paracentesis:
Purpose: Diagnose infections, remove fluid, and check for complications.
Management of Bleeding Esophageal/Gastric Varices:
Endoscopic Techniques: EVL, ES for variceal bleeding control.
Pharmacological Agents: Terlipressin and others for managing variceal hemorrhage.
Nursing Care Protocols during Therapeutic Paracentesis
Before the Procedure:
Aseptic technique, patient identification, consent acquisition, and baseline measurements.
Patient positioning – supine with head elevated.
During the Procedure:
Monitoring vital signs and patient condition; securing catheters and drainage.
Post-Procedure Care:
Frequency of monitoring conditions, ensuring proper drainage, and managing any adverse signs.
References
Carpenito, L. J. (2016). Nursing diagnosis: Application to clinical practice (15th ed.). Philadelphia: Lippincott Williams & Wilkins.
Hinkle, J. L., & Cheever, K. H. (2018). Brunner and Suddarth’s textbook of medical-surgical nursing. Wolters Kluwer India Pvt Ltd.
Ignatavicius, D. D., Workman, M. L., & Rebar, C. (2017). Medical-Surgical Nursing: Concepts for Interprofessional Collaborative Care. Elsevier Health Sciences.
Harding, M., Kwong, J., Hagler, D., Reinisch, C., & Lewis, S. M. (2023). Lewis’s medical-surgical nursing: assessment and management of clinical problems (12th ed.). Elsevier.