Overview
The liver is a complex organ with multiple critical functions including glucose, protein, and fat
metabolism; bile production; bilirubin excretion; drug metabolism; and vitamin storage.
Understanding liver anatomy and physiology is essential for recognizing and managing liver disease
complications.
Liver Anatomy & Physiology
Structure
• Four lobes containing thousands of lobules (working units of the liver)
• Hexagon-shaped lobules containing:
◦Portal vein
◦Bile duct
◦Hepatic artery
◦Hepatocytes (absorb nutrients and oxygen)
◦Central vein (drains to inferior vena cava)
Blood Supply
• 80% from portal vein: blood from stomach, intestines, spleen, and pancreas (carries absorbed
nutrients and toxins for cleansing)
• 20% from hepatic artery: fresh oxygenated blood
• Hepatic vein: drains cleansed blood to inferior vena cava and heart
• Very vascular organ requiring healthy blood flow for proper function
Primary Functions
Glucose Metabolism
• Stores glucose as glycogen for later use
• Glycogenolysis: converts glycogen back to glucose when energy needed
• Gluconeogenesis: synthesizes glucose from proteins or lactate when glucose unavailable
Fat Metabolism
• Breaks down fats for energy production
• Makes lipoproteins and ketone bodies (from fat breakdown)
• Synthesizes all body cholesterol
• Removes LDL (bad cholesterol) from blood
• Converts excess cholesterol to bile salts
Protein Metabolism
• Synthesizes plasma proteins including:
◦Clotting factors (prothrombin, fibrinogen) - requires vitamin K
◦Albumin: maintains colloidal osmotic pressure, keeps fluid in vascular space
• Without albumin: fluid escapes into peritoneal cavity (ascites) or tissues (edema)
Bile Production & Function
• Bile composition: water, electrolytes, fatty acids, cholesterol, bilirubin, bile salts
• Functions: digests and absorbs fats; enables absorption of fat-soluble vitamins (A, D, E, K)
• Critical for vitamin K absorption: needed for clotting factor production
Bilirubin Excretion
• Red blood cells break down every 3 months
• Hemoglobin breakdown produces bilirubin (pigment)
• Bilirubin → bile → bile ducts → duodenum → stool (gives stool brown color)
• Liver responsible for excreting bilirubin from body
Drug Metabolism
• All drugs metabolized in liver for breakdown and detoxification
Vitamin & Iron Storage
• Stores fat-soluble vitamins (A, D, E, K) and iron
Ammonia Conversion
• Ammonia produced from protein breakdown in intestines
• Liver converts ammonia to urea (ammonia is toxic to brain)
• Critical function for neurological health
Kupffer Cells (Macrophages)
• Remove bacteria, debris, red blood cells
• Monitor and cleanse blood from portal vein
• Located in lobule units
Hormone Metabolism
• Metabolizes estrogen and aldosterone
• Liver disease → hormonal imbalances
Physical Assessment
Percussion
• Tympani sound: over non-organ areas (below liver)
• Dullness: indicates liver borders (upper and lower edges)
• Resonance: heard from chest above liver
Palpation
• Most livers not palpable (covered by rib cage)
• Ask patient to take deep breath; liver edge moves down with inspiration
• Healthy liver: soft, slightly sharp edge, smooth surface
• Diseased liver: hard, irregular shape, possible nodules
Diagnostic Tests
Blood Work (Liver Panel)
Important: 70% of liver cells may be damaged before enzymes significantly elevated
Liver Enzymes
• ALT: elevated with liver damage, hepatitis
• GGT: found in liver, kidneys, pancreas, bile duct; elevated with alcoholic liver disease and
cholestasis
• AST: elevated with liver problems; also found in heart, skeletal muscle, kidneys (may elevate after
exercise)
• ALP (Alkaline Phosphatase): found in liver, bile ducts, bone
Other Lab Values
• Serum bilirubin: elevated when liver cannot excrete (backs up into blood)
• Albumin: decreased (diseased liver cannot produce)
• PT/INR: prolonged (insufficient vitamin K for clotting factors)
• LDH: elevated in ischemic hepatitis or sepsis
• Ammonia: elevated in liver failure (cannot convert to urea)
• Cholesterol: may be elevated (obstruction) or decreased (liver cannot synthesize)
• Hemoglobin/Hematocrit: low (nutritional deficits, B12/folate insufficiency)
• Platelets: low (liver regulates production; splenomegaly destroys)
• Protein: low (poor diet)
Imaging
• Ultrasound
• CT scan
• MRI
Liver Biopsy
Preparation
• Obtain consent
• Coagulation studies required (liver very vascular; ensure ability to clot)
• Patient voids prior (large bladder may obstruct)
Procedure Methods
• Percutaneous with ultrasound guidance (most common): needle inserted under ultrasound
visualization
• Transvenous (less common): catheter threaded through jugular vein → right atrium → inferior vena
cava → liver
Post-Biopsy Nursing Care
• Position: right side for 2-4 hours (tamponade effect; prevents bleeding)
• Pressure dressing: tape tightly
• Lung assessment: monitor for pneumothorax (puncture risk); listen for decreased breath sounds
• Pain management: expect mild pain; severe pain indicates complications
• Monitor vital signs: increased heart rate may indicate hemorrhage
• Assess abdomen: should remain soft; hard abdomen suggests peritonitis or bile leakage
Complications (3 Main)
1.
Pneumothorax: decreased breath sounds on right
2.
Peritonitis: rigid, hard abdomen; severe pain
3.
Hemorrhage: increased heart rate; vital sign changes
Stages of Liver Damage
Progression
1.
Fatty liver: reversible if offending agent removed
2.
Liver fibrosis: may be reversible with intervention
3.
Cirrhosis: irreversible; liver full of scar tissue
Causes of Cirrhosis
• Alcoholic (most common): chronic alcoholism over years
• Post-necrotic: scarring after hepatitis
• Biliary: scarring around liver/bile ducts
• Cardiac: from right-sided heart failure
Cirrhosis
Definition
Replacement of normal liver tissue with fibrous scar tissue; destroyed hepatocytes cannot perform
functions.
Compensation & Decompensation
• Compensated: 80% of patients compensate ~10 years; may show minimal symptoms
• Symptoms may be subtle: anorexia, nausea, vomiting, bowel changes (inconsistent)
• Decompensation: occurs when liver can no longer compensate; pronounced symptoms from portal
hypertension
Portal Hypertension
Mechanism
• Scarred liver cannot accept blood flow from portal vein
• Blood backs up in vessels below liver
• Pressure builds (portal hypertension)
• Causes: ascites, edema, varices, encephalopathy, splenomegaly
Consequences
Ascites
• Cause: obstruction of venous blood flow → increased capillary pressure → fluid escapes into
peritoneal cavity
• Cycle: low intravascular volume sensed → kidneys produce aldosterone → retention of sodium/
water → worsens ascites
• Problem: fluid in wrong space; blood pressure may be low
• Manifestations: very large abdomen, thin arms/legs, malnourished appearance, respiratory
difficulty
Management:
• Diuretics: spironolactone (blocks aldosterone, spares potassium)
• Fluid restrictions: typically 2g sodium diet
• Albumin IV: maintains colloidal osmotic pressure; keeps fluid intravascular
• Assessment: daily weights (1L water = 2.2 lbs), abdominal girth measurement, respiratory rate
• Positioning: semi-Fowler's or upright (relieves diaphragm pressure)
• Paracentesis: drain 5-6 liters; monitor blood pressure; give albumin after; patient voids prior;
patient sits upright (fluid pools inferiorly)
Varices (Collateral Vessels)
• Formation: portal vein splits; new abnormal vessels created to bypass congested liver
• Locations: esophagus (esophageal varices), stomach (gastric varices), lower rectum (hemorrhoids),
abdomen (caput medusae)
• Problem: small vessels never meant for high blood flow; inelastic; prone to rupture
• Analogy: like highway traffic diverted onto tiny roads
Esophageal Varices
• Characteristics: dilated, tortuous, inelastic veins in esophagus
• Initial presentation: often asymptomatic; may be found on endoscopy
• Prevention: beta-blockers (propranolol) reduce pressure
Rupture Triggers:
• Heavy lifting
• GERD/acid reflux
• Alcohol consumption
• Vomiting
• Coughing
• Straining with bowel movements
Complications of Rupture:
• Hemorrhagic shock
• Airway compromise
• GI bleeding → protein digestion → ammonia production → hepatic encephalopathy
• Emergency situation
Management:
• Pharmacological:
◦Terlipressin: constricts esophageal veins; stops bleeding; IV drip with dedicated tubing/line
◦Vitamin K: aids clotting
◦Red blood cells: transfusion for bleeding
• Endoscopy: gastroenterologist locates bleeders
◦Sclerotherapy: inject medication into vein; causes scarring/sclerosis
◦Banding/Ligation: place rubber bands around bleeder
◦NPO post-procedure: until gag reflex returns (lidocaine numbing wears off)
• Balloon tamponade (rarely used): Sengstaken-Blakemore tube with inflatable balloons
◦Compresses bleeding site
◦Risks: airway obstruction if dislodged; scissors at bedside for emergency deflation
◦Usually combined with intubation/sedation for airway protection
Spleenomegaly
• Cause: increased pressure in spleen
• Result: spleen destroys platelets, RBCs, WBCs
• Consequences: thrombocytopenia, anemia, leukopenia
• Bleeding risk: high (liver cannot make clotting factors + low platelets)
Hepatic Encephalopathy
Cause: Ammonia and toxins bypass liver (unfiltered blood shunting); ammonia toxic to brain
Sources of Ammonia:
• GI bleeding (hemoglobin breakdown)
• High protein diet
• Bacterial infections (intestinal)
• Hypokalemia and alkalotic states
Signs & Symptoms (spectrum):
• Stage 1: mild confusion, agitation, irritability, sleep disturbance, decreased attention
• Stage 2: lethargy, personality changes, inappropriate behavior
• Stage 3: somnolent but arousable, slurred speech, confusion, possible aggression
• Stage 4: coma
• Motor disturbance: asterixis (abnormal hand flexion when arms extended; "flapping tremor")
• Cognitive changes, weakness, neuropathy
Potential Reversibility: Yes, with treatment
Management:
• Lactulose: laxative; traps ammonia in intestine; expelled in stool (oral or enema)
◦Expected effect: increased bowel movements
◦Excessive doses → diarrhea
• Antibiotics (e.g., Neomycin): decrease intestinal bacteria producing ammonia
• Protein diet: monitored low protein (1.5g/kg/day); cannot eliminate; carbs acceptable
• Avoid: sedatives, opioids, tranquilizers, sleeping pills (liver cannot metabolize; become toxic;
worsen neuro status)
• Nursing: frequent neuro checks, safety precautions, position near nurse's station
Shunting of Unfiltered Blood
• Blood bypasses liver
• Liver cannot cleanse/filter
• Ammonia and toxins enter general circulation → brain damage (encephalopathy)
Signs & Symptoms of Liver Disease
• Pallor: pale appearance
• Malaise: general feeling of unwellness
• Jaundice: orange tone to skin, sclera, mucous membranes
• Petechiae/Bruising: easy bruising (clotting factor deficiency)
• Gynecomastia (males): breast enlargement
• Menorrhea (females): abnormally heavy menstrual bleeding
• Cognitive changes: mild confusion to severe
• Tremor/Asterixis: abnormal hand flexion
• Weakness: generalized
• Neuropathy: peripheral nerve damage
• Right upper quadrant tenderness: liver location
• Large abdomen with thin extremities: ascites with malnutrition
• Edema: peripheral (legs)
• Pruritus: intense itching (bile salts in skin); unrelieved by creams
• Spider angiomas: small spider-like veins
• Palmar erythema: red palms (excess estrogen)
• Elevated respiratory rate: from ascites pressure on diaphragm
Jaundice
Definition
Yellow or yellow-orange discoloration of skin, sclera, mucous membranes; symptom of liver/
gallbladder disease, not disease itself.
Detection
• Visible in sclera and mucous membranes (easier to see on darker skin)
• Bilirubin level >2.5 mg/dL (normal: 0.3-1 mg/dL)
• Icteric phase: beginning stage; sclera starts yellowing
Types
Hemolytic Jaundice
• Cause: massive RBC destruction (e.g., hemolytic transfusion reaction)
• Problem: healthy liver cannot keep up with bilirubin production; cannot excrete all
• Result: bilirubin enters general circulation → deposits in skin, sclera, urine
• Urine: orange (contains bilirubin)
• Stool: normal brown color (bilirubin reached intestines)
Hepatocellular Jaundice
• Cause: diseased liver cannot clear normal bilirubin amounts
• Conditions: cirrhosis, alcoholic liver disease, cancer, hepatitis, gallbladder problems
• Result: bilirubin backs up into blood → deposits in skin, sclera, mucous membranes
• Urine: dark orange, frothy
• Stool: pale/clay-colored (bilirubin didn't reach intestines)
Obstructive Jaundice
• Cause: bile duct occlusion (inflamed gallbladder, tumor, stone)
• Result: bile with bilirubin cannot reach intestines; bilirubin absorbed by body
• Manifestations: orange skin, sclera, mucous membranes
• Urine: dark orange, frothy
• Stool: pale/clay-colored
Manifestations of Liver Disease
Nutritional/Metabolic
• Edema: from hypoalbuminemia (cannot keep fluid intravascular)
• Large abdomen, thin extremities: ascites with malnutrition
• Vitamin deficiency (A, D, E, K): fat-soluble; need bile for absorption
• Bleeding/bruising: clotting factor deficiency; vitamin K deficiency
• Thrombocytopenia: splenomegaly destroys platelets; liver regulates production
Dermatologic
• Pruritus: bile salts absorbed into skin; unrelieved by normal creams
• Spider angiomas: small spider-like veins
• Palmar erythema: red palms (excess estrogen from impaired metabolism)
Endocrine
• Gynecomastia (males): breast enlargement
• Amenorrhea/Menorrhea (females): abnormal menses
• Testicular atrophy (males): from hormone metabolism impairment
Gastrointestinal
• Jaundice: bilirubin accumulation
• Large abdomen: ascites
Respiratory
• Elevated respiratory rate: ascites pushing on diaphragm
Neurological
• Peripheral neuropathy: vitamin deficiency affecting myelin sheath
Nursing Diagnosis & Care Plan Example: Ascites
Medical Diagnosis: Ascites
Nursing Diagnosis: Excess fluid volume related to increased portal pressure and decreased albumin
Goal/Outcome: Restore normal fluid volume
Interventions:
• Administer diuretics (spironolactone)
• Sodium restrictions (2g diet)
• Albumin IV
• Daily weights
• Abdominal girth measurement
• Assess respiratory rate
• Assist with paracentesis or TIPS procedure
• Semi-Fowler's positioning
Hepatitis
Definition
Inflammation of liver; causes inflammation and necrosis of liver cells.
Causes
• Viral: Hepatitis A, B, C, D, E; Cytomegalovirus (CMV); Epstein-Barr
• Drug-induced: overdose
• Alcohol-induced
• Acetaminophen (Tylenol): leading cause of acute liver failure
Lab Values in Acute Infection
• Elevated AST, ALT
• Elevated bilirubin
• Specific antibodies/antigens (varies by type)
Symptoms (All Types)
• Nausea, vomiting, anorexia
• Dark urine (jaundice)
• Malaise, fever
• Jaundice
• GI symptoms (diarrhea)
Hepatitis A
Transmission
• Fecal-oral route: contaminated food/water
• Highly contagious
• Mechanism: virus in food → ingestion → replication in intestines → portal vein to liver → replication
in liver; spread via poor hand hygiene after bowel movements
At-Risk Populations
• Travelers to countries with poor water sanitation
• Restaurant/daycare outbreaks (diaper changes, toilet assistance)
Prevention
• Vaccine: available for children and adults
• Hand hygiene: especially with food preparation and bathroom use
Treatment
• Supportive: bedrest (person feels quite ill)
• Severe cases: Interferon (antiviral)
Course
• Acute only: no chronic state
• Outcome: lifelong immunity after recovery
• Mortality: <1%
Post-Exposure Prophylaxis
• Immune globulin: passive immunity (antibodies from recovered persons)
• Vaccine: takes longer to provide immunity
• Household contacts: use separate utensils for safety
Hepatitis B
Transmission
• Bloodborne and bodily fluids
• Routes: sexual contact, needle sharing, needle stick injuries, birth (mother to baby)
• NOT spread by: casual contact, saliva, coughing, sneezing, kissing
At-Risk Populations
• Multiple sex partners (STI/STD)
• IV drug users
• Hemodialysis patients
• Healthcare workers
Prevention
• Vaccine: given at birth; booster before nursing school; healthcare workers required
• Practices: good hygiene, unprotected sex avoidance, no needle/razor/toothbrush sharing, safe
tattoo parlors (separate needles, hygienic)
Course
• Acute: most do not become chronic; body mounts immune response; lifelong immunity
• Chronic: some become chronic carriers; no cure; antivirals manage symptoms
• Chronic hepatitis B: known cause of liver cancer
Treatment
• Acute: supportive
• Chronic: antivirals (no cure)
Post-Exposure Prophylaxis
• Immune globulin: hepatitis B antibodies
• Vaccine: takes time to provide immunity
Hepatitis C
Transmission
• Bloodborne only (not in other bodily fluids)
• Routes: needle sharing (IV drug users), multiple sex partners (STD), hemodialysis, blood
transfusions prior to 1992 (blood not tested)
• Symptoms: usually none until late disease
Prevention
• No vaccine available
• Practices: good hygiene, avoid needle/razor/toothbrush sharing
Treatment
• Antivirals (since 2013): completely cures hepatitis C
• Course: 8-12 weeks of antiviral therapy
• Cure rate: 85% of acute cases can become chronic (20-30 years to cirrhosis), but should not with
treatment
Chronic Carriers
• May have chronic state if untreated or if past point of return
• Antivirals may not work if too advanced
Important Notes
• No lifelong immunity: can reinfect with hepatitis C after cure
• Leading cause of liver transplants: historically, now decreasing due to antiviral treatment
• Screening: pregnant women and IV drug users screened for B and C
Hepatitis C Testing
• HCV antibody negative/non-reactive: no exposure or antibodies not yet produced
• HCV antibody reactive: presume current hepatitis C infection
• HCV antibody positive + RNA/antigen detected: current infection
• HCV antibody positive + RNA/antigen NOT detected: no current infection; prior exposure; treated
patients have antibodies but not protected from reinfection
Hepatitis D
Characteristics
• Co-infection with Hepatitis B only: cannot get D without B
• Same transmission/prevention as Hepatitis B
• Everything about B applies to D
Prevention
• Hepatitis B vaccine
• Good hygiene, unprotected sex avoidance, needle/razor avoidance
Hepatitis E
Transmission
• Fecal-oral route: contaminated food/water
• Spread by: poor hygiene (bathroom → food preparation)
• Common sources: raw/undercooked shellfish and pork
At-Risk Populations
• Pregnant women (especially last trimester): high mortality risk for mother and baby
• Underdeveloped countries (more common)
• Rising rates in US in recent years
Prevention
• No vaccine
• Hand hygiene: especially bathroom and food preparation
• Pregnant women: avoid shellfish and pork
Treatment
• Supportive: like Hepatitis A
• May need: hospitalization, IV fluids
Course
• Acute: supportive treatment
• Outcome: lifelong immunity after recovery
Hepatitis B Serology (Complex)
Antigens & Antibodies
• Surface antigen (HBsAg): outer surface
• E antigen (HBeAg): indicates virus replicating
• Core antigen (HBcAg): inner core
Body's Response
• Makes antibodies to antigens from inside out
• First: antibody to core antigen (HBcAb) - person still considered infected
• With recovery/treatment: antibody to surface antigen (HBsAb) - protected/immune
Vaccine
• Gives antibody to surface antigen (HBsAb)
• Protection = HBsAb present
Panel Interpretation
• Multiple antigens and antibodies (IgM, IgG) show where person is in infection
• Key: to be protected, need antibody to surface antigen
Summary: Hepatitis Types & Nursing Interventions
Bloodborne Hepatitis
• B: think body fluids and blood
• D: goes with B only
• C: blood only
Foodborne Hepatitis
• A: fecal-oral
• E: fecal-oral
Nursing Education & Interventions
Safe Behaviors:
• Target high-risk groups (IV drug users, multiple sex partners)
• Importance of vaccines (B available; no vaccine for C)
• Healthcare workers: sharp safety (prevent needle sticks)
Foodborne (A & E):
• Hand washing education (before/after bathroom)
• Safe food preparation (clean hands)
• Vaccine importance (A has vaccine; E does not)
All Hepatitis Types:
• Lifestyle modification: no alcohol for 6 months after acute phase (liver healing); avoid
acetaminophen or use sparingly
• Diet: low fat, small frequent meals during acute phase
• Post-exposure: immunoglobulin + vaccine for A and B
Liver Cancer
Types
• Primary: rare; usually from Hepatitis B or C or cirrhosis
• Secondary: more common; metastasized from GI, lung, or breast
Symptoms
• GI symptoms (range)
Diagnosis
• Blood work (liver panel)
Treatment
• Chemotherapy, radiation
• Lobectomy: if cancer in one lobe only (healthy liver regenerates)
Progression
• Often end result of Hepatitis C
• Follows cirrhosis in disease progression
Liver Transplantation
Indications
• End-stage liver disease
Procedure
• Diseased liver removed
• Replaced with whole liver from deceased donor OR lobe from living donor
Success Requirements
• Immunosuppressant therapy: anti-rejection medications for life
• Non-compliance = failure: critical adherence
• Extensive screening (psychological, nutritional) before transplant
Complications
• Infection (from immunosuppression)
• Bleeding
• Rejection
Living Donor Risks
• Pulmonary embolism (high risk)
• Thrombosis in portal vein → PE
• Bile duct injury
Recipient Education
• Strict immunosuppressant adherence
• High infection risk (immunosuppression quiets immune response)
• Longstanding systemic problems from original disease may persist
Nursing Interventions Summary for Liver Patients
Cirrhosis/Portal Hypertension/Ascites
• Assess vital signs (focus on respirations)
• Daily weights, abdominal girth measurement
• Semi-Fowler's positioning
• Administer IV diuretics, albumin
• Sodium restrictions
Hepatic Encephalopathy
• Neuro checks frequently
• Safety precautions
• Administer lactulose
• Avoid sedatives, opioids
Esophageal Varices
• Suspect in all liver disease patients (may be asymptomatic)
• If bleeding: start terlipressin immediately
• Prepare for endoscopy
• Anticipate RBC transfusion
• Move fast (emergency)
Diet
• Early cirrhosis (no ascites): regular protein
• Late cirrhosis (decompensated): low protein, low sodium, high carb
• Vitamin supplementation
• Avoid alcohol (6 months post-acute hepatitis)
• Avoid acetaminophen
• Avoid toxic medications
Procedures
• Review paracentesis and liver biopsy guidelines (Choral Point Chapter 43)
Patient Teaching
• Hepatitis prevention and transmission
• Bleeding precautions
• Avoid alcohol and acetaminophen
• Safe medication use (liver-toxic drugs)
• Increased lung cancer risk with cirrhosis
Clinical Exam Questions & Answers
Question 1: Ascites with Vital Signs
Scenario: BP 128/78, Pulse 118, RR 28, Temp normal, O₂ 89% on room air
Best First Action: Raise head of bed
Rationale: Patient likely positioned too flat; large abdomen pushes diaphragm up, preventing lung
expansion. Semi-Fowler's or upright position relieves pressure, improves breathing.
Question 2: Hepatitis A Education
Incorrect statement: "I can take cinnamon for arthritis" (or similar acetaminophen reference)
Rationale: Acetaminophen contraindicated in hepatitis; can cause acute liver failure
Question 3: Hepatitis C Teaching Plan
Most helpful history: IV drug use or multiple sex partners (bloodborne transmission)
Not relevant: Recent uncooked meat in South America (suggests Hepatitis A or E - foodborne)
Question 4: Lactulose Effect
Expected effect: Increased bowel movements
Rationale: Lactulose traps ammonia in intestine; expelled in stool; goal is bowel movements to
eliminate ammonia
Key Takeaways
1.
Liver disease severity: 70% of liver cells damaged before enzymes significantly elevated
2.
Cirrhosis: irreversible; fatty liver and fibrosis may be reversible if offending agent removed
3.
Portal hypertension: causes ascites, varices, encephalopathy, splenomegaly
4.
Esophageal varices: emergency; rupture → hemorrhagic shock, airway compromise
5.
Hepatic encephalopathy: potentially reversible with lactulose and treatment
6.
Hepatitis types: A & E (foodborne), B & D (bloodborne), C (bloodborne only)
7.
Hepatitis C: only type with complete cure via antivirals (8-12 weeks)
8.
Nursing focus: safety, monitoring, preventing complications, patient education