Hepatic Disorders1
Hepatic Disorders Overview
Liver Anatomy and Function
The liver is the largest internal organ in the body, second only to the skin, and it plays a vital role in various physiological processes.
Location: Found in the Right Upper Quadrant (RUQ) of the abdomen.
Functions:
Detoxification: Breaks down and eliminates toxins, drugs, and metabolic byproducts from the bloodstream.
Drug Metabolism: Modifies pharmaceutical substances to enhance their excretion.
Blood Clotting: Produces clotting factors essential for proper hemostasis.
Synthesis of Albumin: Regulates osmotic pressure and transports various substances in the blood.
Bile Production: Necessary for digestion, particularly in the emulsification of fats.
Regenerative Capacity: The liver can regenerate itself following injury, allowing for the recovery from acute damage.
Cirrhosis Pathophysiology Overview
Cirrhosis is a progressive disease characterized by severe liver scarring and dysfunction. Key features include:
Extensive Fibrosis: Formation of fibrotic bands disrupts normal liver architecture.
Nodular Regeneration: Growth of nodular structures in response to damage.
Bile Duct Blockage: Leads to cholestasis (impaired bile flow), impacting both hepatic and systemic circulation.
Consequences of Cirrhosis: Ultimately results in liver shrinkage, difficulty in function, and potential liver failure.
Common Types of Cirrhosis
Post Necrotic Cirrhosis:
Causes: Viral Hepatitis (notably Hepatitis C), exposure to hepatotoxic substances such as certain drugs and toxins.
Laennec’s Cirrhosis (Alcoholic Cirrhosis):
This is the most prevalent type, resulting from chronic alcohol abuse.
Biliary Cirrhosis:
Often linked to chronic biliary obstruction or autoimmune issues that affect bile flow.
Common Causes of Cirrhosis
Primary Causes:
Alcoholic liver disease.
Viral Hepatitis Types B and C.
Autoimmune hepatitis.
Nonalcoholic fatty liver disease (NAFLD).
Exposure to drugs and chemical toxins.
Contributing Factors:
Gallbladder disease.
Metabolic syndromes and genetic predispositions.
Cardiovascular disease.
Complications of Cirrhosis
Complications arise from liver dysfunction, including:
Portal Hypertension: Increased pressure in the portal vein can lead to serious health issues.
Ascites: Accumulation of fluid in the abdominal cavity.
Esophageal Varices: Enlarged veins that can rupture, leading to hemorrhage.
Splenomegaly: Enlargement of the spleen due to increased pressure.
Jaundice: Yellowing of the skin and eyes due to bilirubin accumulation.
Hepatic Encephalopathy: Cognitive dysfunction resulting from the liver's inability to detoxify ammonia.
Anemia and Hepatorenal Syndrome:
Portal Hypertension
Portal hypertension is characterized by elevated blood pressure in the portal vein,
leading to the development of varices that pose a risk for lifethreatening bleeding and high morbidity/mortality rates.
Splenomegaly
The spleen’s normal functions include filtering blood and storing platelets. Complications from splenomegaly can lead to severe hematological issues:
Anemia: Signs may include pallor and fatigue.
Thrombocytopenia: Symptoms include increased susceptibility to bleeding and bruising. 1st sign that pt has liver dysfunction.
Lymphocyte Dysfunction: Results in decreased immunity and increased infection risk.
Ascites and Gastroesophageal Varices
Ascites: Characterized by excessive fluid accumulation in the peritoneal cavity, requiring monitoring and potential therapeutic interventions.
Esophageal Varices: occurs when fragile, thin-walled esophageal veins become distented from increased pressure; management may require endoscopic procedures to prevent rupture
bleeding from the increase pressure is a life threatening medical emergency.
hematemesis (vomiting blood) or melena black, tarry stools)
treatment
sengstaken blakemore tube used for controlling bleeding in upper GI tract
Biliary Obstruction
Impairments in bile production can affect fat absorption, particularly concerning fat-soluble vitamins K
jaundice
yellowish coloration of the skin
late-stage cirrhosis
What is Bile?
Bile is a substance produced by the liver and stored in the gallbladder, crucial for digestion:
Functions:
Aids in the digestion and absorption of dietary fats and fat-soluble vitamins (A, D, E, K).
Facilitates the excretion of bilirubin formed during the breakdown of red blood cells.
imbalance in bile production
Gallstones (cholelithiasis): imbalance of bile salts, cholesterol, and bilirubin leads to stone formation
jaundice: buildup of bilirubin in the bloodstream due to bile flow obstruction
Malabsorption of fats: inadequate bile production results in steatorrhea (fatty stools) and vitamin deficiencies
cholecystitis: inflammation of gallbladder, often due to gallstones blocking bile flow
Late Stages of Cirrhosis Symptoms
Common symptoms indicative of advanced liver disease include:
Jaundice and Icterus: Yellowing of the skin and sclera.
Purpuric lesions, such as petechiae, pinpoint, red-purple hemorrhagic lesions) or ecchymoses (large purple, blue, or yellow brusies)
Skin Changes: Presence of rashes, purpuric lesions, palmar erythema, and spider angiomas.
Ascites: Visible abdominal distension due to fluid accumulation.
Vitamin Deficiencies: Including but not limited to A, D, E, and K deficiencies.
Hepatic Encephalopathy
PSE: a complex cognitive syndrome that results from liver failure and cirrhosis.
pt reports; sleep disturbances, mood disturbance, mental status changes, and speech problems
stage 1
subtle manifestations that may not be recognized immediately
personality changes (agitation, belligerence)
emotional lability (euphoria, depression)
impaired thinking
inability to concentrate
fatigue, drowsiness
slurred or slowed speech
sleep pattern disturnances
stage 2
continuing mental changes
mental confusion
disorientation to time, place or person
Asterixis (hand flapping)
stage 3
progressive deterioration
marked mental confusion
muscle twitching
hyperreflexia
asterixis (hand flapping)
stage 4
unresponsiveness, leading to death in most pt
unarousable, obtunded
no asterixis
seizures
fetor hepaticus ( liver breath-musty, sweet, odor)
Cirrhosis Assessment
History: Obtaining details about age, gender, medication use, employment history, alcohol intake, needlestick injury, sexula, fmaile, social histories
Physical Assessment: Monitoring signs such as fatigue, weight fluctuations, anorexia, vomiting, and abdominal discomfort, abdo pain, abdominal assessment (measuring girth)
Abdominal Girth Measurement: Essential for evaluating ascites.
Psychosocial Assessment: Considering social and alcohol-related histories.
Lab Findings for Cirrhosis
Serum Enzymes: hepatic cell destruction, hepatitis
Elevated levels of AST (0-35) and ALT (4-36) signal liver damage; ALT is the more specific marker.
Bilirubin Levels: (0.3-1.0)
Elevated total and direct bilirubin levels indicate liver dysfunction. (hepatic cell disease)
elevated serum indirect unconjugated bilirubin: cirrhosis
Serum Proteins:
A decrease in total protein and albumin levels is observed in severe liver disease. (UNDERNUTRITION)
increased serum total protein: acute liver disease
Ammonia Levels: Increased serum ammonia concentrations suggest advanced liver dysfunction.(10-80)
Prolonged PT/INR: hepatic cell damage and decreased synthesis of prothrombin
Diagnostics for Liver Issues
Imaging Assessments:
Utilize CT, MRI, abdominal x-rays, and liver ultrasound for diagnosis.
Specialized Assessments:
Include transient elastography and arteriography, alongside EGD (directly visualize upper Gi tract to detect complication of liver failure) and ERCP for biliary concerns.
Treatments for Liver Disorders
Fluid Management: Administer diuretics (spironolactone and furosemide)
caution sodium, potassium imbalances
monitor intake and output
Electrolyte Imbalances: Correct elevated BUN and hematocrit levels through appropriate interventions.
Nutritional Support: Implement low-sodium diets and ensure vitamin and mineral supplementation.
Paracentesis: A medical procedure used to remove excessive fluid from the abdomen, alleviating discomfort.
Hemorrhage Prevention: Regularly assess for esophageal varices due to their potential to cause significant GI bleeding.
Ammonia Management: Administer lactulose to facilitate ammonia excretion and reduce confusion risks.
Pruritus Management: Address skin itching associated with bilirubin build-up.
Medication Guidance: Avoid narcotics that can further delay drug metabolism.
Hepatitis Overview
A group of infectious conditions characterized by inflammation of liver cells, resulting from five primary viral pathogens:
Hepatitis A (HAV): Typically an acute infection; vaccination is available.
Hepatitis B (HBV): Can be both acute and chronic; vaccination is effective for prevention.
Hepatitis C (HCV): Primarily chronic and can lead to serious liver damage; no vaccination is available.
Hepatitis D (HDV): Co-exists with HBV; no vaccine exists.
Hepatitis E (HEV): Generally acute; also associated with contaminated water.
Routes of Transmission for Hepatitis
HAV: Fecal-oral transmission, commonly through shellfish caught in contaminated water sources
preventing
proper handwashing
avoiding contaminated food or water
receiving immunoglobulin within 14 days if exposed to the virus
receiving HAV vaccine before traveling to areas where disease is common
receiving vaccine if living or working in enclosed areas with others
HBV: Transmitted via blood and body fluids, often through unsafe sexual practices or sharing of needles.
sharing razors, accidental needlesticks, birth, blood transfusion (before 1992), hemodualysis
preventions
HCV: Primarily blood-to-blood contact,
illicit IV drug needle sharing
blood, blood products or organ transplant before 1992
needstick
healthcare workers
prisoners
sharing of drug paraphernalia
HDV: parenteral (occurs with hepB)
defective RNA virus that needs helper function of HBV
parenteral routes, especially in those who use IV drugs
HEV: Fecal-oral route similar to HAV, associated with contaminated drinking water.
Hepatitis Signs & Symptoms
Common manifestations of hepatitis include:
Abdominal discomfort, particularly in the RUQ.
Jaundice indicated by yellowing of the skin and sclera.
Gastrointestinal symptoms such as diarrhea or constipation, light-colored stools, and dark urine.
General systemic symptoms: fever, fatigue, malaise, loss of appetite, nausea/vomiting, dry skin, and pruritus.
Diagnostics for Hepatitis
Laboratory Assessments:
Liver enzyme tests (AST, ALT) alongside serological analyses for antigen detection.
Diagnostic Procedures:
Consider liver biopsy or ultrasound for definitive diagnosis.
Prevention of Viral Hepatitis in Healthcare Workers
Adhere to standard precautions for infection control.
Utilize needleless technology to minimize risks of needle-stick injuries.
Ensure vaccinations are up to date, particularly for Hepatitis B, where applicable.
Promptly follow up post-exposure to provide appropriate prophylaxis and monitoring.
Hepatitis Management Summary
Hepatitis A: Transmitted via fecal-oral route, managed with supportive care and vaccination.
Hepatitis B: Requires blood/body fluid precautions; vaccination is essential.
Hepatitis C: Managed mainly with antiviral therapy; no vaccine available.
Hepatitis D: A concurrent infection requiring active Hepatitis B; lacks a vaccine.
Hepatitis E: Generally self-limiting; associated prevention strategies target hygiene and water safety.
Liver Transplant Considerations
Liver transplantation becomes necessary for advanced liver disease cases such as end-stage renal disease (ESRD) or acute liver failure. Factors to consider include:
Exclusion Criteria: Severe cardiovascular or respiratory complications, or failure to comply with treatment protocols.
Post-transplant Management: Ongoing monitoring for acute graft rejection and risk of infections, alongside managing potential hepatic complications.
Psychosocial Support: Addressing emotional well-being and medication side effects during recovery.
side effects of immunosuppressive drugs
long- term manangamet
Postoperative Assessment and Prevention
Acute Graft Rejection: Monitoring for signs such as tachycardia, fever, jaundice, and RUQ pain or flank pain, diminished bile drainage or changes in bile color or increased jaundice
lab changes: increased levels of bilirubin, prolonged PPT, transaminases, alkaline phosphate
prevention: prophylaxis with immunosuppressants agents, cyclosporine plus antirejection drugs
Infection Prevention Strategies: Employing antibiotic prophylaxis and maintaining a sterile environment.
Hepatic Complications Monitoring: decreased bile drainage, increased RUQ abdo pain with distention and guarding, N/V, increased jaundice, clay-colored stools, Lab values (increased bilirubin, transaminases)
report s/s to surgon immediately
Acute Kidney Injury Monitoring: Closely observe urine output and report any immediate concerns.
monitor all drugs with nephrotoxic side effects
prevent hypotension