Liver Anatomy, Physiology, and Metabolic function

Liver Anatomy and Physiology

• The liver is the largest gland
• It is located in the upper right abdomen
• It's a vascular organ that receives blood from the GI tract via the portal vein and the hepatic artery

Metabolic Functions of the Liver

• It plays a role in glucose metabolism via glycogenolysis and gluconeogenesis
• Glycogenolysis converts glycogen back to glucose
• Gluconeogenesis uses amino acids or lactate from exercising muscles
• It is involved in ammonia conversion to urea, protein metabolism, and fat metabolism
• It is essential for vitamin and mineral storage, specifically vitamin A, B, D, several B vitamins, iron, and copper
• The liver is responsible for bile formation and bilirubin excretion
• It's involved in drug metabolism

Assessment of Patient with Liver Alterations

• Focus on health history and physical assessment on page 1368
• Health history should include exposure to hepatotoxic substances, infectious agents, travel, lifestyle, medical/family history, and COLDSPA
• Physical assessments should cover the skin, musculoskeletal, genitourinary, cognitive status, neurological, palpation, and percussion

Liver Function Studies

• Serum aminotransferase levels must be studied
• Aspartate aminotransferase (AST) is present in high metabolic activity tissues and increases in cirrhosis, hepatitis, and liver cancer
• Alanine aminotransferase (ALT) is primarily in liver disorders and monitors hepatitis or cirrhosis
• Gamma-glutamyl transferase (GGT) is associated with cholestasis
• Gamma-glutamyl transpeptidase (GGTP) is also known as GGT
• Lactic dehydrogenase (LDH) is also important
• Serum protein studies such as total protein, albumin, and globulins should be considered
• Assess bilirubin and urobilinogen, clotting factors, serum alkaline phosphatase, serum ammonia, and lipids
• Review clinical functions of labs in Table 43-1

Additional Diagnostic Studies

• Liver biopsy, ultrasonography, CT, MRI, and laparoscopy all can be used

Hepatic Dysfunction

• Liver cells are damaged
• Can be acute or chronic
• Causes include infection, anoxia, metabolic disorders, toxins, and malnutrition

Manifestations of Hepatic Dysfunction

• Jaundice
• Portal hypertension
• Ascites and varices
• Hepatic encephalopathy or coma
• Nutritional deficiencies

Jaundice

• Yellow or greenish-yellow sclera and skin
• Bilirubin levels greater than 2 mg/dL cause it
• Types include: Hemolytic(↑serum bilirubin & urobilogen), Hepatocellular, Obstructive, and Hereditary hyperbilirubinemia
• Gilbert and Dubin-Johnson syndrome are hereditary hyperbilirubinemia's

Signs/Symptoms of Hepatocellular and Obstructive Jaundice

• Hepatocellular jaundice manifests as being mild to severely ill, and can cause a lack of appetite, nausea/vomiting, weight loss, malaise, fatigue, weakness, headache, fever/chills, and jaundice may/may not be detected
• Obstructive jaundice presents with jaundice (mucus membrane), dark orange-brown urine, clay-colored stools, dyspepsia, impaired fat digestion, and pruritus

Portal Hypertension

• Obstructed blood flow increases pressure in the portal venous system
• Manifestations include splenomegaly, hypersplenism, ascites, and esophageal varices

Ascites

• Albumin-rich fluid moves into the peritoneal cavity
• Factors include portal hypertension, splanchnic circulation, liver inability to metabolize aldosterone, and decreased synthesis of albumin
• Increased abdominal girth, bulging flanks, weight gain, shortness of breath, abdominal striae, distended veins, umbilical hernia, fluid, and electrolyte imbalance can all manifest

Ascites Assessment and Management

• Record abdominal girth and weight daily
• Assess for fluid in the abdominal cavity by percussion for shifting dullness or fluid wave
• Closely monitor fluid and electrolyte imbalances
• Measure input and output accurately
• Implement a neurological and respiratory assessment
• Watch for encephalopathy

Treatment of Ascites

• Follow a low-sodium diet
• 1st Line diuretic is Spironolactone, can also use Furosemide
• Bed rest
• Paracentesis
• Administer salt-poor albumin
• Use of Transjugular intrahepatic portosystemic shunt (TIPS)
• Peritoneovenous shunt

Hepatic Encephalopathy

• This is a life-threatening complication
• It results from hepatic insufficiency and portosystemic shunting
• Mental changes, motor disturbances, moodiness, altered sleep, coma, seizures, asterixis, constructional apraxia, abnormal DTRs, flaccid extremities, and fetor hepaticus will manifest

Hepatic Encephalopathy Assessment

• Electroencephalogram (EEG) to assess
• Assess for changes in LOC and other manifestations
• Monitor fluid, electrolyte, and ammonia levels

Hepatic Encephalopathy Management

• Reduce serum ammonia levels via Lactulose
• Eliminate the precipitating cause
• Administer IV glucose to minimize protein catabolism
• Use gastric suction, enemas, or oral antibiotics to reduce ammonia from GI tract
• Discontinue sedatives, analgesics, and tranquilizers
• Monitor and treat complications and infections
• Maintain patient safety

Esophageal Varices

• Dilated, tortuous veins develop in the submucosa of the esophagus
• Occurs with cirrhosis
• Elevated pressure in veins draining into the portal system is the cause
• Is a life-threatening complication
• Manifestations include hematemesis, melena, general deterioration, and shock

Esophageal Varices: Assessment & Diagnostic Findings

• Endoscopy
• Ultrasonography
• CT scanning
• Angiography
• Portal Hypertension Measurements
• Labs: LFTs
• Splenoportography
• Hepatoportography
• Celiac angiography

Treatment of Bleeding Varices

• Treat for shock
• IV fluids, electrolytes, volume expanders, blood and blood products
• Use Vasopressin and octreotide to decrease bleeding
• Give Beta-blockers, such as Propranolol, nadolol, or carvedilol, to decrease portal pressure
• Use Nitrates, such as Isosorobide
• Balloon tamponade

Treatment of Bleeding Varices

• Endoscopic sclerotherapy and variceal ligation treatment option/tools
• Transjugular intrahepatic portosystemic shunt
• Use tissue adhesives, fibrin glue, and embolization for additional therapies
• Surgical bypass procedures and devascularization and transection can be used for surgical management

Nursing Management of Esophageal Varices

• Assess for encephalopathy
• Maintain safe environment
• prevent injury, bleeding, and infection
• Maintain comfort
• Administer prescribed treatments and monitor for potential complications
• Educate and support patient and family

Other Manifestations of Hepatic Dysfunction

• Edema and bleeding
• Vitamin deficiency
• Metabolic abnormalities
• Pruritis and skin changes

Viral Hepatitis

• A systemic viral infection causing necrosis and inflammation of liver cells
• Types include A, B, C, D, E, G, and GB virus-C
• A and E are transmitted via the fecal-oral route
• B and C are bloodborne
• Those with hepatitis B are at risk for hepatitis D
• Hepatitis G and GB virus-C can be spread through blood

Nonviral Hepatitis

• Includes toxic and drug-induced hepatitis causes

Phases of Hepatitis Infection

• Hepatitis infections consists of Viral Replication, Preicteric or Prodromal, Icteric, and Convalescent

Hepatitis A (HAV)

• Infection occurs through fecal-oral route transmission
• Incubation period is generally 2-6 weeks
• Can last 4-8 weeks
• Mortality rate is 0.5% if younger than 40 and 1-2% if older than 40 years old
• Usually Asymptomatic or anicteric
• Manifestations: mild flu-like symptoms, low-grade fever, anorexia, jaundice, indigestion, epigastric distress, and enlargement of liver/spleen

Management of Hepatitis A

• Prevention is done via handwashing, safe water, proper sewage disposal, vaccine, and immunoglobulin for contacts
• Medical management: bed rest, nutritional support, hydration
• Nursing management: emotional support and education

Hepatitis B (HBV)

• Spread through blood, saliva, semen, and vaginal secretions
• Those who are in close contact, healthcare worker, IV drug user, or homosexual are at risk (see chart 43-7)
• Incubation is between 1-6 months
• Can last 6 months and can become chronic
• May have rashes, loss of appetite, dyspepsia, abdominal pain, generalized aching, arthralgias, malaise, weakness, or jaundice
• Hepatomegaly and tenderness
• Splenomegaly
• Posterior cervical lymph node enlargement
• Serum antigen and antibody detected

Management of Hepatitis B

• To prevent, screen blood donors, use disposable IV equipment, disinfect, give vaccine and immunoglobulins, safe sex practices, and avoid IV drug use
• Medical Management: Alpha interferon, Nucleoside analogs(entecavir/tenofovir), bed rest, and nutritional support
• Nursing management: emotional support and education

Hepatitis C

• Spread through blood contact
• Affects those who are 40 -59 years of age and African Americans
• Hepatitis C is a common cause of liver cancer and transplant
• IV drug users, those who practice high risk sex, and those exposed to blood products are at highest risk
• Incubation period is 15-160 days
• May have symptoms similar to HBV
• May have mild or absent symptoms
• Sufferers frequently are in a chronic carrier state

Management of Hepatitis C

• Public health programs teaching safe needle sharing, screening blood supply, safety needles in heath care, and disinfecting
• Direct-acting antivirals (DAA): Glecaprevir-pibrentasvir; ledipasvir-sofosbuvir
• Educate about reducing/eliminating infection, transmission, how treatment works, and follow-up care guidelines

Hepatitis D

• Only those with hepatitis B are at risk
• Transmission: same as HBV but through blood, saliva, semen, and vaginal secretions
• Those who are IV drug users, on hemodialysis, or who have had blood transfusions are at risk.
• Incubation: 30 - 150 days
• Similar to HBV
• This form of the virus will likely develop acute liver failure or turn into chronic active hepatitis and cirrhosis
• Treatment: Interferon alfa

Hepatitis E

• Fecal-oral route transmissed
• Incubation period: 15 to 65 days
• Symptoms may be similar to the HAV
• Usually self-limiting
• Abrupt or immediate onset of Jaundice
• Generally does not develop into a chronic illness
• Prevention done through hand washing

Nonviral Hepatitis: Cause, Manifestations, and Treatment

• Cause: Hepatotoxins- carbon tetrachloride, phosphorus
• Manifestations: Anorexia, N/V, jaundice, hepatomegaly. Liver failure and death possible and depends on length of exposure
• Treatment: Liver transplant, fluid and electrolyte balances, blood transfusion, and comfort measures

Nonviral Hepatitis: Drug-induced Hepatitis

• Cause: Hepatoxic drugs: isoniazid, halothane, acetaminophen
• Manifestations: Chills, fever, rash, pruritis, arthralgia, anorexia, nausea, jaundice, and hepatomegaly
• Liver failure and death possible
• Treatment: stop use of causative medication, antidotes, and liver transplant

Acute Liver Failure (ALF)

• Syndrome characterized by sudden and severely impaired liver function in a previously healthy individual
• Causes: viral hepatitis, hepatoxic agents, metabolic conditions, structural changes
• Manifestations:
• Neurologic dysfunction, elevated PT/INR, jaundice, anorexia, kidney disease & hepatic encephalopathy
• Cerebral edema
• Electrolyte disturbances
• Cardiovascular abnormalities
• Infection
• Hypoglycemia

Acute Liver Failure (ALF): Management

• Treatment: Liver transplant is best
• Plasmapheresis, prostaglandin therapy, and extracorporeal liver assist devices (ELAD) & Bioartificial liver (BAL) are therapies
• Manage encephalopathy by providing Mannitol, monitoring fluids/electrolytes. Also using quiet and low stimulation with sedation.
• Constantly check the status of ICP and glucose levels for irregularities. Also monitor for infections.