EP 192: How Cirrhosis Impacts the Liver

EP 192: How Cirrhosis Impacts the Liver

How Cirrhosis Impacts The Liver

How cirrhosis affects the liver is one of the many interesting medical cases you’ll encounter as a nurse. But what is it? Cirrhosis is a liver disease where liver cells become extremely damaged. This leads to the damaged cells being replaced with fibrous tissue or scarring of the liver. It also alters the liver’s structure and normal vasculature impairs blood and lymph flow and causes hepatic insufficiency.

Causes

Excessive alcohol consumption

  • Too much alcohol intake is the most common cause of cirrhosis

Injury

  • Problems with the bile duct: bile stays in the liver and damages cells.
    • Bile duct: carries bile from the liver to the small intestine

Hepatitis

  • Different types of hepatitis can cause postnecrotic cirrhosis.

Other diseases

  • Viral Infection, autoimmune 
  • Too much fat collecting in the liver (nonalcoholic)
  • Obesity, hyperlipidemia, diabetics

Right-sided heart failure

  • Hepatic congestion secondary to right-sided heart disease

How the liver works:

  1. The liver takes substances in our blood and metabolizes and detoxifies them. 
  2. Stores and produces substances help digestion, clotting, and immune health. 
  3. When it stops working every system in our body struggles.

Types of Liver Cells and How They Work

Two main types of cells perform the tasks listed above.

  • Kupffer cells
    • Remove bacteria, debris, parasites, and old RBCs 
  • Hepatocytes
    • Bile production, metabolism, storage, conjugating bilirubin, and detoxification.

Functions of the Liver

Metabolization

Glucose: 

  • The excessive amounts will be synthesized and stored as glycogen 
  • The liver can’t synthesize glycogen properly and store it, so more stays in the blood, leading to hyperglycemia
  • Converts glycogen into glucose when blood glucose levels are low to increase sugar levels 
  • If the patient is sick or not eating, the liver is unable to convert the glycogen to glucose so the patient can have episodes of hypoglycemia

Lipids and Proteins: 

  • The liver converts ammonia, which is a byproduct of protein breakdown, into urea which is then excreted via the urine.
  • Urea is much less toxic to the brain than ammonia. 
  • Ammonia = neuro changes + hepatic encephalopathy 

Storage

  • Stores vitamins (vitamins B12, A, E, D, and K), minerals, and iron and glycogen. 
  • Remember, bile is essential for the absorption of fat-soluble vitamins. 
  • In cirrhosis, bile production is impaired, which will lead to decreased absorption and storage of those fat-soluble vitamins (vitamins A, D, E, and K)

Digestion

How cirrhosis affects the body? When epatocytes produce bile to help with the absorption of fats and those fat-soluble vitamins. 

Bile is stored in the gallbladder:

  • In the bile and stool is a substance called bilirubin. 
      • Bilirubin: RBCs are removed by the Kupffer cells and components of the RBCs are recycled. The Kupffer cells break down the hemoglobin into heme and globin groups.
      • Then hepatocytes metabolize heme into iron and bilirubin. The bilirubin is put into the bile and leaves via the stool (which is why stool is brown because bilirubin is a yellow-brown substance).
  • In cirrhosis, the hepatocytes are damaged and CAN’T do this so the hepatocytes leak bilirubin in the blood (rather than it entering the bile to leave the body in stool) and the levels increase in the blood and are present in the urine.
    • This is why the patient will be jaundiced and have yellowing of the skin, sclera, mucous membranes, dark urine along with clay-colored stool.

Production of blood plasma proteins: 

  • Albumin 
    • Maintains oncotic pressure and water regulation within the interstitial tissue,
  • Fibrinogen and prothrombin 
    • Aids in clotting.
Coagulation factors
  • Bleeding within the body activates a complex system of plasma proteins called coagulation factors, which promote blood clot formation. The liver is responsible for producing most of these coagulation factors.
  • Fibrinogen, thrombin = factor II, and factors V, VII, IX X, and XI
  • Protein C, protein S, and antithrombin III

Detoxification

  • Decreases the efficacy of drugs. 
    • In cirrhosis, the patient is very sensitive to drugs because the liver can’t protect them from their harmful effects. It also removes toxins from the body (alcohol) and hormones our glands produce. 
      • Ex: estrogen is metabolized in the liver. However, in cirrhosis, it is unable to metabolize estrogen which leaves more of the hormone in the body. This can lead to enlarged breast tissue in men (gynecomastia).

Complications of Cirrhosis:

Portal Hypertension

  • The portal vein becomes narrowed due to scar tissue in the liver. This restricts the flow of blood to the liver and increases pressure in the portal vein. This will affect the organs connected to the portal vein…..like the spleen, and vessels to the GI structure (varices).

Enlarged spleen

  • “Splenomegaly” What does the spleen do? Stores platelets and WBCs. With portal HTN the platelets and WBCs are kept in the spleen. They can’t leave and this leads to a low platelet and WBC count.

Esophageal Varices 

  • (as well as gastric varices): due to the increased pressure via the portal vein. This increased pressure causes the veins to become weak, and they can RUPTURE!
  • Life-threatening if the varice ruptures: WHY? Remember the platelet count will be low along with clotting factors available AND levels of Vitamin-K…they are at risk for a total bleed out.

Fluid overload in legs and abdomen

  • Ascites (fluid in the abdomen). If the patient has ascites, they are at risk for infection from bacteria in the GI system. Remember the immune system is compromised because of low WBC production. Swelling in the legs and ascites is happening due to venous congestion from the portal HTN and low albumin levels (the water is not being regulated in the body and is entering the interstitial tissue).

Jaundice

  • Yellowing of the sclera of the eyes, mucous membranes, and skin. This is due to the hepatocytes leaking bilirubin into the blood rather than the bile.

Hepatic Encephalopathy

  • the liver is unable to detoxify. Ammonia builds up along with other toxins that collect in the brain. This leads to an altered mental system, coma, neuromuscular problems, asterixis (involuntary hand-flapping), hepatic foetor “fetor hepaticus” (late sign; A pungent, musty, sweet smell to the breath)

Clotting problems

  • Thrombocytopenia is seen in most patients with cirrhosis.
    • Reduced production due to impaired hepatic synthesis of thrombopoietin
  • Chang in INR. maybe low or elevated
    • Most clotting factors are synthesized by the liver.  Reduction in these clotting factors tends to cause reduced enzymatic coagulation.
    • Naturally occurring anticoagulants are also synthesized by the liver.  A deficiency of these tends to augment enzymatic coagulation.
    • Factor VIII is produced by endothelial cells and tends to be upregulated in cirrhosis, augmenting coagulation.

Renal Failure

In severe cases known as Hepatorenal Syndrome.

Miscellaneous

  • Liver Cancer
  • bone fractures (low vitamin D)
  • Diabetes

Signs and Symptoms of Cirrhosis:

Early stages of how cirrhosis affects the body:

  • Patients may be asymptomatic

Late stages of how cirrhosis affects the body:

  • GI system. 
    • Early indicators usually involve gastrointestinal signs and symptoms such as anorexia, indigestion, nausea, vomiting, constipation, or diarrhea.
  • Respiratory system. 
    • Respiratory symptoms occur due to hepatic insufficiency and portal hypertension.
    • pleural effusion, and limited thoracic expansion due to abdominal ascites, interfering with efficient gas exchange and leading to hypoxia.
  • Central nervous system. 
    • Lethargy, mental changes, slurred speech, asterixis (flapping tremor), peripheral neuritis, paranoia, hallucinations, extreme obtundation, and ultimately, coma.
  • Hematologic.
    • The patient experiences bleeding tendencies and anemia.
  • Endocrine. 
    • The male patient experiences testicular atrophies
    • the female patient may have menstrual irregularities, gynecomastia, and loss of chest and axillary hair.
  • Skin. 
    • There is severe pruritus, extreme dryness, poor tissue turgor, abnormal pigmentation, spider angiomas, palmar erythema, and possibly jaundice.
  • Hepatic. 
    • Cirrhosis causes jaundice, ascites, hepatomegaly, edema of the legs, hepatic encephalopathy, and hepatic, renal syndrome.

Diagnosed:

  • Liver scan: The liver scan shows abnormal thickening and a liver mass.
  • Liver biopsy; a Liver biopsy is a definitive test for cirrhosis as it detects destruction and fibrosis of the hepatic tissue.
  • Liver imaging: Computed tomography scan, ultrasound, and magnetic resonance imaging may confirm the diagnosis of cirrhosis through visualization of masses, abnormal growths, metastases, and venous malformations.
  • Cholecystography and cholangiography visualize the gallbladder and the biliary duct system.
  • Splenoportal venography: Splenoportal venography visualizes the portal venous system.
  • Percutaneous transhepatic cholangiography: This test differentiates intrahepatic from extrahepatic obstructive jaundice and discloses hepatic pathology and the presence of gallstones.
  • How cirrhosis affects blood count: There is decreased white blood cell count, hemoglobin level, and hematocrit, albumin, or platelets.

Medical Management

Treatment is designed to remove or alleviate the underlying cause of cirrhosis.

  • Diet. The patient may benefit from a high-calorie and medium to high-protein diet.
    •  Once a patient has hepatic encephalopathy, restrict protein intake.
  • Sodium restriction.is usually restricted to 2g/day.
  • Fluid restriction. Fluids are restricted to 1 to 1.5 liters/day.
  • Activity. Rest and moderate exercise is essential.
  • Paracentesis. Paracentesis may help alleviate ascites.
  • Sengstaken-Blakemore or Minnesota tube. The Sengstaken-Blakemore or Minnesota tube may also help control hemorrhage by applying pressure on the bleeding site.

Pharmacologic Therapy

Drug therapy requires special caution because the cirrhotic liver cannot detoxify harmful agents effectively.

  • Octreotide. For esophageal varices.
    • improves renal function, total exchangeable sodium, and peripheral hemodynamics in cirrhotic patients with ascites
    • Helps with esophageal varies by decreasing portal vain hypertension
    • It also controls the emptying of the stomach and bowel
  • Diuretics. Diuretics may be given for edema, however, they require careful monitoring because fluid and electrolyte imbalance may precipitate hepatic encephalopathy.
  • Lactulose. Encephalopathy is treated with lactulose.
  • Antibiotics. Antibiotics are used to decrease intestinal bacteria and reduce ammonia production, one of the causes of encephalopathy.
  • beta blockers. Slow the heart rate, decreases the force of contraction, and also helps with the treatment of esophageal varices
  • Nitrates. Vaso dilator to treat portal hypertension
  • Administer blood products and vitamin K to help with clotting

Surgical Management

Transjugular intrahepatic portosystemic shunt (TIPS) procedure. The TIPS procedure is used for the treatment of varices by upper endoscopy with banding to relieve portal hypertension.

Liver transplant: surgical resect or implantation of a new liver, partial or full

How Cirrhosis Affects the Body and What is the Nursing Management

Nursing management for the patient with cirrhosis of the liver should focus on promoting rest, improving nutritional status, providing skin care, reducing the risk of injury, and monitoring and managing complications.

  • Monitor blood glucose levels (hyperglycemia and hypoglycemia)
  • Assessing sclera and skin color for Jaundice along with urine color: very dark
  • Monitor I’s and O’s very closely, daily weight, monitor ascites and swelling in extremities
  • Activity intolerance, difficulty breathing (no supine), at risk for skin breakdown (turning every 2 hours), elevating feet
  • Administering Lactulose per MD order:  decreases ammonia levels

Nursing Assessment

Assessment of the patient with cirrhosis should include assessing for:

  • Bleeding. Check the patient’s skin, gums, stools, and vomitus for bleeding.
  • Fluid retention. To assess for fluid retention, weigh the patient and measure abdominal girth at least once daily.
  • Mentation. Assess the patient’s level of consciousness often and observe closely for changes in behavior or personality.

Learn more about cirrhosis of the liver by watching this full episode here

TIMESTAMPS:

00:00 Introduction
01:25 What is Cirrhosis
02:32 What causes Cirrhosis
04:12 What does the liver do
05:39 Functions of the liver
17:32 Complications of Cirrhosis
22:39 What are the signs and symptoms of cirrhosis
29:43 How to diagnose cirrhosis
34:54 Pharmacologic Therapy
37:44 Surgical Management
39:18 Nursing Assessment
42:28 Wrapping up the show