Cirrhosis NCLEX Review

This NCLEX review will discuss cirrhosis.

As a nursing student, you must be familiar with cirrhosis along with how to care for a patient experiencing this disease.

These type of questions may be found on NCLEX and definitely on nursing lecture exams.

Don’t forget to take the cirrhosis quiz.

You will learn the following from this NCLEX review:

• Definition of cirrhosis
• Types
• Signs and Symptoms
• Complications
• Nursing Interventions
• Treatment

Cirrhosis Nursing Lecture

Cirrhosis NCLEX Review

Cirrhosis: It’s a liver disease where liver cells become extremely damaged due to long term/severe damage. This leads to the damaged cells being replaced with fibrous tissue, hence, scarring of the liver.

What causes Cirrhosis?

• Viral Infection: Hepatitis C*, B
• Alcohol Consumption: Heavy amount*
• Too much fat collecting in the liver (nonalcoholic): obese, hyperlipidemia, diabetics
• Problems with bile duct (carries bile from liver to small intestine): bile stays in liver and damages cells
• Autoimmune

*most common causes in the U.S.

Role of the Liver (helps to understand the complications and nursing interventions):

In a nutshell, the liver takes substances in our blood and metabolizes and detoxifies them along with storing and producing substances to help with digestion, clotting, and immune health. In other words, it is SO VERY important for our survival. When it stops working every system in our body struggles!

How does the liver receive its blood supply to do its job?

The liver receives it blood from two sources:

• First Source: Majority of the blood flow to the liver comes from the hepatic portal vein (remember this structure for complications seen in portal hypertension).
  • This is a venous network that delivers blood high in nutrients (lipids, proteins, carbs, GLUCOSE etc.) from organs that aid in digestion of food, but this blood is very poor in oxygen. The organs connected to the hepatic portal vein are:
    • small/large intestine, pancreas, spleen, stomach
  • Second Source: Hepatic artery: it delivers rich oxygenate blood that just came from the heart to the liver, but it’s poor in nutrients.

—–these two blood supplies mix together as they enter the functional units of the liver called the liver lobules (there are thousands of them in the liver). These lobules contain hepatocytes, which perform most of the liver’s function and kupffer cells (macrophages that cleanse the blood coming from the hepatic portal vein and artery), and the blood will exit via the hepatic vein to go back to the heart to be re-oxygenated.

As blood flows through the lobules there a two types of cells performing special jobs (as stated above):

• Kupffer cells: removing bacteria, debris, parasites, old RBCs (remember this because this plays a role with bilirubin)
• Hepatocytes: does most of the work of the liver by performing bile production, metabolism, storage, conjugating bilirubin, and detoxification.

Highlights of the Functions of the Liver

(need to understand these functions to help with understanding the complications and signs/symptoms):

• Metabolizes:
  • All the fresh nutrient-rich blood entering into the hepatic lobule passes by the hepatocytes which METABOLIZES :
    • Glucose: the excessive amounts will be synthesized and stored as glycogen (monitor blood glucose…in cirrhosis the liver can’t synthesize glycogen properly and store it, so more hangs out in the blood, leading to hyperglycemia) AND converts glycogen into glucose when blood glucose levels are low to increase sugar levels (in cirrhosis, if the patient is sick or not eating the liver is unable to convert the glycogen to glucose so the patient can have episode 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 that ammonia. This doesn’t happen in cirrhosis which is why the patient will have neuro change, asterixis, HEPATIC ENCEPHALOPATHY, etc.
  • Storage:
    • Stores vitamins (vitamin B12, A, E, D, and K) and minerals along with 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 (vitamin A, D, E, and K)
  • Digestion:
    • hepatocytes produce bile to help with the absorption of fats (bile is stored in the gall bladder) and those fat soluble vitamins.
      • In the bile and stool is a substance call BILIRUBIN. How does the bilirubin get there?
        • Remember 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 present in the urine. This is WHY the patient will have yellowing of the skin, sclera, mucous membranes, dark urine along with clay-colored stool… JAUNDICE!

Production of blood plasma proteins: albumin (maintains oncotic pressure and water regulation within the interstitial tissue), fibrinogen, prothrombin (aids in clotting).

Detoxifies: makes drugs less harmful to the body. In cirrhosis, the patient is very sensitive to drugs because the liver can’t protect the patient from their harmful effects. It also removes toxins from the body (alcohol) and hormones produced by our glands. For example, 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, 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 RUPURE!

• 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).

• What is Hepatic Foetor? A pungent, musty, sweet smell to the breath (discussed more below)

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: patients may be asymptomatic, but in the late stages will have:

Remember the mnemonic: “The Liver is Scarred”

Tremors of hands (asterixis: hand-flapping due to increased toxins in the blood)

Hepatic foetor or “fetor hepaticus”: very late in the disease and is a pungent, sweet, musty smell. This is from the buildup of toxins (mercaptans) in the blood. Why in the breath? The portal hypertension shunts these toxins where they pass through the lungs allowing the smell to be noticed.

Eye and skin yellowing (jaundice)

Loss of appetite (spleen pushing on stomach…feel full)

Increased Bilirubin (skin and urine….jaundice) and ammonia

Varices (esophagus and gastric…at risk for bleeding…watching for activities that can increase rupture: coughing, vomiting, drinking ETOH, constipation)

Edema in legs (low albumin and congestion of hepatic veins)

Reduced platelets and WBCs (bleeding and infection risk)

Itchy skin (toxins the blood)

Spider angiomas (chest) (increased estrogen in the blood)

Splenomegaly (low platelets and WBCs), stool clay colored (no bilirubin in the stool…should be there not in the urine or blood)

Confusion or coma (high toxin and ammonia level)

Ascites (low albumin and venous congestion)

Redness on the palms of the hands (increased estrogen in the blood)

Renal failure (hepatorenal syndrome)

Enlarged breast in men (decrease metabolism of estrogen so there is more in the blood)

Deficient on vitamins (B12, A, C, D, E, K and iron) (no longer able to store and have bile to help absorb these fat soluble vitamins)

Diagnosed:

• Liver biopsy
• Labs: liver enzymes (albumin), platelet levels, PT/INR, hepatitis B or C, bilirubin levels

Nursing Interventions for Cirrhosis:

Monitor for bleeding (PT and INR)

• limit invasive procedures and hold pressure at injection sites for 5 minutes or more, soft tooth brushes, safety, assessing stools, urine, petechiae

Monitor Esophageal varices

• Monitor very closely for bleeding, darky tarry stools, vomiting blood, (bleeding is an emergency!!) Watch for activities that can increase rupture: coughing, vomiting, drinking ETOH, constipation

Check reflexes, mental status very closely (mental status change, irritability, confusion), hepatic encephalopathy, and for flapping of the hands “asterixis”

Diet:

• If neuro system is compromised: low protein diet: protein breaks down into ammonia
• If neuro system NOT compromised: high lean protein (fish, poultry) NO ETOH, or raw seafood (oysters….contain bacteria that the immune system is too weak to fight and detoxify from the body), fluid restriction, needs vitamin (administer PO vitamins per MD order)

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, and measuring abdominal girth (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

Treatment:

• Liver transplant
• Shunting surgery (helps alleviate the ascites)
• Diuretics
• beta blockers (slows the heart rate..decreases force of contraction and also helps with the treatment of esophageal varices) and Nitrates (dilate vessels) to treat portal hypertension
• Administer blood products and vitamin K to help with clotting
• Lactulose (to decrease ammonia level)
• Paracentesis (to remove fluid from abdomen)

References: