Liver: Largest internal organ and gland
Gerontologic Consideration of Liver Disease * Increase liver disease rate with age because of liver structure changes with age * Decrease liver volume – Because liver size will change with age * Decrease in hepatobilary function * Decrease drug metabolism: which increases the vulnerability for drug-induced hepatitis and increase risk for drug interactions * Decrease ability to respond to injury
Hepatitis
Most common cause for liver inflammation is viral infection
Acute Infection: * Inflammation causes damage liver cell and may develop into hepatic cell necrosis. * If there are no complications, the liver cells can regenerate and regain its normal appearance and function.
Chronic Infection: * Last longer than 6 months * May persist for years * Continuous inflammation and damage done to the liver will slowly develop into liver cirrhosis, then liver failure, and then liver cancer.
Clinical Manifestations:
Acute Phase: 1-4 Months: Icteric Phase * Jaundice begins * Clay Color stools
Convalescence Phase: Post-Icteric phase (healing phase) * Jaundice starts to disappear * Last about 2-4 months. * Major complaint is easy fatigue and malaise.
Priority Nursing Diagnosis: * Activity Intolerance r/t decrease physical energy and strength.

Recovery Phase: Most patients recover completely
Chronic Infection/Condition: * Develops into: Chronic hepatitis, Cirrhosis, Hepatic Failure, Heptocellular cancer
Assessment:
Health History: * Medications: Some medications that can be toxic to the liver
Physical Assessment: * Normal liver cannot be palpated * Percussion is used to determine if the liver is normal size. (8 to 10cm)
Diagnosis:
Liver Enzyme: * Elevated ALT and GTT * Alk Phos will be elevated. * Damaged liver cells release alk. Phos. Enzymes * Protein will be decrased because the liver is unable to produce the proteins * Increase Bilirubin * Indirect or unconjugated bilirubin * Prolonged prothrombin time (increase clotting time): because the liver is unable to produce clotting factors.
*IMPORTANT CONCEPT* RBC are broken down, broken down in 3 pieces , globin, iron, heme. Heme will be further broken down into greenish pigment call biliverdin, quickly converted to yellow pigment call bilirubin. This bilirubin is known as indirect /Unconjugated bilirubin(In the blood). This bilirubin will go into the liver by binding with albumin(transporter), and once it enters the liver, it will mix with glucuronic acid. The glucuronic acid will make the indirect/unconjugated bilirubin into more solid form call direct/conjugated bilirubin. Will go back into the biliary system and mix with bile and use the biles for digestive process.
*If you understand the concept, then you understand how this works* That is why patients with hepatitis will have elevated indirect/unconjugated bilirubin because the liver cannot process all that unconjugated bilirubin, and that is also why the patient has clay color stools. This is also why the person looks jaundice.

Patient who have uncompatable blood transfusion will have pre-hepatic jaundice
Patient who has viral hepatitis or cirrhosis will have hepatic jaundice
Patient who problems with the biliary system(gallbladder and pancreas), they will have First-Hepatic Jaundice.
General Home Care:
Not everyone goes to hospital when they have mild or moderate case of hepatitis and go through home remedy. * Rest * Well Balanced Diet * Low Fat, High carbohydrate, High Protein * Maintain fluid & electrolyte balance * Vitamin supplement: B-Complex(help regenerate liver tissues)
Viral Hepatitis * 6 types of hepatitis virus: A-E, & G * To determine which viral antibody a patient has, it will depend on what antigen and antibodies are found in the system.
Hepatitis A(HAV)
Transmitted through fecal to oral route (touching feces, putting it in the mouth)
37% of outbreaks of HepA are from eating contaminated food or drinking contaminated water.
Risk Factors: * Poor hygiene * Improper handling of foods * Crowded situations * Poor sanitary conditions
Diagnosis:
* Replication starts at the oropharynx/GI tract * Transport to liver-Major site for replication, and then sheds into the bile and transported into the intestine. * And the bile is excreted into the feces which is why we can get viral culture from feces. * There is a brief viremia(virus in the blood) * And then our immune system will control the virus.
Average Incubation period: 28 days(15-50 days)
Virus can be found in the stool 2 weeks before symptoms starts to show or up to 1 week after begin to have jaundice.
You will get a negative stool test for virus if you get it after incubation period, BUT we can still find the virus in the blood because of brief viremia. * If we find antibodies, hepA virus, IgM in the blood, then the patient has acute HepA. * IgM first response, IgG means the person has past exposure to infection and has lifelong immunity. * Help A is not an ongoing or long-term disease process * No chronic carrier state (meaning you can’t give it to someone else, through sex and is not in your feces) * Inflamed & swollen liver will heal completely * No permanent liver damage * Infection will cause life-long immunity and therefore there will be no recurrence of the disease.
Management:
* Best Treatment: Best treatment: Vaccination will pre-exposure prophylaxis * HepA vaccine(Havrix,Vaqta,Avxim) may be given at 1 to 18 years old. * Combined Vaccine(Hep A& B) Twinrix can be given to people 18 years or younger. * Side Effect: Soreness & Redness at the IM injection site.
Immune Globulin (IG) injection
Pre-Exposure: Non-immunized people. Will provide passive immunity for a short period of time.
*Note* So these injections are for people who are going to places that may increase their risk of getting the HepA virus(foreign country), and then because the HepA vaccine requires 2 dosage, they do not have the full protection, and therefore they will get this IG injection that will temporarily protect them. Furthermore, they might be given the first dose of HepA injection along with this IG injection.
Post: Exposure: If the patient becomes exposed to the virus, then we can give IG injection within 2 weeks to decrease severity of illness.
Environmental Controls:
Hand Washing, watch out for drinking water(making sure they are clean), and cleaning food properly
Post-Exposure Management: After exposure, the patient should not be too worried and go to the hospital in mild cases. (my personal thoughts on this, so HepA will cause nausea and vomiting, and they might just go to the hospital if their fever spikes too high, or if their fluid and electrolyte imbalance is too severe, then they might want to go to the hospital).
They will just receive home care because the problem will usually fix itself and usually does not require medical treatment. Just encourage the family members to wash their hands frequently.
Medical Management for severe cases: * Bed Rest * Enteric/contact precaution: Prevent secondary transmission (prevent transmission to other people) * Means wear gloves, gown.
Hepatitis B(HBV)
Acute Infection: * When we find Hepatitis B surface antigen in all body fluids(including: semen, vaginal secretions, blood)
Chronic Infection: * If patient has HepB surface antigen for more than 6-12 months. * HepB Surface antibodies would mean that the patient has HepB immunity from vaccine or they had a past HepB infection.
Mode of Transmission:
Transmitted percutaneously (any blood to blood contact or secretions to blood). * Direct contact with the blood infected person * Unprotected sexual activity with infected person(Recommended to use condoms). * Needle sharing among intravenous drug users * Sharing razors/personal items with infected person * Being pierced/tattooed with contaminated instrument * Blood Transfusion(Very Rare in the USA) * Childbirth: Pass the virus from mother to child
Cannot get HepB from: * Shaking hands with infected person * Hugging infected person * Sitting next to infected person

Medical Management: PREVENTION
Immunization: HepB Vaccine is the most effect method, and is part of the routine vaccination schedules for newborn and adults in major risk groups. There are 3 dosages given at birth, 1 month, and then 6 month.
HepB Immune Globulin Injection (post-exposure ) AFTER EXPOSURE * If a pregnant lady has HepB, we will give her HepB Immune globulin and tell her to stay away from alcohol until she is done with her pregnancy. * If baby is positive for HepB at birth, we will give HepB Immune globulin AND vaccine(remember two different things), and we will give the other 2 doses of vaccine at 1 month, and 6 month.
Post-Exposure:
We can give HepB immune globulin to post-exposure within 24-hours of exposure and start vaccine series.
Acute Infection: * Symptoms will start to appear 1-4 months after exposure * Patient usually recover on their own, without medical treatment, and symptoms will resolve itself over weeks to months and the patient will become cured. * In severe cases, the patient will need to restore their fluid and electrolyte imbalances.
Chronic Infection: * Longer than 6 months * The virus never completely left the body * Life-long chronic liver disease * 15%-25% mortality from chronic liver disease, because it will cause cirrhosis, to liver failure, to liver cancer.
Drug Therapy:
SubQ: Interferon: * Major Adverse effect is flu-like symptoms. So if patient comes in and complains of flu-like symptoms, it might be because of interferon. * We teach our patients to let us know when flu-like symptoms develop. Physician might decrease dose, or just let them continue. But side-effects should go down when the patient gets use to the medication.
So there are two types of interferon: Conventional interferon-A drug, which is given 3times/week subQ and pegylated. The pegylated interferon(This is a better choice over Interferon-A) is mixed with polyethylene glycol to make the drug stay in the body longer, and therefore have a longer acting effect. And therefore, only needs to be given once a week subQ. (This is for convenience purposes, instead of having to give 3 times a week, we can just give it once a week with the pigylated interferon). (To remember what it does, pigyLATED, think of later to leave the body).
Nucleoside & Nucleotide Analogs: Given PO * Is used to decrease HBV replication * These drugs are nephrotoxic drug. Therefore we have to monitor kidney function are up to level. Therefore watch serum creatinine levels. * We also want to teach the patient to watch out for weigh gains for 2-3kg over 2-3 days, because that could mean fluid overload.
Hepatitis C * Most common mode of transmission is IV drug use: sharing needles * Most people don’t have symptoms * Incubation periods: 45 days. * Most people go into Chronic HepC(75-85%), therefore going into cirrhosis, liver failure, liver cancer.
Self Care: * Rest * Increase fluid intake(2500-3000ml/day) * No Alcohol consumption, because liver is already damage.
Medical Management:
Weekly pegylated interferon subQ injection
Ribavirin given PO * The problem with ribavirin is that the side effects are worse than the HepC the disease itself.
Hepatitis D: * Defected virus, meaning that the virus cannot replicate by itself. People with HepD infections will also have HepB. * HepD is transmitted percutaneously (Blood to blood, or mucous with blood). * Only occurs with people with HepB, and when people have HepB&D, they are a greater risk for liver failure.

Hepatitis E and Hepatitis G(not seen a whole lot, don’t worry)
Drug-Induced Hepatitis
Similar to acute viral hepatitis, but is more extensive functional liver damage.
Common drug that causes Drug-Induced Hepatitis is Tylenol (Acetaminophen). * Maximum amount of Acetaminophen/day is 4 grams. Each pill contains 500 miligram, therefore a patient cannot exceed 8 pills over 24-hours. * People who drink and take Alcohol will put them at the greatest risk for Drug-Induced Hepatitis. * If medication is stopped, then symptoms will gradually go away, unless they have been taken the drug for a long time(which means their liver damage is severe, and therefore fatal).
Cirrhosis
* Liver cirrhosis usually develops insidiously(over a long time). * Irreversible, chronic, degenerative liver disease * Liver cells regenerate, but the regeneration process is distorted or disorganized. (that is why we get the gross looking liver) * New fibrous connective tissue is the cause of the distorted appearance of the liver.(This is how scarring works) and the scarring will disrupt blood flow, thus no nutrition ,oxygen, blood will reach the liver cells, resulting in decrease liver function. * The scarring tissue will replace damaged liver cells, and then the liver cannot provide the liver protein, in which 6 of them are clotting proteins. * That is why cirrhosis patients will have bleeding problems because of insufficient clotting protiens. * The liver is also used for detoxifying toxins in our body on the daily basis. When there is liver cirrhosis, the liver is unable to detoxify the poison, and therefore the toxins accumulate and lead to decrease mental functioning and even coma. * We refer Cirrhosis as “End-Stage Liver Disease”

There are many different types of cirrhosis: * Post-Necrotic Cirrhosis, cause by chronic, viral hepatitis * Biliary Cirrhosis: When the small bile ducts in the liver is obstructed * Cardiac Cirrhosis: Vascular Cirrhosis: * Cause by patient with long-standing right sided heart failure. (think about it, when patient with right sided heart failure, the blood is backed up to the rest of the body, most importantly the liver, because there are a lot of blood that goes from the liver to the inferior vena cave), When this happens the large amount of blood stored in the liver causes the liver to become enlarged, and hepatic tissues become necrotic due to lack of oxygenated blood flow. * Alcohol cirrhosis: * Most common type of cirrhosis
Alcoholic Cirrhosis
Alcohol has a direct toxic effect on liver cells, and cause inflammation and cause metabolic changes in the liver. The most common metabolic change in the liver is the accumulation of fat within the liver cells call “Fatty Liver”, and the fatty liver will cause further inflammation and destroying liver tissues. Eventually the scar tissues will form and extensive liver scarring can be seen.
Normal Hepatic Circulation:
Portal Vein: * Collects venous blood from stomach, spleen, and intestine and transfer it to the liver.
Portal Hypertension:
Excessive scarring will cause obstruction of the portal vein, which will lead to an increase pressure in the portal vein, which increases capillary hydrostatic pressure (which means fluid is going to be pushed out of the intravascular space into the interstitial spaces.)
Decrease Capillary Oncotic Pressure:
Because patient with liver cirrhosis does not have enough protein, they have a decrease capillary oncotic pressure (which pulls the fluid from interstitial space to intravascular).
The accumulation of fluid in the tissue spaces will lead to peripheral edema, pleural effusion and ascites.

Clinical Manifestations:
The most important thing to remember is that the patient will have coagulation problem with liver cirrhosis. Bleeding problems, easy bruising
Ascites due to fluid being pushed out, and because of the decrease protein production by the liver, then there is less fluid being pulled back in.
Spider Angioma: Spider Veins
Palmar Erythema: Red Palms, when you press on it, it will be blanched.
Caput Medusae: Multiple Vein distension in the abdomen.
Diagnostic Studies: * Lab Studies: In cirrhosis there is an increase AST, in Hepatitis increase ALT * Ultra Sound: to see enlargement of the liver * CT: Scan to see tumors and how far the tumor has spread.
Liver Biospy: * Used to confirm liver cirrhosis. * Done guided with ultrasound * Post-Procedure Care: * Keep patient laying on the right side for 2 hours to put pressure on the site to prevent bleeding. Then they can be on bed rest in flat position for 12-24 hours. * If patient is bleeding, access for hypovolemia, shock, pneumothorax.
Medical Managements: * There is no specific treatment to cure cirrhosis; therefore we focus on mainly treating the underlying cause and managing symptoms. * For early stages, we can slow down the progression by telling the patient to stop drinking to slow down the progression.

Drug Therapy:
Mainly for symptom relief: * Antihistamine is given to relieve pruritis * Give them stool softeners because we do not want them to be straining during bowel movement. It can cause rectal bleeding (hemorrhoids). This is important because here are not enough clotting factors due to decrease in liver function. * Diuretics: This is mainly used to treat signs of ascites or fluid overload. * Loop diuretic + Potassium: To remove the fluid while controlling potassium levels. * We can see a therapeutic effect when we see a decrease in weight, urine output that is greater than 30ml/hour, and decrease abdominal girth. * Give Albumin, because of the decrease protein production due to decrease liver function * Giving Antiacid for G/I symptoms:
Dietary Management: * Alcoholism and Malnutrition goes hand-in-hand because they drink, but don’t feel like eating. * They need a well-balanced diet * If they have no complications: they can eat a high calorie, high carbohydrate, moderate to low fat diet. * In order to prevent fluid overload, we might want restrict sodium and fluid intake.
Promote Oral Intake: * Provide oral hygiene before meals: promote taste sensation * Provide between-meals nourishments * Provide small, frequent meals.
Activity:
* Patients are usually extremely fatigued, and cannot tolerate activity well. * Assist them with activities as much as they can tolerate.

Ascites
Treatment:
* Sodium and Fluid Restriction * Diuretics: Lassix(Loop) and Aldactone(K-sparing)
Comfort measures: * Dyspnea because of increase abdominal pressure that leads to limited lung expansion * We want to keep the patient in semi-fowler to fowler’s patient depending on what they can tolerate. * More comfortable sitting up in a chair with feet elevated to decrease dependent edema.
Patients have impaired skin integrity: Therefore we have to provide meticulous skin care and provide a special pressure-relieving mattresses.
Paracentesis:
* When none of the effects are working, we do a paracentesis(which is manual removal of the fluid). * This can be done at the bed side, or it can be done under ultrasound guidance. * This is a sterile procedure.
How to prepare procedure: 1. First receive consent from patient 2. Then have them voice prior to procedure to reduce the risk for bladder punctures. Even when they say they went to the bathroom already, we tell them to do it anyways. 3. Assist patient in the upright position. This will move all the fluid down, and move all the organs behind the fluid. This will decrease the risk for puncturing organs. * Stay away from abdominal aorta(paracentesis sites located near the right and left flanks of the belly button, and right under it). * Physician may insert needle to the peritoneal cavity to aspirate fluid, or they might insert a drainage bag if there is a lot of fluid.
Post-Procedure Care: * Monitor fluid volume: Because we are took the fluid out, the patient might be fluid volume deficit, and the complication that might occur with it is hypovolemia. * Patient will be on bed rest * Monitor vital signs every 15 minutes until patient is stable

Surgical Management:
Peritoneovenous Shunt(LeVeen Shunt): http://www.youtube.com/watch?v=PRVHon-Mv9o
This is when a catheter is put in the in the abdomen subcutaneously and up into the superior vena cava, in which when we put pressure in our abdomen, it will push the fluid from the peritoneal cavity into the superior vena cava.
Pre-Op: Remember that we want our patient in the best condition as possible before bringing them into surgery.
Post-Op Care:
Patient will usually spend the night in the ICU because we want to monitor system fluid volume-overload(because we are putting too much fluid into the blood stream, we can cause an increase in hemodilution)
Hepatic Encephalopathy:
Pathophysiology:
Major complication due to cirrhosis and is characterized by an increase ammonia levels in the blood and cerebral spinal fluid.
*Important Concept* Normal Process: is that protein(that is ingested) is broken down by bacteria and it crease ammonia, and the liver would convert ammonia to urea so that the kidney can excrete it.
But, with Liver cirrhosis, because of decrease function, the liver cannot convert ammonia into urea, and therefore ammonia is accumulated in the body and therefore the ammonia levels are increased.
Grading System: 0-4(4 being the most advanced).
Clinical Manifestations pay attention * Ammonia is a toxic substance for our CNS, which means that most of the clinical manifestations are neurological problems. * Mild Confusion – Deep coma within a few days * Primarily changes in levels of consciousness and A&Os, so one second the patient may be A&O x 3, and then suddenly the patient is A&Ox1. * Motor Disturbance: Asterixis - http://www.youtube.com/watch?v=sEnp2ss8VoA

Medical Management: * Goal is to decrease protein intake(this will decrease the amount of protein breakdown into ammonia). * Decrease the bacteria that breaks down protein

Drug Therapy: * Decrease ammonia levels by manipulating intestinal tract,

Neomycin Sulfate: * This antibiotic will destroy the bacteria that breaks down protein into ammonia. * Undersiable Side Effect: * Diarrhea * Hearing impairment * Vitamin K deficiency: Because the antibiotic also kills E.Coli, in which it produced vitamin K in the body. Because there is a deficit in vitamin K, there is a decrease in clotting factor, and the patient is at risk for bleeding.
Lactulose:
* It is a laxative that will clear out the ammonia through diarrhea. * It can be given PO, NG tube, or Enema. (if given through enema, they have to hold for 30 to 60 minute) * Patient neuro functioning will improve when the ammonia levels are decrease. * 4 bowel movement/day and because of diarrhea, we want to monitor fluid and electrolyte levels.
Dietary Therapy: * Low Protein Diet: * If we are going to give a little protein, it is better to give vegetable and dairy protein better than red meat because vegetable protein contains few amino acids producing ammonia. * Eating vegetable will also prevent constipations: which will reduce ammonia production.

Nursing Managements: * Focus on reducing ammonia production * Assess neurological status * Give laxative & Enema as ordered * Encourage oral fluid intake if not contraindicated * Avoid drugs that cause constipations (opiods medications, dehydration). remember constipations means the GI tract is slowed, which means that this allows time for the bacteria to break down more protein.
Remember that these patients are also liver cirrhosis patients, and therefore we also have to manage their symptoms too which are: * Meticulous skin care(edema) * Avoid straining for bowel movement to prevent rectal bleeding, in which because they have liver cirrhosis, they have decrease clotting factors.
Comfort Measures for pruritus (itching)
Bleeding Esophageal Varices(BEV) * Most dangerous complication caused by cirrhosis. * 90% of patients with portal hypertension will have Bleeding Esophageal Varices. * The morality rate(chances of death) is 50%.
Portal Hypertension: Normal Portal Pressure is 9 mmHg, and if it is more than 9 mmHg, the they have portal hyper tension.
Remember that portal hypertension is caused by the distorted cirrhosis and caused a backflow of blood. Because of the backflow of blood, the varices(small veins located before the portal) are going to be dilated and bleed.
Diagnostic Test:
ESD(Esophagogastroduodenoscopy) Major Diagnostic tool

Medical Management: * Physician may insert Salem sump tube. * Lavage the area with normal saline until clear fluid returns. * Mix NS with Nor-Epinephrine to cause vasoconstriction(which will help stop the bleeding) * If patient has severe hemorrhage, then we want to monitor for hypovolemic shock. * Fresh frozen plasma, Packed RBC – to replace blood loss * Histamine receptor Blockers- Because it is in the stomach, we want to decrease acidic content from irritating the stomach. * Vitamin K – Promote clotting
Pharmacologic Therapy:
Drugs are used to control acute bleeding by decreasing portal pressure.
Vasopressin, Inderal(betal blocker), Sandostatin. These drugs are used to decrease the portal pressures, and therefore either prevent the varices from popping or decrease the bleeding.
Endoscoptic Therapy:
Schlerotherapy and Ligation We might not be tested on these, just and FYI
Post Procedure Care: * Retrosternal Pain(pain around the sternum area), we will give pain medication * Fever: is common, and we will give antipyretics.

Balloon Tamponade:
If all procedures fail to stop the bleeding, the doctor may want to insert esophagogastric tube: Senstaken-Blackmore tube.
Nursing Management: * Keep pair of scissors at the bedside, in which if the patient shows signs of respiratory distress, we can just cut and remove the tube immediately.
TIPS: (Transjugular Intrahepatic Portosystemic Shunt) * This is done for SECOND major bleeding after first initial bleeding. * This is a non-surgical procedure and done under fluoroscopy in x-ray department. * And the point of this procedure is to redirect the flow of blood directly from the portal vein into the superior vena cava. This will decrease the pressure and decompress the varices.
Post-Op care: Administer pain reliever, but no sedatives due to hepatotoxicity.