N440 Study Guide Exam 2 - Lecture notes 4-8 PDF

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Cirrhosis Cirrhosis= extensive, irreversible scarring of the liver, usually caused by a chronic reaction to hepatic inflammation and necrosis  

Typically develops slowly and has a progressive, prolonged, destructive course resulting in end-stage liver disease Most common causes of cirrhosis= alcoholism, chronic viral hepatitis, nonalcoholic steatohepatitis (NASH), bile duct disease, gallbladder disease, CVD, chemicals/toxins, and genetic diseases

Pathophysiology Characterized by widespread fibrotic (scarred) bands of connective tissue that change the liver’s normal makeup Inflammation caused by either toxins or disease results in extensive degeneration and destruction of hepatocytes (liver cells) As cirrhosis develops, the tissue becomes nodular  

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Nodules can block bile ducts and normal blood flow throughout liver In early disease, the liver is usually enlarged, firm, and hard. As the pathologic process continues, the liver shrinks in size, resulting in decreased liver function (weeks to years) Some patients have NO s/s until serious complications occur Impaired liver= elevated serum liver enzymes

Complications Portal hypertension= a persistent increase in pressure within the portal vein greater than 5 mm Hg; MAJOR INDICATOR OF CIRRHOSIS Results from increased resistance to or obstruction (blockage) of the flow of blood through the portal vein and its branches The blood meets resistance to flow and seeks collateral (alternative) venous channels around the high-pressure area Splenomegaly (spleen enlargement) = caused by blood flow back into the spleen; veins in the esophagus, stomach, intestine, abdomen, and rectum become dilated Ascites= collection of free fluid within the peritoneal cavity caused by increased hydrostatic pressure from portal hypertension 

Plasma protein collects in the peritoneal fluid reduces amount of circulation plasma protein in blood  this plus inability of liver to produce albumin because of impaired cell functioning= serum colloid osmotic pressure is decreased in circulatory system (third shift)  hypovolemia and edema at same time

Esophageal varices= result from portal hypertension; blood backs up from liver and enters esophageal and gastric veins  fragile, thinned-walled esophageal veins become distended and tortuous from increased pressure     

Size of veins is what determines potential for bleeding Can occur in distal esophagus and present in the stomach and rectum LIFE THREATENING if bleeding= severe blood loss  shock from hypovolemia Bleeding is either hematemesis (vomit blood) or melena (black, tarry stools) LOC can occur before bleeding, spontaneous or from any activity that increases abdominal pressure (heavy lifting, exercise, coughing/sneezing, trauma)

Jaundice= yellowish coloring of the skin caused by one of two mechanisms Hepatocellular disease= liver cells cannot effectively excrete bilirubin; this decreased excretion results in excessive circulating bilirubin levels Intrahepatic obstructive= results from edema, fibrosis, or scarring of the hepatic bile channels and bile ducts, which interferes with normal bile and bilirubin excretion; patient often report pruritus (itching) Portal-systemic encephalopathy= complex cognitive syndrome that results from liver failure and cirrhosis     

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Report sleep disturbances, mood disturbance, mental status changes, and speech problems EARLY May be reversible with EARLY interventions Altered LOC, impaired thinking processes, and neuromuscular problems LATER My develop slowly in patients with chronic liver disease and go undetected until late stages Exact cause are not clear, but probably are the result of shunting of portal venous blood into central circulation so that the liver is bypassed  substances absorbed by the intestine are not broken down or detoxified and may lead to metabolic abnormalities (elevated serum ammonia)  results from inability of liver to detoxify protein and by-products Factors that may lead to PSE= high protein diet, infection, hypovolemia, hypokalemia, constipation, GI bleeding (caused by large protein load in intestine), or drugs (opioids, analgesics, sedatives, hypotonic, diuretics) Symptoms develop rapidly in acute liver dysfunction= four stages o Stage 1- subtle manifestations that may not be seen immediately, personality changes, behavior (agitation), depression, impaired thinking, can’t concentrate, fatigue, drowsy, slurred speech, sleep pattern disturbance o Stage 2- continue of mental changes, confusion, disorientation to time, place, or person, Asterixis (hand flapping)

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o Stage 3- progressive deterioration, marked mental confusion, muscle twitching, hyperreflexia, asterixis o Stage 4- unresponsiveness death, unarousable, usually no response to painful stimuli, no asterixis, positive Babinski’s, muscle rigidity, fetor hepaticus (liver breath- musty, sweet odor), seizures Hepatorenal syndrome= indicates poor prognosis; often cause of death**, sudden decrease in urinary flow, elevated BUN and creatinine with abnormally decreased urine sodium excretion, increased urine osmolarity o Often occurs after deterioration from GI bleeding or onset of PSE

Etiology and Genetic Risk **Hepatitis C is second leading cause of cirrhosis and liver failure; it is an infectious bloodborne illness that usually causes chronic disease Inflammation caused by infection over time leads to progressive scarring of the liver Hepatitis B and D are most common causes of cirrhosis worldwide; B causes inflammation and low-grade damage over decades = cirrhosis; D can infect liver but only if patient already has B Also cause by NON-alcoholic fatty liver disease= obesity, diabetes mellitus type 2, and metabolic syndrome; Hispanics at highest risk Other common cause is excessive alcohol us; direct toxic effect on the hepatocytes and causes liver inflammation, (alcohol hepatitis)  liver becomes enlarged with cellular degeneration and infiltration of fat, leukocytes, and lymphocytes  inflammation decreases and destructive phase increases over time damage to live tissue progresses as malnutrition and repeated exposure to alcohol continue; if alcohol is stopped= fatty infiltration and inflammation is reversable Assessment Obtain history= age, gender, employment, history of alcohol or drugs and chemical toxins, sexual history (infectious diseases/hepatitis A, B, and C), hepatitis history, family history of alcoholism/liver disease, describe alcohol intake/amount consumed during given period/how long sober, drug history/type/route, tattoos= Behaviors causing the liver disease occurred YEARS before onset of current illness and they can be regretful and embarrassed*** Physical= fatigue? Weight change? GI symptoms (anorexia, vomiting)? Abdominal pain and liver tenderness? Liver function tests! Usually show problems even with no s/s Advanced stage cirrhosis usually has patient finally seek treatment= GI bleeding, jaundice, ascites, and spontaneous bruising

Assess for= yellowing of skin or eyes, dry skin, rashes, purpuric lesions (petechiae or ecchymoses), warm and bright palms of hands, vascular lesions with red center and radiating branches (spider angiomas), ascites, peripheral dependent edema of extremities and sacrum, vitamin deficiency Abdominal assessment for ascites, distention, dilated abd. Veins, liver enlargement, **measure abdominal girth to evaluate progression of ascites (lay flat, pull tape measure around largest diameter and measure at end of exhalation) Stool/vomit for blood, enlarged breasts, neurologic function (especially in late stage/hepatic cirrhosis), asterixis, labs (AST, LDH, ALT, LFT, GGT) X-rays to show ascites, hepatomegaly, or splenomegaly, CT scan, MRI, ultra sound (first assessment for someone with suspected liver disease) Planning and implementing Decrease fluid in ascites, fluid and electrolyte balance, low sodium diet to control fluid/restriction**, vitamin supplements, IV fluids, diuretics, respiratory support in case of ascites (dyspnea, orthopnea, crackles in lungs) Paracentesis= performed at bedside, explain it, vitals/weight**, void before and after**, HOB elevated, monitor vitals, measure drainage/record, describe fluid, label and send to lab, maintain bedrest, weight again** Sengstaken-Blakemore tube= short-term esophagogastric balloon tamponade, very effective way to control bleeding; can cause life threatening complications= aspiration, asphyxia, and esophageal perforation**; placed through nose and into stomach balloon is inflated to apply pressure to bleeding variceal area TIPS= shunt for patients who have not responded to other modalities for hemorrhage/long-term ascites; doppler ultra sounds and general anesthesia  place large sheath through the jugular vein needle is guided through sheath and pushed through liver into portal vein  balloon enlarges this tract and stent keeps it open 

No serious complications, discharge after ½ days

Nutrition High carb, high protein, moderate fat diet need protein to heal Small, frequent meals especially if the patient has encephalopathy Teach patient to avoid excessive vitamins and minerals that can be toxic to liver (iron, fat-soluble vitamins, ad niacin) Take potassium supplement if on diuretic Drug therapy

Used sparingly because they are difficult for the failing liver to metabolize (opioid analgesics, sedatives, and barbiturates) Lactulose or lactitol may be prescribed to eliminate ammonia levels in the stool; given orally or NG tube; works by increasing osmotic pressure to draw fluid into colon and prevent absorption of ammonia in colon 

Watch for bloating/cramping, hypokalemia and dehydration from excessive stools

PPIs or H2 blockers to help reduce acid reflux AVOID ALL NSAIDS and hepatic toxic herbs, vitamins, and minerals Hepatitis Hepatitis= widespread inflammation of liver cells. Viral hepatitis is the most commo type and can either be acute or chronic. After the liver has been exposed to any causative agent, it becomes enlarged and congested with inflammatory cells, lymphocytes, and fluid, resulting in right upper quadrant pain and discomfort. As disease progresses, the liver’s normal lobular pattern becomes distorted because of widespread inflammation, necrosis, and hepatocellular regeneration increases pressure within portal circulation, interfering with the blood flow into hepatic lobules  edema of liver’s bile channels results in obstructive Jaundice Hepatitis A= RNA virus that survives on the human hands; resistant to detergents and acids but is destroyed by bleach and extremely high temps  

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Usually mild course similar to flu-like infection and often goes unrecognized **Spread mostly by fecal-oral route by fecal contamination either from personto-person contact (oral-anal sexual activity) or by consuming contaminated food/water Common sources of infection include shellfish caught in contaminated water and food contaminated by food handlers infected with HAV Incubation period is 15-50 days, with peak of 25-30 days Usually not life threatening, but more severe in elders and pre-existing liver disease such as HCV or chronic liver disease; small percent have severe illness Some adults have HAV and do not know it; course is similar to that of GI illness, recovery is usually uneventful

Hepatitis B= Not spread like HAV, circulates through blood 

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Spread through these common modes= unprotected sex with infected partner, sharing needles, accidental needle sticks or injuries from sharp instruments (health care workers low incidence), blood transfusions (from before 1992), hemodialysis, close person-to-person contact by open cuts and sores Immunosuppressed people** (HIV)

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Symptoms usually occur within 25-180 days of exposure= anorexia, fever, fatigue, RUQ pain, dark urine with light stool, joint pain, jaundice Blood test to confirm disease Most adults who get HBV recover, clear the virus from their body, and develop immunity; small amount do not form immunity Hepatitis carriers can infect others even though they are not sick and have no obvious s/s Chronic carriers are at high risk for cirrhosis and liver cancer**

Hepatitis C= single-stranded RNA virus, transmission is blood to blood  

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The rate of sexual transmission is low in couples but increases with multiple sex partners Spread most commonly by= illicit IV drug needle sharing, blood, blood products, or organ transplants received by 1992, needle stick injury with HCVcontaminated blood (health care workers at high risk), unsanitary tattoo equipment, and sharing of intranasal cocaine paraphernalia NOT transmitted by casual contact or by intimate household contact Those infected are advised not to share razors, toothbrushes, or pierced earrings because of microscopic blood Average incubation period is 7 weeks; acute infection and illness is not common Most people are unaware they have been infected; asymptomatic and not diagnosed until many months/years after exposure abnormal lab test or liver problem occurs HCV does its damage over decades by causing chronic inflammation in liver and eventually causes liver cells to scar  cirrhosis Unlike HBV, most people with HCV do not clear the virus and a chronic infection develops

Hepatitis D= caused by a defective RNA virus that needs the helper function of HBV. It usually only occurs only with HBV to cause viral replication   

Usually develops into chronic disease Incubation period is about 14-56 days Like HBV, HDV is transmitted primarily through parenteral routes, especially in patients who are IV drug users; having sexual contact with someone who has HDV is also a high-risk factor

Hepatitis E= causes a waterborne infection associated with epidemics in the Indian subcontinent, Asia, Africa, the Middle East, Mexico, and Central and South America    

Large outbreaks after heavy rain//flooding Caused by fecal contamination of food and water In US HDV has only been found in international travelers; looks like HAV Incubation period of 15-64 days; no evidence of a chronic form of the disease; tends to be self-limiting and resolves on its own

Complications Chronic Hepatitis= usually with hepatitis B or C; chronic hepatitis can lead to cirrhosis and liver cancer, superimposed infection with hepatitis D in patients with chronic hepatitis B may also result in chronic hepatitis Incidence and Prevalence= HAV and HBV have declined due to vaccinations, however, HBV and HCV are a concern because of their association with cirrhosis and liver cancer HCV is the most common type and there is no vaccination for it currently cases of HCV will rise over the next decades due to increasing illicit drug use  more transplants and death Health promotion and maintenance Vaccinations for infants, children, and adolescents decrease A and B Other preventatives= washing hands, avoid contaminated food/water, receiving the HAV vaccine before travel, receiving immunoglobulin within 14 days if exposed to virus, and receive vaccine if working/living in enclosed areas with others (colleges, care facilities, day-cares, prison) Assessments History of known exposure, lab tests*** (elevated ALT or AST levels), use of herbal supplements, drugs, ingestion of shellfish, exposure to possibly contaminated water, travel, sexual activity, illicit drug use, IV or intranasal, needle exposure, close living accommodations, blood or blood products or transplants before 1992, place of birth, history of alcohol use, HIV positive S/S= Abdominal pain, changes in skin or eyes, joint pain, muscle pain, diarrhea/constipation, changes in color of urine or stool, fever, lethargy, malaise, N/V, itching Cholecystitis Cholecystitis is an inflammation of the gallbladder that affects many people. Most commonly in affluent countries. It may be either acute or chronic; mostly acute One type of acute cholecystitis in which chemical irritation and inflammation result from gallstones (Cholelithiasis) that obstruct the cystic duct, gallbladder neck, or common bile duct 

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When the gallbladder is inflamed, trapped bile is reabsorbed and acts as a chemical irritant to the gallbladder wall; reabsorbed bile, in combo with impaired circulation, edema, and distention of the gallbladder, causes ischemia and infection tissue sloughing with necrosis and gangrene within gallbladder itself; the gallbladder wall may eventually perforate (rupture) if small/localized perforation= abscess may form if large/not localized= Peritonitis Exact formation is unknown, but abnormal metabolism of cholesterol and bile salts play important role in formation Chronic results when repeated episodes of cystic duct obstruction cause chronic inflammation; Calculi are always present gallbladder becomes fibrotic and contracted  decreased motility and deficient absorption

o Pancreatitis and bile duct inflammation can occur as chronic complications from backup of bile throughout the biliary tract  jaundice Risk factors Four F’s= female, forty, fat, fertile Other risks= Mexican, prolonged fasting/rapid weight loss, increased serum cholesterol, cholesterol =-lowering drugs, hormone replacement therapy or birth control, pregnancy, Crohn’s disease, genetics, family history of gallstones, athletic women (chronic) S/S Vague upper abdominal pain/discomfort that can radiate to right shoulder, pain triggered by high-fat or high-volume meal, anorexia, N/V, dyspepsia (indigestion), belching/gas/ feeling full, rebound tenderness (Blumberg’s sign), fever, jaundice, clay-colored stools, dark urine, steatorrhea (most common with chronic) Assessment Height, weight, vitals, food preferences (see if eat a lot of fat/cholesterol), does food cause pain, gas/belching/indigestion after eating, abdominal pain, type of pain and where/when *** Diets in high-fat, high calorie, low fiber, and high refined white carbs= higher risk for gallstones **Rebound tenderness (Blumberg’s sign) and deep palpation= performed by doctor Diagnostics Labs= increased WBC, AST and LDH elevated, serum bilirubin levels are elevated X-Ray= shows calcified gallstones Ultrasound= URQ to test for cholecystitis ERCP= show biliary obstruction Interventions Non-surgical= avoid fatty foods, IV for hydration, NSAIDS for mild-moderate pain (monitor for signs of GI bleeding), anti-emetics to control N/V, ESWL (break up gallstones by shock wave) and used for patients who have normal weight, cholesterol based stones, and good gallbladder function, percutaneous biliary catheter to open the blocked ducts so that bile can flow (internal, external, or both to drain) Surgical= Laparoscopic Cholecystectomy ***(most performed, less complications, deaths, injuries to Bile duct, better recovery, less severe pain)- small midline puncture at the umbilicus, carbon dioxide is insufflated into the abdominal cavity, trocar catheter is inserted then a

laparoscope with video, aspirate the bile and crush any large stones and then extract the gallbladder through the umbilical port 

After surgery watch for N/V (give antiemetic like Zofran), opioid for pain only right after surgery, IV, elevated head, early ambulation to prevent infection and to promote absorption of CO2, resume activities within 1 week, introduce foods high-fat one at a time to see tolerance, no large fatty meals, teach incision care

Open Cholecystectomy- greatly declined, patients who have this usually have severe biliary obstruction and ducts are explored, remove gallbladder through incision and explores the biliary ducts for presence of stones/obstruction, JP placed to prevent fluid accumulation (serosanguineous) 

After surgery give opioid for pain, cough/deep breathe when pain is controlled, antiemetics for N/V, care for incision and drain (drain is removed after 24 hours), NPO until fully awake, ambulate asap to prevent DVT, resume solid foods in 1-2 days, avoid excessive fatty food intake, teac...