Hepatic System Exam 2 Med-Surg III PDF

Hepatic System Quick Pathophysiology Review: 1. Liver creates bile 2. Gallbladder stores that bile 3. Bile is released from the gallbladder into the digestive tract to help breakdown fat from foods! 4. Pancreas s...

Hepatic System Quick Pathophysiology Review: 1. Liver creates bile 2. Gallbladder stores that bile 3. Bile is released from the gallbladder into the digestive tract to help breakdown fat from foods! 4. Pancreas secretes digestive enzymes (lipase, amylase, protease) to further breakdown the fat, protein and carbohydrates in the small intestine 5. The liver ends up absorbing the nutrients from digestion and aids in detoxifying substances absorbed from the digestive tract Chronic Inflammation of the Liver (Cirrhosis/Liver Failure) - Liver is in the RUQ under rib cage - Liver that has suffered chronic inflammation to the point where it is completely scarred (scarred tissue is no longer functional) - Functions on normal healthy liver: - Filter waste - With cirrhosis: keeps waste in body leading to failure of other organs - Production of albumin - With cirrhosis: keep the oncotic pressure LOWER than the hydrostatic pressure which leads to fluid to leak out of blood vessels into tissues, causing swelling. - S/S: Generalized edema (anasarca) & swelling in interstitial space, Ascites → compromised diaphragm, delayed wound healing, increase risk of infection, muscle wasting and weakness - Metabolism - With cirrhosis: dosage of medication must be adjusted due to insufficient function of metabolism which may cause toxicity to dosages not adjusted - Coagulation (production of clotting factors) - With cirrhosis: bleeding, hematoma, bruises, gum bleeding, prolonged bleeding from cuts or minor injuries (BASICALLY know thrombocytopenia s/s) - Management: administer Vitamin K (if pt is LOW in vitamin K this leads to high risk for bleeding as vitamin K helps synthesize clotting factors!), monitor PT/INR (may be increased due to low vitamin K → if so this can also indicated a slower blood clotting process) and Platelet (if low → cannot cause clotting → high risk  for bleeding), Fresh frozen plasma transfusions for acute bleeding (since pt is lacking them), avoid invasive procedures if possible - Production of bile (bile: dead RBCs; stored in gallbladder) - With cirrhosis: leads to Jaundice, clay colored feces, orange/brown urine (increased bilirubin since the liver is not processing the bili) - Storage of vitamins A, D, E, K, and B12 and minerals like iron and copper. - With Cirrhosis: leads to deficiency of vitamins A, D, E, K, B12, iron and copper which may also lead to blood/bleeding issues - Glycogen (stored glucose from foods;but made from pancreas) → Glucose (needed when you are sleeping, 6 - 8 hrs of no eating) - With cirrhosis: you may go into hypo/hyperglycemia - Controlling the ammonia levels → protein - With cirrhosis: the ammonia levels with increase and irritates the brain and causes LOC changes - Hepatic encephalopathy: - S/S: confusion, forgetfulness, altered LOC, asterixis (flapping tremor/extension of wrist), slurred speech, personality changes - Treatment: diet!: low protein, small frequent meals, avoid alcohol and hepatotoxic substances, increase fiber, LACTULOSE (increase amount of poop to get rid of that ammonia!!!) ← ON TEST - Reasons why this chronic inflammation may happen: - #1 MOST COMMON → Alcohol - Medication (Acetaminophen, TB medications, Chemotherapy/Radiation) - Hepatitis (Viral: B & C) - Hepatitis B vaccine - Antiretroviral (Suppress multiplication of virus to reduce damage) - Hepatitis C cure, pill for 90 days, once a day that will eliminate the virus from the body ( pt with Hep C usually only 20% develop cirrhosis) Portal Venous System Hypertension - Pathophysiology: the portal vein carries blood from digestive organs to the liver, but because of the scarred tissue in the liver (cirrhosis), this carrying of blood becomes harder and creates resistance in the blood flow through the liver → INCREASE in BP - The PVS starts in the mouth → all the way to the anus area, The PVS collect the blood that is full of CO2 from the GI system, to the superior vena cava, to the heart, to the lungs, through the aorta back to the body - Arteries are hard because they need to support a lot of pressure from the blood - S/S: this may lead to varices, splenomegaly (enlarged spleen), ascites (fluid accumulation in abdomen), and hepatic encephalopathy - Esophageal varices ← EASIEST TO RUPTURE (laughing, coughing, bending over → rupture and bleeding)  - Hematemesis: bleeding out due to insufficient clotting factors and 50% of patients die due to this - Other s/s: Gastric varices, Intestinal varices and Rectum varices (hemorrhoids) Easy the rupture veins, Caput medusae (abdominal veins dilated;looks like Medusa's head is on the abdomen of patient), Gynecomastia (small testicles), Liver is HARD as a rock when palpated, Spider angioma (dilated blood vessels on skin that look like spider web), Umbilical hernia, Sparse body hair (due to hormone imbalance from liver dysfunction), Jaundice (yellow skin and eyes, dark urine, pale stool, fatigue, itching, abdominal pain and confusion), Muscle wasting, Fetor hepaticus: breath smells like feces - Ascites (pt intakes fluid and goes into the interstitial space due to no albumin to absorb fluid) → SOB - Paracentesis: removal of fluid (10-13L removed with needle and ultrasound to not puncture organs) this is done 2x a week - Procedure: prep pt (empty bladder, monitor vitals, assess coagulation, pt is given local anesthesia, needle inserted into abdomen to drain fluid, post care: monitor for hypotension, infection and electrolyte imbalance - Nursing Interventions: sit or lay pt down for procedure, bed rest slows down ascites, low sodium diet decreases ascites, fluid restriction, monitor weight and i & o, accu-check to prevent hypoglycemia, adjust medication to avoid toxicity, give Diuretics such as Spironolactone and Furosemide - Nursing Management/Treatment - prevent GI bleeding → give stool softener to not increase PVS pressure (no straining,no valsalva maneuver, no laughing, no bending over), HOB elevated 30-40 degrees - Hepatic Encephalopathy: Altered Mental Status (AMS) due to increased ammonia, if pt has no hepatic encephalopathy (they may have a normal diet), if pt has hepatic encephalopathy (low protein & sodium diet) - Lactulose → ammonia attaches to intestine (have pt do at least 2-3 bowel movements to remove ammonia from body (results in improved LOC) - Nursing Interventions lactulose: inform pt the purpose is to lower ammonia levels by pooping them out basically!, inform pt this may lead to dehydration due to diarrhea, take as prescribed (may be 2-4 times a day), and nurse should monitor for signs of electrolyte imbalance - Neomycin (antibiotic) kill bacteria in intestine (these bacterias in our GI work good for us but also create ammonia so its best to kill it since its doing more bad for us) - Bleeding pt (hematemesis/esophageal varices) we can give octreotide (Sandostatin) which is a vasoconstrictor for the varices to  decrease amount of bleeding and it reduces portal pressure, Antidiuretic hormone, Vasopressin also vasoconstricts to stop the bleeding, Sengstaken-blakemore tube inflates in stomach and esophagus to put internal pressure on the walls where the varices are (AE: airway obstruction (if pt starts having respiratory arrests, use scissors to cut the tube and deflate the balloon tube) #1 Reason for death: - UNCONTROLLABLE BLEEDING OUT! - Monitor bleeding through mouth, feces, and anus…monitor blood labs too! Acute Inflammation of the Liver (Hepatitis) - Inflammation of liver tissue due to infection - Types: - A: spread through fecal oral route (contaminated water) - has vaccine - B: blood and bodily fluids (Blood, sexual contact, perinatal transmission) - has vaccine - C: blood and bodily fluids (IV drug use, transfusions) - D: blood and bodily fluids (transmits always with B) - E: spread through fecal oral route (contaminated water) - G: not known very well (common in blood donors) - Hepatitis A virus (HAV) - RNA Virus - Patient will feel sick for 2 weeks and recover after with no liver damage - Prevention: Vaccine for Hepatitis A - Cause: Transmitted fecal-oral route, parenteral (rarely), frequently occurs in small outbreaks - S/S: Low grade fever, Malaise, flu-like symptoms - Treatment: Bed-rest (Sleep and rest for those 2 weeks), hydrate and a balanced diet - Diagnosis: Present in blood briefly - IgM Test: Anti-HAV immunoglobulin M(sick NOW) - Appears in the serum as the stool becomes negative for the virus - Detection of IgM anti-HAV indicates acute hepatitis (active disease) - IgG Test: Anti-HAV immunoglobulin G (cured and IMMUNE or VACCINATED) - IgG anti-HAV: Indicator of past infection - Presence of IgG antibodies provides lifelong immunity! - Hepatitis B Virus (HBV) - DNA virus (More infectious than HIV) - Prevention: Vaccine for Hepatitis B - Cause: Perinatally by mothers infected, Percutaneously (IV drug use), Horizontally by mucosal exposure to infectious blood, blood products, or other body fluids, Sexually transmitted, Can live on dry surface for 7 days, Kissing/sharing food items may spread the virus through saliva - S/S: flu-like symptoms, fatigue, nausea, abdominal pain (URQ) , loss of appetite, low-grade fever, jaundice, dark urine, clay stools - Diagnosis: - IgM Test: Surface Antigen (HBsAg), Core Antigen (HBcAg), E Antigen (HBeAg): all antigens that can be detected in blood to indicate CURRENT INFECTION OF HEP B - IgG Test: S-Antibody (Anti-HBs), E-Antibody (Anti-HBe): detected in blood which indicates the patient is now immune to HBV for life - NOTE: There are 10% of people who do not develop these antibodies and therefore are chronic carriers of the disease → 🙁 These pt need to be on cirrhosis medication to prevent the inflammation of liver - Treatment: Antivirals (Tenofovir & Entecavir) to suppress viral replication, monitor liver function - Hepatitis C Virus (HCV) - RNA virus - Cause/Risk factor: IV drug use (accidental needle sticks), Blood transfusion, High-risk sexual behavior, Hemodialysis, Occupational exposure, Perinatal transmission (mother baby), Body piercing, Tattooing, Intranasal drug use - S/S: flu-like symptoms, fatigue, nausea, abdominal pain (URQ) , loss of appetite, low-grade fever, jaundice, dark urine, clay stools - Diagnosis: - Asymptomatic (usually found as a causal finding) - IgM Test: Anti-HCV - Blood test that indicates exposure to virus, PCR test (HCV RNA) to confirm if pt is currently infected and this also measure the viral load - Body CANNOT create any antibodies for HEP C (There is NO vaccine because the body can NOT create antibodies so no IgG meaning you can get Hep C more than once) NO IgG! ← ON TEST - Treatment: There is a cure that is $9,000, which is 90 pills for 90 days - Medications: Zepatier, Mavyret, Harvoni, Copegus, Rebetol, Ribasphere, Sovaldi, Epclusa, Vasevi (general side effects: fatigue, nausea, headache, diarrhea and sometimes insomnia) - In some cases this may resolve itself spontaneously  - Note: Only 20% of pt will develop cirrhosis, the remaining are chronic carriers **HIV opens the door for HCV - Hepatitis D Virus (HDV) Delta virus - Defective single-stranded RNA virus - Cause: Hepatitis B (Cannot survive on their own, requires the helper function of HBV to replicate. You will never get HDV if you dont get HBV) - S/S: flu-like symptoms, fatigue, nausea, abdominal pain (URQ) , loss of appetite, low-grade fever, jaundice, dark urine, clay stools, in some cases: acute liver failure (fulminant hepatitis) treat with supportive care, underlying cause and continuous monitoring - Diagnosis: - IgM Test: HDV Antibodies (Anti-HDV): blood test, indicates exposure to virus - HBV Marker: indicates co-infection (HBV + HDV) - PCR Test (HDV RNA): confirms active infection - IgG ← same as HBV - Treatment: Interferon may be used but its not effective for everyone, mainly control HBV, and if fulminant hepatitis (liver failure) occurs then there may be more extensive treatments such as liver transplant - Hepatitis E Virus (HEV) - RNA Virus - Cause: spread through fecal oral route (contaminated water), Zoonotic (undercooked pork or wild caught animals), person to person (in developing countries) - S/S: flu-like symptoms, fatigue, nausea, abdominal pain (URQ) , loss of appetite, low-grade fever, jaundice, dark urine, clay stools - Diagnosis: - IgM and IgG (anti-HEV antibodies): indicates current or past infections - PCR Test (HEV RNA): confirm active HEV infection - Treatment: supportive care, bed-rest, hydrate, balanced diet  - Hepatitis G virus (HGV) ← not very well researched/known - RNA virus - Cause: poorly characterized parenterally and sexually transmitted virus, found in some blood donors - S/S: usually asymptomatic, some mild symptoms are: fatigue or malaise - Diagnosis: - Anti-HGV antibodies: blood test to indicate exposure to the virus - PCR Test (HGV RNA): not routinely done, but this will show infection - NOTE: Hep G co-exists with other Hep viruses and HIV - Treatment: monitor liver functions although it does not appear to cause liver damage Complications: - Hep: ABG (USUALLY benign) - Hep: BD (fulminant hepatic failure) - Hep: BDC (Cirrhosis, Hepatocellular carcinoma) - Hepatocellular carcinoma: primary liver cancer originating from hepatocytes (main liver function cells) - S/S: unexplained weight loss, loss of appetite, abdominal pain/discomfort, jaundice, ascites and fatigue & weakness) TEST: How they are transmitted, how to prevent them, which are chronic carriers, which give you cirrhosis, Which have IgG ? Pancreatitis - The pancreas release the digestive enzymes: Lipase, Amylase and Protease which are activated to break down food the patient has eaten - Cause of Pancreatitis: The gallbladder, may create a gallbladder stone (cholelithiasis) which can travel and end up blocking the main pancreatic duct, which lead to the digestive enzymes becoming prematurely activated within the pancreas (since their natural path is blocked) instead of the small intestine to actually break down food. This leads to the pancreas essentially digesting itself (autodigestion), causing damage and inflammation. - The enzymes are active once they leave the pancreas but if the gall bladder stone is blocking the path then they will return to pancreas and begin to injure and autodigest the pancreatic cells - Cause of Cholelithiasis: may be due to alcohol, trauma, high triglycerides and high dosage of medications - Common in middle-aged men and women - African american rate 3 times higher than that of white people - Biliary tract diseases (most common in women) - Alcoholism (most common in men) - Acute Pancreatitis: gallstones, alcohol abuse, medications, infections, trauma. - Chronic Pancreatitis: Chronic alcohol abuse, genetic mutations, cystic fibrosis, autoimmune diseases. - S/S of Pancreatitis: Pain is 20/10, they suffer belt pain (loops around body, starts on LUQ and goes to back and then back to the front), Sudden & severe, Aggravates with feeding, If pt lays flat they get worse, SOB, Vomiting does NOT relieve pain, Abdominal sounds are absent, WBC elevated, Hypotension, Tachycardia, Abdominal tenderness, Crackles (cause of vasodilation/pulmonary edema), Discoloration of abdominal wall (Cullen & Gray Turner's sign), Pseudocyst (accumulation of fluid) - Diagnosis: Elevated serum amylase and lipase, Elevated WBC, Blood glucose (hypo/hyperglycemia), Triglycerides, Bilirubin, Serum calcium, Abdominal endoscopic ultrasound, X-ray, CT scan, Endoscopic retrograde cholangiopancreatography (ERCP) remove the stone from the area OR cholecystectomy - Treatment/Management: - #1 KEEP PT NPO! ← on TEST (if pt eats then more amylase and lipase are produce) - Follow up: monitor blood glucose levels (prevent hypoglycemia), check electrolytes, liver and kidney function and monitor for signs of infection at the catheter site - HOB elevated, Prevent hypotension (IV fluids) - Pain management - Semi-fowlers (no abdominal pressure) - Morphine/Hydromorphone - Monitor blood glucose levels - Shock - Plasma or plasma volume expanders (dextran or albumin) - Fluid/electrolyte imbalance - Lactated Ringer’s solution - Ongoing hypotension - Vasoactive drugs: dopamine (Intropin) - High carb, low fat and high protein diet ← HELP WITH HEALING ON TEST - Monitor triglycerides - Complications - Edematous pancreatitis (Pseudocyst) - Mild and self-limiting - May lead to pseudocyst due to accumulation of fluid → becomes an abscess - S/S: pain, infection and may rupture (this leads to hemorrhage) - Treatment: drainage/surgical intervention - Hemorrhage pancreatitis - Bleeding will travel to the front of abdomen (Cullen's Sign) - Bleeding will travel to the back of person (Grey Turner's Sign) - Notify PCP, pt may need surgical abdominal lavage  - - Systemic pancreatitis (Systemic inflammatory response syndrome: SIRS) - The inflammation is so severe that it causes vasodilation in entire body - S/S: Fluid starts escaping from the arteries, pulmonary edema, pericardial effusion, hypotension - Treatment: identify and treat underlying cause (sepsis=antibiotics, trauma/burn=iv fluids…), O2 as needed, monitor kidney and liver functions, control inflammation with corticosteroids (Methylprednisolone, Dexamethasone) - Hypotension (treat with IV fluids) - Tetany: hypocalcemia - S/S: positive Trousseau’s Sign: Spasm of the hand and wrist when inflating a blood pressure cuff, muscle cramps, spasms, tingling sensation, Chvostek’s Sign: Twitching of facial muscles when tapping the facial nerve - Hypo or Hyperglycemia: due to impairment of insulin production in pancreas - Pleural effusion: fluid in pleural space (between lung and chest wall) - S/S: SOB, cough, chest pain - Treatment: thoracentesis (drain fluid) - Atelectasis - Prevention: incentive spirometry, deep breathing and coughing exercise, early ambulation, HOB 30 degrees/semi-fowlers - Pneumonia ON TEST: causes, how it is diagnosed, pain, look of pain, priority and management and complications