hepatic and pancreatic notes
hepatic and pancreatic notes Nurs 4020
Popular in MedSurg
Popular in Department
verified elite notetaker
verified elite notetaker
verified elite notetaker
MATH 102 004
verified elite notetaker
verified elite notetaker
verified elite notetaker
This 0 page Class Notes was uploaded by Brenna Notetaker on Monday February 8, 2016. The Class Notes belongs to Nurs 4020 at East Carolina University taught by Mrs. Swift in Fall 2015. Since its upload, it has received 19 views.
Reviews for hepatic and pancreatic notes
Report this Material
What is Karma?
Karma is the currency of StudySoup.
You can buy or earn more Karma at anytime and redeem it for class notes, study guides, flashcards, and more!
Date Created: 02/08/16
Hepa s 102 32015 In ammation of the liver caused by viruses drugs and chemicals bacteria autoimmune disorders can be acute 6 mo or less or chronic gt6 mo causative agent gt in ammation of liver tissue gt cell degeneration gt cell regeneration acute or failure chronic why it s a problem 0 O O O 0000 prone to infections because liver cells are unable to assist with RBC WBC or bacteria breakdown decreased emulsi cation of fats because liver cannot produce bile salts like it previously did jaundice from excess bilirubin hypo or hyperglycemia because liver is responsible for carbohydrate metabolism increased cholesterol because fat metabolism is altered and body cannot break down cholesterol decreased albumin synthesis because liver is no longer synthesizing albumin like it used to decreased blood clotting due to decreased vitamin K production and decreased blood clotting factor production ammonia build up anemia from decreased iron storage no fatsoluble vitamin storage no detoxi cation of hormones and drugs because liver is not ltering them Viral hepatitis 0 caused by one of ve major viruses A n Fecaloral transmission virus is found in stool of infected person for two weeks before they show symptoms a RNA virus a daycare workers a acute severe short lasting a fully recovered within 6 months a antihepatitis A immunoglobulin G anti HAV IGG indicates person has been affected in the past a prevent by washing hands wash all raw fruits and vegetables before eating don t consume raw or undercooked shell sh or seafood B Hepatitis A vaccine especially for people working or traveling to countries where Hepatitis A is common central or south America men engaging in sexual activity with other men chronic liver disease food workers working with primates infected with hepatitis A a DNA virus a transmission blood 0 sex with an infected partner 0 sharing needles or syringes 0 sharing anything with tissue razors or toothbrushes direct contact with open sores exposure to blood infected mother to baby 0 any blood or bodily uids saliva a carrier state 210 carrier state have the virus but don t show symptoms a immunity 0 Hep B titer shows immunity to Hep B antibodies from the vaccination or having the disease in the past prevention HBV vaccine serious of 3 booster of vaccine or get all 3 series if titer is low or if you ve been exposed o injected with Heb B immunoglobin o handwashing hygiene wearing gloves standard precaution do not recap dirty needles RNA virus transmission blood 0 blood or bodily uids 0 high risk sexual behaviors most common needle sticks 100 more likely to get it 0 mother to baby chronic hepatitis C is most common disease in US 1 reason for liver transplants in US 25 of Hep C will progress to cirrhosis within 25 30 years prevention 0 no vaccine screening 0 do not engage in high risk sexual behaviors be careful with needles standard precautions handwashing uncommon diagnosis El cannot survive on own must be with hepatitis B defective RNA virus transmission blood percutaneous sexual blood or bodily uids prevention 0 prevent hepatitis B vaccine very common in the US seen in developing countries India Mexico Africa Asia RNA virus transmission fecaloral wash hands and fruits and vegetables undercooked shell sh prevention not normally seen in US El El El RNA virus transmitted by blood transfusion and sex frequently coexist with other hepatitis viruses such as HBV and HCV no evidence that it alone causes liver damage 0 history engaged in at risk behaviors if they know their partner is positive eating undercooked or raw shell sh not washing fruits and veggies 0 physical exam jaundice quotglowquot look at whites of eyes for darkskin people palpate liver for tenderness hepatomegaly splenomegaly which may be tender upon palpation o diagnostic studies lab studies pg 1011 El El El liver enzymes AST ALT serum bilirubin increased because it is not being excreted in the bile depekote is bad on the liver taken for psych or seizures prothrombin time increased ammonia levels increased due to decreased liver clearance serology tests 0 clinical manifestations 0 some patients are symptomatic 0 can be classi ed into two phases acute El El El may have no symptoms common symptoms are anorexia fatigue NV abdominal pain RUQ weight loss cigarettes taste nasty if a smoker headache low grade fever urine may be dark usually resolves in 14 months chronic El El may still be asymptomatic very tired muscle and joint pain all acute symptoms can progress to cirrhosis those at greater risk are males use of alcohol hyperlipidemia obesity diabetes 0 three phases preicteric u when they start feeling bad may feel like u vague abdominal pain urine that gets progressively darker increased liver enzymes joint pain weight loss icteric peak phase a progress into jaundice I increased direct bilirubin clay colored stools severe RUQ pain dark or tea colored urine itchy skin bowel deposits on skin spider angiomas posticteric start to improve a may still be tired I jaundice increased a stool and urine normal color a appetite returns complications of viral hepatitis 0 chronic persistent hepatitis stays in the background doesn t cause much problems may cause fatigue 0 chronic active hepatitis with B amp C not with A or E with D is also with B o Fulminant hepatitis severe necrosis of liver cells gt liver failure particularly if B amp D combined 0 cirrhosis 0 liver cancer treatments 0 primary goals is to rest liver and promote cellular regeneration prevent complications jaundice dehydration weight loss 0 treat signs and symptoms 0 physical rest essential to decrease metabolic demands of liver and to increase blood supply to liver to carry nutrients and oxygen for cell regeneration collaborative care o pharmacologic vaccines nucleoside and nucleotide analogs to keep Hep B virus from reproducing interferon alfa2b HBV and HCV given subQ or Ribavirin HCV prevent replication can be given at home 2xday by mouth Rebetron combination of interferon and ribavirin HCV given by mouth supportive drugs antiemetic sedative pain relief 0 nutrition increased calories high carbs protein is needed for cell regeneration but if liver function is severely impaired you should not increase it low fat vitamin B and K green leafy vegetables if pt has intractable NV they may need IV nutrition or tube feedings monitor uids and electrolytes closely 0 others no alcohol at all mouthwash emphasize rest may need drugs to help them rest teaching about reducing spread and prevention if they are a carrier they are still able to transmit disease nursing care 0 assessment past history medications social IV drug use alcohol use multiple partners SS urine color suddenly tired RUQ pain 0 toxic and druginduced hepatitis toxic systemic poisons drugs acetaminophen most common ibuprofen ASA isonizide INH chlorothiazides methyldopa Aldomet methotrexate idiopathic hepatitis 0 probably autoimmune 7080 are women 0 treated with corticosteroids other immunosuppressive agents lmuran Cirrhosis Chronic and progressive disease of the liver where liver cells are degenderized and destroyed degeneration causes in ammation all across liver and brosis normally happens after decades and chronic liver disease 0 types 0 alcoholic fatty in ltrated of the liver if the person doesn t stop drinking it can cause scarring not functioning tissue 0 postnecrotic after damage to liver from toxins or viral heanUs O O O biliary biliary obstruction stone or longterm untreated gallbladder disease cardiac rightside heart failure gt increased preload gt blood backed up into circulatory system into liver gt hepatic cell injury postnecrotic biliary and cardiac causes brosis and scar formation without the initial fatty in ltrations clinical ndings compensated cirrhosis has no symptoms decompensated shows symptoms 0 O 0 management of ascites table 449 diagnostic studies liver enzymes will be elevated but with endstage they may be decreased protein and albumin decreased because protein metabolism isn t working globulin increased antibodies decreased cholesterol dt abnormal fat metabolism not a good thing PT may be increased dt decreased synthesis of vitamin K and decreased prothrombin bilirubin liver biopsy to nd changes in liver cells can be done in OR open biopsy or under sterile at the bedside percutaneous watch for bleeding monitor labs before and after type and cross blood baseline vitals and vitals after biopsy informed consent lay on right side after to prevent bleeding for about 2 hours and need to stay in bed for at least 12 hours after monitor for hypovolemic shock dt bleeding at risk for pneumothorax listen to lung sounds paracentesis provides relief to patient and also allows analysis of uid explain procedure before procedure and get consent empty bladder before to prevent puncture get baseline vitals and abdominal girth and weight before and after may need to provide replacement of uids monitor BP for changes internal bleeding complications of cirrhosis O O portal hypertension with esophageal varices emergency needs immediate attention if you see signs of any bleeding notify provider immediately coughing or sneezing can cause bleed peripheral edema and ascites o hepatic encephalopathy ammonia is not being converted to urea by liver gt build up ammonia in the body gt effects brain CNS depressant 55 of impending coma disorientation asterixis later signs are slowed speech labile impaired judgment hiccups positive Babinski sign hyperactive re exes o hepatorenal syndrome blood backs up into kidneys collaborative care 0 treat underlying cause 0 rest 0 pharmacologic diuretics H2 blockers to keep gastric secretions down PPl to keep gastric secretions down vitamin K to correct clotting abnormalities antibiotics to help reduce risk of hepatic encephalopathy lactulose laxative to bind to ammonia and gets rid of it in stool 0 nutrition high calories up to 3000day low to moderate fat protein varies depending on liver clearance normally only severely restricted for hepatic encephalopathy vitamin B and K o ascites sodium restriction albumin low in salt bed rest diuretics paracentesis topical lidocaine peritoneovenous shunt shunt into abdomen and into vascular system jugular veins to reroute uid out of abdominal cavity and back into circulation only for symptom management lots of risks 0 care for portal hypertension esophageal and gastric varices goal is to avoid bleeding I avoid alcohol ASA irritating foods promptly treat URI control coughing and sneezing betablockers Inderal to decrease CO gt decreases HR gt decreased pressure gt decreases risk of bleeding if bleeding occurs a medications sandostatin reduces portal vessels pressures vasopressin causes loss of uid volume decreased portal vessel pressure NTG causes vasodiation to put less pressure on walls of veins n endoscopic sclerotherapy go in a quotzapquot occlude distended veins 0 ligation or banding clips distended vein a balloon tamponade mechanical compression to stop bleeding Hepatic Encephalopathy Ammonia eve gets to high gt uid shift in brain gt LOC changes 0 Stages 0 Prodromal change in personality 0 Impending periods of confusion o Stuporous severe mental de cits o Coma Management O Caused by increased ammonia in bloodstream Reduce ammonia level with lactulose like kayexalate for ammonia neomycin xifaxan antibiotics that reduce in ammation and ora in the gut 39 assessment 0 00000 history risk factors meds nutrition vitamins elimination clay colored poop and dark urine general survey assess skin respiratory GI neurologic assess for encephalopathy LOC changes 0 areas of concern 000000000 0 rest nutrition response to jaundice edemaascites may be giving diuretics assistance with paracentesis dyspnea skin care uidelectrolyte balance hemorrhage varicies esophagus or gastric system low prothrombin factor gt increased P39IT infection especially with antibiotics hard on liver harder for body to fight infection neurologic status pay attention to what family and friends say about small changes to baseline neuro status 0 teaching for home care diet rest ss bleeding changes in neuro status nursing diagnosis 0 O ineffective airway clearance dt ascites and varicies treatments gt edema in airway impaired gas exchange VS WNL clear lung sounds blood gases WNL and pulse ox WNL uid volume excess balanced ampO decreased edema in LE decreased abd girth and daily weight risk for impaired skin integrity skin intact skin free of infection risk for injury free of infection free from bleeding improved P39IT able to describe bleeding precautions altered nutrition lt body requirements decreased NN able to ingest meals demonstrate no signs of malnutrition liver transplant Hep C is most common reason 0 major post op complications 0 rejection 0 infection lifelong immunosuppressant therapy 0 liver is less likely to be attacked by antigens pancreatitis two cell types 0 exocrine o endocrine acute pancreatitis 0 Diffuse in ammation of the pancreas caused by activation of the pancreatic enzymes auto digestion 0 Most common causes are gallstones bile gt pancreas gt pressure build up or alcoholism o Other causes surgery pancreatic tumors 3rCI trimester pregnancy 3rCI trimester and right after delivery viral bacterial or parasitic infections medications and pancreatic trauma 0 Early onset ss Abdominal pain worse with eating because it activates pancrease Nausea and vomiting Low grade fever Leukocytosis Hypotension Tachycardia Jaundice Decrease Absent bowel sounds Crackles in lungs Bruising of abdominal wall a Grey Turners spots a Cullen s sign bruising around belly button Dehydration Increased serum amylase and lipase o Complications Pseudocysts cavity on the outside of the pancreas Usually goes away but if it ruptures gt pancreatitis Abscess cavity including uid inside pancreas Can rupture and cause infection Pleural effusion atelectasis pneumonia Hypotension dt vascular permeability Hypocalcemia fat necrosis causes calcium to leave cells gt tetany Chronic pancreatitis 0 Progressive brosis and degeneration o irreversible 0 two types calcifying in ammation and sclerosis in the head of the pancreas around the pancreatic duct can be tied back to alcohol consumption common to see it with cirrhosis obstructive usually caused by biliary disease obstruction is a stone pancreas become hard cells die malabsorption of nutrients gt nutritional de ciencies insulin is not being secretes gt hyperglycemia clinical manifestations Same as acute pancreatitis Malabsorption of nutrients Weight loss Diabetes Mellitus Steatorrhea fat in the stool Dark and frothy urine from bile 0 Diagnosis for acute and chronic History gallbladder disease alcohol intake ss labs Serum amylase serum lipase urinary amylase serum glucose serum calcium serum triglycerides other a Abdominal xray chest xray abdominal US contrast enhanced CT MRI n cholangiopancreatography n endoscopic retrograde cholangiopancreatography ERCP upper GI scope collaborative care 0 acute and acute attack of chronic OOOO El surgic El El El drug t nutriti El El conservative hydration NPO LR or other electrolyte solutions if shock occurs 0 blood volume replacement 0 plasma 0 dextran o albumin al ERCP laparoscopic cholecystectomy drain placement for abscess pseudo cyst and severe peritonitis herapy pain medications painful even when they aren t eating Demerol usually avoid morphine because it can cause spasm of sphincter of oddi which makes pain worse antispasmodics carbonic anhydrase inhibitor Diamox decreases amount of bicarbonic secretions of pancreas antacids decrease HCL acid in stomach gt decrease pancreatic activity H2 receptor antagonistPPI decrease HCL acid gt reduce pancreatic activity PPl may also have anti in ammatory effect on pancreas onal NPO initially to reduce pancreatic secretions possible NG to suction to decrease vomiting and abdominal pain n TPN or low fat enteral feedings u when food it allowed small frequent feedings low fat high carbs carbs are less stimulating to the exocrine portion of pancreas a vitamin supplements 0 chronic not an acute attack drug therapy a pancreatic enzymes with each meal a insulin or oral hypoglycemic surgery a sphincteroplasty n pancreatojejunostomy n subtotal panreatectomy portion of pancreas removed usually only done for patients that have disabling pain not relieved by other interventions nursing management 0 assessment past history meds past surgeriestreatments GI surgery gt increased risk of pancreatitis nutrition extra calcium fat intake vitamins enzymes with meals general survey and head to toe skin discoloration respiratory complications CV system for perfusion cardiac output GI nursing diagnosisgoals o acute pain reports adequate pain control uses nonpharmacologic techniques of pain mng NG tube is maintained to suction o de cient uid volume equal ampO stable weight moist mucous membranes 0 imbalances nutrition maintain appropriate weight food and uid intake adequate o ineffective therapeutic regimen describe therapeutic regimen with regard to disease process and management express commitment to lifestyle changes and participation in treatment for alcohol dependence support group
Are you sure you want to buy this material for
You're already Subscribed!
Looks like you've already subscribed to StudySoup, you won't need to purchase another subscription to get this material. To access this material simply click 'View Full Document'