Hepatic Biliary and Pancreas Disorders

  1. Calculouscholecystitis
    inflammation of the gallbladder due to stones obstructing the gallbladder duct.
  2. formations of gallstones the 4 F's?
    • Fertile, female, fluffy, and forty
    • Main problem is when the stones obstruct bile flow.
  3. Cholecystitis? Main cause?
    • almost always occurs when the gallstones partially or completely obstruct bile flow.
    • Gall pain after a fatty meal may be a precursor
  4. Diagnostic tests for cholecystitis?
    • ERCP: Endoscopic Retrograde Cholangio-Pancreatography
    • CT scan
    • Ultrasound
    • HIDA scan-hepatobiliary iminodiacetic acid scan
    • CBC-Elevated WBC & bilirubin
  5. icterous?
    Jaundice of the eyes
  6. steatorrhea
    Fatty stool
  7. Treatment for cholecystitis
    • Pain management-opioids
    • low fat diet-decrease of bile
    • cholecystectomy-laparoscopic is treatment of choice
    • may need to remove stones in the ducts.
  8. Post op care for Cholecystectomy?
    • Diet change
    • education
    • pain management
    • pulmonary hygiene 
    • I&O
    • Fluid and electrolytes
  9. Acute Pancreatic disorders?
    Pancreatitis-which causes premature activation of excess pancreatic enzymes-pancreatic and ductal tissue may be destroyed (Pancrease starts to digest itself)-can be acute or chronic. Also may causes pancreatic scarring and obstruction of the ducts.
  10. Acute pancreatitis info? risk factors for disease?
    • Endocrine function: Management of insulin
    • Exocrine function: management of digestive enzymes
    • Etiology: Alcohol use, biliary tract disease, trauma (blunt), gastric ulcers, peritonitis, infections, thiazide diuretics.
  11. Presentation of Pancreatitis?
    • Severe pain: Sudden, epigastric, radiates to the back (boring-feeling goes through body)
    • More comfortable in fetal position
    • Jaundice (cullins sign (brusing around umbilicus/ turners sign-flank bruising)
    • LABS: Specific to pancrease
    • Elevated Lipase, amylase, trypsin, glucose, bilirubin, ALT, WBC and decreased serum calcium
  12. Acute Pancreatitis treatment?
    • Pain management
    • decrease inflammation
    • anticipate and treat complications
    • NPO, hydrate with maintance fluids, opioids, proton pump inhibitor
    • May need NG tube (ileus is common)
    • Antiemitics 
    • If NPO for longer than 24-48 hours Jejunal tube feedings or TPN (total pertoneal nutrition)
    • If not NPO will need small feedings High carb, High protein Low fat.
  13. Nursing interventions for Pancreatitis?
    • Side lying position
    • frequent oral hygiene
    • Assess respirtory status: risk for complications of ARDS, fluid overload, pleural effusions
    • Assess for hypocalcemia: Chvosteks (possible perioral paresthesia) 
    • Assess vitals: looking for tachycardia, hypotension and fever
    • Assess glucose: may lead to hyperglycemia
  14. Chronic pancreatitis? S&S and complications?
    • Abd pain
    • lack of enzymes leads to malabsorption of nutrients
    • anorexia, weight loss, nausea, vomiting.
    • Will eventually lead to diabetes
    • Streatorrhea
  15. Chronic pancreatitis treatment?
    • Opioid analgesia
    • Pancreatic enzymes (Pancrealipase) (contains amylase, lipase and protease. Don't mix with foods due to enzymes braking down the food.
    • Proton pump inhibitors decrease gastric juice
    • Assess glucose levels and treat
    • Collaborate with nutritionist pt. may need 4k-6k calories low in fat
    • Avoid alcohol.
  16. Pancreatic abscess?
    • If untreated will be fatal
    • purulent liquefaction of necrotic pancreas may occur after  acute pancreatitis, episode of chronic pancreatitis and gallbladder surgery.
    • Fever and pleural effusion may occur
    • diagnosed with an ultrasound
    • abscess must be drained
    • Antibiotics are given as well
  17. Pancreatic pseudocyst?
    doesn't produce more fluid like a normal cyst.
    • sac like structure formed on pancreas
    • can cause number of complications similar to abscess on the pancreas. 
    • Bowel obstructions, hemorrhage, infections, fistula formation. treated with percutaneous drainage, or endoscopic drainage/ laparoscopic drainage.
  18. Pancreatic cancer? Treatment?
    • 4th leading cause of cancer death
    • difficult to diagnose 1st sign may be jaundice, clay colored stool, dark urine.
    • diagnosed with CT, ERCP and or abdominal ultrasound
    • treatment is with chemo, radiation and and/or whipple surgery
  19. Whipple surgery?
    • open surgical or laparoscopic surgery. Where they will remove any potential cancerous  tissue from the head of the pancreas, duodenum, portion of jejunum, stomach, and the gallbladder, maybe the spleen.
    • They then reconnect the organs appropriately to allow proper digestion and physiology. Recovery takes up to a month.
  20. How much of your pancreas do you need to manage BG?
    At least 10% of pancreas. Sometimes you may need enzyme supplementation or DM meds.
  21. Nursing interventions for Whipple care?
    • Assess for BG: risk for lack of insulin production
    • Assess for Hemorrhage: post op bleeding?
    • Assess for Ileus: GI obstruction? nausea? 
    • Assess for peritonitis: possibility for fistula leading to leakage of pancreas/gallbladder juices leaking into peritoneal cavity.
    • Assess lab values: F&E, Glucose imbalance, check albumin and calcium levels.
  22. Hepatitis Types?
    • HepA: Transmitted Oral/Fecal, Vaccine avail.
    • HepB: transmitted via blood, STI
    • HepC: transmitted via blood, IV drug abuse, STI
    • HepD: Can tag along with B
    • HepE: Oral/Fecal-developing countries 
    • HepG: Usually tied to C
  23. HEP A?
    • Incubation period: 2-6 weeks
    • Replicates in the liver-excreted in bile and is shed in stool
    • S&S: fever, malaise, nausea and anorexia, abdominal discomfort, dark urine and jaundice.
    • Children younger than 6 may not exhibit S&S, older than 6=70% become jaundice.
    • Convalescent phase: 9-10 weeks maybe up to 16 weeks.
  24. HEP A Blood tests?
    • IgM anti-HAV indicates acute hepatitis A (appears 1st week of disease and declines over 3-4 months)
    • IgG anti-HAV documents past infection(peaks at one month-may last for life)
    • Vaccine avail. for oversea travels.
  25. Hep B?
    • 100 times more virulent than HIV
    • Mother to baby transmission possible at 85%
    • Infected infants have 25% chance to die from disease.
    • Vaccine available.
  26. Hep B Blood tests?
    • HBsAg: Hepatitis B surface antigen- contagious may disappear after acute episode and they may become carriers-(INcrease risk for Liver cancer and cirrhosis.)
    • HBsAb: Hepatitis B suface antibody-recovery and immunity-positive means you have been vaccinated.
    • May check viral count.
  27. Hep B treatment? pediatric treatment?
    • Hep B immune globulin within 12 hours then the series.
    • if exposure administer hep B immunoglobulin
    • and vaccinate against Hep A and B.
  28. Chronic hepatitis treatment?
    • Boost immune system
    • antivirals
    • Interferon alfa or PEG interferon (30-40%) will respond to this treatment.
    • Lamivudine (epivir)- Therapy last a year-resistant strains are becoming a problem.
    • Following are more for Hep B.
    • Adefovir (hepsera): 48 weeks of therapy 50% respond. nausea, headache, fatigue, nephrotoxicity. are possible
    • Entecarvir (baraclude): newer treatment for resistant strains
    • Tenofovir: used mostly for HIV, but also for Hep B
  29. Hep C? Most common chronic bloodborne infection in the USA
    • No vaccine
    • more prevalent than hep B
    • most common reason for liver transplant
    • 10% transmission at birth
    • more than 50% of HIV pt's have Hep C
    • many infected prior to 1992 blood testing
    • 70% develop chronic hepatitis and 30% end stage cirrhosis.
  30. Autoimmune Hepatitis?
    • Body recognizes own liver as foreign and will attack it. More likely with people who have an autoimmune disease already (DM, MS, celiac disease, lupus)
    • 100-200k cases per year
    • 6% of all liver transplants, 78% are women.
    • Type 1, 2, 3
    • Type one: most common blood tests show positive antinuclear antibodies (ANA) and smooth muscle antibody (SMA)
    • Type two: more common among women and girls
    • Type three: may not have antibodies, but subtle liver changes may occur.
  31. Hepatitis care?
    • Encourage healthy diet of high carbs, protein and low in fats. Abstain from alcohol. avoid acetaminophen
    • Activity and rest
    • proper skin care
    • educate on how to prevent transmission to others.
  32. Liver function?
    • Fat digestion
    • Processing and storage of fats
    • Converts fatty acids to ketones
    • Metabolizes fat soluble drugs (CYP 450 system)
    • Can build carbohydrates from protein
    • Can convert sugar to fat
    • Liver breaks down Ammonia and converts it to urea Amino acids (breakdown of proteins) ammonia, which will be converted to urea, then excreted
    • Protein metabolism-primary is albumin-contributes to osmotic colloidal pressure.
  33. Liver Lab tests?
    • ALT-Most specific to liver alanine aminotransferase: enzyme released from hepatocytes when the liver is injured.
    • AST: Aspartate aminotransferase found in hepatocytes and cardiac cells may increase more than 10 times normal, and stay elevated, less specific than ALT
    • ALP: Alkaline phosphatase Primarily found in liver and bone, may be markedly elevated
    • GGT: Gamma-glutamyltransferase: elevated with liver, heart and kidney injury. 
    • Serum ammonia: increases with liver issues Due to the liver being unable to convert ammonia to urea
    • Serum albumin: decreases with liver issues due to liver being unable to create albumin 
    • PT: Will increase due to liver being unable to  synthesize clotting factors.
    • Bilirubin may inrease and can lead to anemia due to bleeding/malnutrition due to vitamin deficiencies.
  34. Cirrhosis of the liver?
    • inflammation caused by toxins or other disease processes results in extensive degeneration of the liver, destruction of hepatocytes and leads to scarring and liver failure. Liver becomes impaired and starts to shrink.
    • Most common cause in US: Alcohol and Hep C
    • Worldwide: Hep B
  35. Other causes of Hepatic failure
    • drugs and toxins
    • biliary cirrhosis hemachromatosis
    • wilsons disease
    • alpha 1 antitrypsin deficiency 
    • cystic fibrosis
  36. Portal Hypertension?
    • liver stores about 450cc of blood when sclerosed blood flow is interrupted
    • increases resistance to hepatic blood flow
    • will cause increased pressure on venous channels splenomegaly, ascites, and esophageal varices. May also present with caput medusae
  37. esophageal varices?
    • Due to chronic liver disease, cirrhosis or portal hypertension
    • thin walled varicosities in the submucosa of the esophagus can rupture leading to massive hemorrhage often fatal.

  38. Treatment for Portal hypertension?
    • sengstaken/ blakemore tube
    • sclerotherapy/ ligation
    • Bands
    • TIPS: Transjugular intrahepatic portal systemic shunt. Catheter is inserted through the jugular vein down into the hepatic vein where a new route for blood flow through the liver is created.
    • procedure to create new connections between two blood vessels in your liver. to relieve pressure
  39. Treatment for esophageal varices?
    • Decrease the likelihood of this happening by decreasing chances of liver disease, portal hypertension. 
    • B-adrenergic blockers can be helpful along with vitamin K SQ 10mg
    • other treatments are used to manage portal hypertension which can prevent varices.
    • there is also endoscopic injecting sclerosing agent to control bleeding from varices if it occurs.
  40. Ascites ?
    • fluid accumulation 
    • common in advanced cirrhosis
    • increased cap pressure due to portal hypertension
    • kidney disease leading to salt/water retention
    • decreased oncotic pressure due to impaired synthesis of albumin.
  41. Liver responsibilities continued?
    • Endocrine organ: Metabolism of glucocorticoids, mineralcorticoids and sex hormones
    • Hematologic organ: Temporary storage of blood (about 450 cc), synthesis of clotting factors, Kupffer cells-phagocytic cells that forms the lining of the sinusoids of the liver and is involved in the breakdown of red blood cells.
    • Excretory organ: Bile, cholesterol, urea, detoxification of drugs and other harmful substancesCYP 450: enzymes responsible for the absorption and utilization of many drugs;-- also produced by the liver
  42. Hep C diagnosis
    • Anti-HCV: doesn't tell if acute or chronic
    • Diagnosed with ELISA Enzyme linked immunosorbent assay.
    • RIBA: recombinant immunoblot assay
    • HCV PCR RNA test to determine viral load in body-detectable at 1-3 weeks after exposure.
    • Oraquick HCV is a rapid antibody test for the disease.
  43. HEP C Genotypes?
    Six "Known" types
    Types (2 and 3) are 2 or 3 times more likely to respond to interferon therapy than type 1.
    Genotype determines course of treatment.
    • Genotype one: most american fall into this category-more difficult to treat up to 48 weeks. (heavier dose of ribavirin)
    • Genotype two and three: better response usually 24 weeks of treatment (peginterferon and ribavirin)
    • Genotype four and five: 48 weeks of treatment
    • Genotype six:  found mainly in asia
    • Liver biopsy can be useful in determining severity of disease.
  44. Hep C treatment?
    • Combination therapy: antivirals: check Pharm.
    • Newer treatments can cure the disease: Harvoni: combination of sovaldi and ledipasvir
  45. Healthy liver education?
    • Vaccinations are available for Hep A and B
    • No alcohol or at least in moderations
    • Avoid high doses of acetaminophen can lead to liver damage.
    • Healthy life style choices in regards to nutrition and exercise
    • Milk thistle/ herbal supplements may or may not be beneficial.
  46. Albumin is responsible for?
    binding and transportation of certain drugs/ contributes to osmotic colloidal pressure: oncotic pressure
  47. Liver failure S&S?
    • Fatigue
    • malaise
    • Jaundice 
    • Muscle wasting
    • Bleeding
    • Hypoalbuminemia
    • Glucose imbalance
    • feminization
  48. Nursing care for ascites?
    • weigh daily
    • monitor I&O
    • Measure girth of abdomin
    • Assess labs, electrolytes, albumin, rising BUN and Creatinine
    • Nutrition: less than body requirments 
    • High calories, Low protein, low sodium.
    • Skin Integrity-risk for impaired: Cool, lightweight clothing, trimmed nails
    • Risk for hemorrhage: give vitamin k as ordered, soft toothbrush, assess for bleeding, soft foods that will not cause trauma to the esophagus and cause varices to bleed.
  49. paracentesis for Ascites?
    • Monitor for Hypotension and tachycardia and F&E shifts.
    • 500-1000cc is considered safe larger volume may lead to the list above.
  50. Hepatic encephalopathy? treatment?
    • ammonia build up may lead to a neurotoxic effect
    • Asterixis: flapping tremor due to liver issues. AKA: liver flap
    • Personality changes: euphoria, irritability, anxiety.

    • Treatment: Treat underlying cause if possible. 
    • Lactulose: can decrease ammonia in intestine
    • Low protein diet and decrease bacteria in intestine by giving antibiotics
  51. Nursing care for encephalopathies?
    For hepatic encephalopathy?=ways to decrease the ammonia build-up.
    • Ensure safety: bed alarms,
    • 1:1 staffing
    • regular assessments
    • Reorient to surroundings
    • Calm approach
  52. Gastric bypass surgery-potential complications?
    30-40% develop gall stones.
  53. T-tube placement after cholecystectomy?
    Drains bile from liver into a bag outside the body temporary: 2-3 days normally.
  54. what's the prevalence of hepatitis C being transmitted to infants at birth?
    5 out of every 100 babies born to infected HCV mothers. 5%. 2-3 times more likely to aquire HCV if the mother has HIV.
  55. PSE?
    And treatment?
    • Portal systemic encephalopathy due to a build up of ammonia in the blood.
    • Treatment: to decrease ammonia in the blood. Bacteria in the intestine create ammonia-may be treated with neomycin, low protein diet( liver can't process protein which leads to ammonia build up), lactulose (binds to ammonia and helps to excrete)
  56. ERCP?
    • Endoscopic retrograde cholangiopancreatography
    • specialized technique used to study the bile ducts, pancreatic duct and gallbladder.
  57. Pancreatic enzymes
    • proteolytic enzymes (trypsin, chymotrypsin and others) that break down dietary proteins
    • The pancreatic enzymes are secreted in an inactive form and become active in the intestine. In the case of pancreatitis, the enzymes are activated early and begin to auto digest the pancreas.
Card Set
Hepatic Biliary and Pancreas Disorders
Liver and Endocrine 89% of exam