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  1. Functions of the Liver
    • •Stores glucose (as glycogen) and iron
    • •Controls the production and removal of cholesterol.
    • •Metabolizes drugs and removes toxins.
    • •Produces clotting factors
    • •Role in immune system.
    • •Produces bile.
  2. What is hepatitis?
    Liver Inflammation
  3. Age related changes of the liver:
    • Steady decrease in size and weight of the liver, particularly in women
    • • Decrease in blood flow
    • • Decrease in replacement/repair of liver cells after injury
    • • Reduced drug metabolism
    • • Slow clearance of hepatitis B surface antigen
    • • More rapid progression of hepatitis C infection and lower response rate to therapy
    • • Decline in drug clearance capability
    • • Increased prevalence of gallstones due to the increase in cholesterol secretion in bile
    • • Decreased gallbladder contraction after a meal
    • • Atypical clinical presentation of biliary disease
    • • More severe complications of biliary tract disease
  4. Types of Hepatitis:
    • Infectious Hepatitis
    •    •Viral – A, B, C, D, E, G
    •    •Less common infections
    •      -Bacterial, protozoal, fungal, mycoplasmal

    • Noninfectious Hepatitis
    •    •Autoimmune
    •    •Drug-induced
  5. S/S of Hepatitis
    • •Jaundice 
    • •Dark Urine
    • •Fatigue/malaise
    • •Light Stools
    • •Abdominal Pain 
    • •Joint pain
    • •hepatomegaly
    • •Anorexia
    • •Nausea
    • •Vomiting
    • •Diarrhea
    • •Pruritis
  6. Which stage of Viral Hepatitis is the pt most symptomatic
    Acute (icteric stage: jaundice)
  7. Stage of viral hepatitis that begins with resolution of jaundice.
    2-6 weeks in uncomplicated cases.
    Convalescent Hepatitis
  8. Liver inflammation >3-6 months
    • CHRONIC hepatitis
    • •With B, C
    • •Detectable RNA levels can fluctuate
    • •In hepatitis B, the HbSAb is not seen
  9. Hep A
    • •Fecal/Oral transmission
    • •Anti-HAV antibodies
    •    IgM , IgG
    • •Vaccine x 2 doses, 6 mos apart
  10. Hep E
    • •Uncommon in US
    • •endemic to SE Asia
    • Transmission: drinking contaminated water
  11. Hep D
    • •Uncommon in the US
    • •Blood-borne
    • •Structurally different from A, B, and C viruses
    • •“incomplete virus”
    • •Needs presence of hepatitis B virus to replicate
    • •Co-infection or super-infection to hepatitis B
  12. HBsAg – hepatitis B surface antigen
    current acute or chronic infection
  13. HBsAb – Hepatitis B surface antibody
    Successful vaccination OR prior resolved infection
  14. HBcAb or anti-HBc
    • hepatitis B core antibody
    • Intracellular, signifies current or past infection
  15. Hepatitis B RNA
    Signifies presence of active virus
  16. Hep C
    • •If seropositive, genotyping necessary
    • •6 main genotypes, > 50 subtypes
    • •Genotype 1 most prevalent in US
    • •also the most difficult to treat
    • •48 months treatment vs. 24 for other types
    • •Roughly 80% of Hep C infections will become chronic
    • •Chronic Hep C high risk for Cirrhosis
    • •High risk for hepatocellular carcinoma (HCC)
    • •Liver ultrasound q 6 months to monitor
    • •Sustained Viral Response (SVR)
    • •More than one measure of viral level necessary to confirm
  17. Tests coresponding to Hep C
    • •PT is prolonged
    • •ALT and AST elevated
    • •Alkaline phosphatase slightly elevated
    • •Serum/urine bilirubin levels elevated
    • •Serum albumin level low, globulin levels high
    • •Liver biopsy shows extent of cirrhosis
  18. Treatment goal for Hep A
    Self Limiting: Manage symptoms
  19. Treatment Goal for Hep B
    sometimes self-limiting (manage symptoms), but if chronic:

    • Combination of drugs:
    •     x- Interferon (Intron A) Sub-Q  
    • Adverse effects: fever, chills, anorexia, nausea, myalgias, fatigue, alopecia, bone marrow suppression, thyroid dysfunction and depression
    •    Antiviral agents -- 
    • lamivudine (Epivir) and Entecavir (baraclude)
  20. Treatment for Hep C
    Drug treatment is decided by HCV genotype.

    • •Genotypes 1 - 6
    •   48 week course of treatment for genotype 1
    •    (Most common genotype in US)

    •24 week treatment for other genotypes

    • Regimens:
    • interferon alfa-2b (Intron A) & ribavirin (Rebetol)

    peginterferon alfa-2a (Pegasys) & ribavirin (Copegus)
  21. Yellow discoloration of the skin r/t alteration in bilirubin metabolism or a problem with the flow
    of bile.
  22. 3 Categories of Jaundice
    • •Hemolytic
    • •Hepatocelluar
    • •Obstructive
  23. Nursing Interventions for Hepatitis
    • •Reduce fatigue- promote rest
    • •Pruritis – antihistamines, emollients
    • •Maximize nutrition
    •    -Avoid fatty foods
    •    -Suggest multiple small meals.
    •    -Avoid Alcohol.
    •    -Vitamin supplementation
    •    -Relieve nausea and vomiting
    • •Provide client teaching
    • •Administer medications
    • •Promote rest
    • •Parenteral Vitamin K for prolonged PT.
    • •Avoid drugs with hepatotoxic properties:
    • Chlorpromazine, ASA, Acetaminophen, etc.
  24. Fulminant Hepatitis
    • •Massive hepatic necrosis
    • •Rare
    • •Seen primarily with B , D and E
    • •Progression of manifestations: jaundice, hepatic encephalopathy, and ascites.
    • •Mortality rate reaches 90-100% in patients over 60.
  25. Autoimmune Liver Diseases
    • •Autoimmune hepatitis
    • •Wilson’s disease
    • •Hemochromatosis
    • •Primary biliary cirrhosis
    • •Nonalcoholic fatty liver disease and nonalcoholic steatohepatitis (NASH)
  26. Alcoholic Hepatitis
    • •May be acute or chronic
    • •Parenchymal necrosis from heavy alcohol ingestion.
    • •Most frequent cause of cirrhosis of the liver
  27. Cirrhosis of the liver
    • •Chronic, progressive disease
    • •Widespread fibrosis (scarring) and nodule formation.
    • Some causes:
    •   Chronic hepatitis B or C
    •   Alcohol
    •   Non alcoholic steatohepatis
    •   10th leading cause of death in the United States.
  28. Risk Factors of Cirrhosis
    • •Excessive alcohol ingestion.
    • •Viral Hepatitis for postnecrotic.
    • •Use of drugs
    • •Acetaminophen
    • •Methotrexate
    • •Isoniazid
    • •Hepatic Congestion-- via biliary blockage or invasion by fatty tissue
  29. Patho of Cirrhosis
    • •Irreversible chronic injury to the liver.
    • •Extensive fibrosis, and nodular tissue growth
    • •Hepatocyte necrosis
    • •Distortion of the vascular bed
    • •Nodular regeneration of remaining liver tissue
  30. Med Management for Cirrhosis
    • •Monitor for complications
    • •Maximize Liver function
    • •Treat the underlying cause
    • •Prevent Infection
  31. Cause of Portal Hypertension
    • Persistent increase in blood pressure in the portal venous system
    • Increased resistance to or obstruction of blood flow through the portal venous system into the liver.
  32. Most severe complication of portal hypertension...
    • Esophageal Varices 
    • Causes of rupture:
    • •Increased portal venous BP
    • •Increased intrathoracic pressure (coughing and straining at stools)
    • •Irritation by food or alcohol
    • •Erosion by gastric juices
    • •Rupture constituents a medical emergency.
    • •Control of Hemorrhage
    •    Sclerotherapy
    •    Transjugular Intrahepatic Portosystemic shunt
    •    Vasopressin IV
    •    Beta-Adrenergic Blocking Agents
    •    Balloon Tamponade.
  33. Ways to control hemorrhage of esophageal varice
    • Sclerotherapy
    • Transjugular
    • Intrahepatic
    • Portosystemic shunt   
    • Vasopressin IV   
    • Beta-Adrenergic 
    • Blocking Agents   
    • Balloon Tamponade
  34. Accumulation of fluid in the peritoneal cavity
    • Ascites
    • Caused by:
    • •Portal hypertension
    • •Lowered plasma colloidal osmotic pressure
    • •Sodium retention
  35. Management of Ascites
    • Correct fluid and electrolyte balance
    • Perform Paracentesis
    • Administer Albumin and diuretics
    • Diet modifications
    • (Low Na with restriction of fluids)
    • Promote effective breathing patterns
    • Maintain skin integrity
  36. Diuretics used for Ascites
    • •Spironolactone (Aldactone)
    • •Chlorothiazide (Diuril)
    • •Furosemide (Lasix)
  37. Dangerous complication of severe liver disease or liver failure
    • Hepatic Encephalopathy
    • Causes:
    • •Liver’s inability to metabolize ammonia to form urea so it can be excreted.
    • •Ammonia is a CNS depressant
  38. Hepatic Encephalopathy
    • •Manifestations are neurologic-range from mild mental confusion to deep coma
    • •Mortality is high among clients who progress into coma with hepatic failure
  39. Kills bacteria in gut that break down pro
  40. Supportive Measures for Hepatic Encephalopathy
    • •Blood Products-- Fresh Frozen Plasma
    • •H2 Blockers
    • •PPIs
    • •Prevent Hepatic Encephalopathy
    • Antibiotics lessen NH4 production by intestinal bacteria breaking down protein
    • •Reduced protein diet
    • •Lactulose given to promote elimination ammonia in stool
  41. Complications of Hepatic Encephalopathy
    • •Asterixis
    •    Characteristic symptom
    •    Flapping tremors involving arms and hands
    • •Fetor hepaticus
    • •Musty, sweet odor on patient’s breath
    • •Accumulation of digestive by-products that liver is unable to degrade
  42. Nursing management for hepatic encephalopathy
    • •Assess LOC
    • •Orient to time and place
    • •Check handwriting
    • •Monitor I&O, daily wts. Measure abd. girth
    • •Watch for signs of complications
    • •Low protein diet
    • •Protein contains nitrogen
    • •Promote rest and comfort
  43. Test results for hepatic encephalopathy
    • •Elevated Ammonia Levels
    • •ABG’S-Respiratory Alkalosis common
    • •EEG-slow waves as disease progresses
    • •Elevated Bilirubin, and Elevated PT
    • •Elevation in transaminases (AST/ALT)
    • •Elevated bilirubin total and direct (conjugated)

    • Bilirubin is elevated for 2 reasons.... bilirubin byproduct of hemolyzed RBCs and typically
    • binds to albumin to travel to the liver and then be conjugated for excretion in urine/stool. Albumin levels are decreased.....conjugation does not occur b/c of hepatocyte destruction.
  44. Cholesterol Gallstones
    Most common

    • Risk factors:
    • •Female
    • •Obesity
    • •Diabetes
    • •High Cholesterol
    • •OCP/hormone replacement
    • •Pregnancy
    • •“fair, fat, and forty”
  45. Pigmented Gall Stones
    • •Less common
    • •Typically from hemolysis
    • •Sickle cell anemia
    • •E. coli infection
  46. Biliary Colic
    • •Due to spasms
    • •Gallstone blocks the cystic duct
    • •RUQ pain after eating high fat meal
  47. Cholecysectomy
    •Usually done laparascopically “lap chole”

    •General anesthesia

    •Approx ½ inch incision made near umbilicus

    •three other quarter to half inch incisions

    • Four narrow tubes “laparoscopic ports” placed through incisions

    • Laparoscope inserted through umbilical port

    • Instruments inserted through other ports
  48. Cholecysectomy Post Op
    •Pain Management

    •Referred rt shoulder pain common (r/t gas used in surgery)

    •Turn (at least q 2h), cough, and deep breathe until ambulating

    •Bandages on small puncture sites can be removed 1 day post op

    •patient can shower

    •Monitor sites for drainage, redness, s/s infection

    • •Most patients will go home next day so teaching crucial
    • •Encourage patients to ambulate/add activity gradually
    • •Lift nothing heavier than gallon of milk for 2 weeks
    • •May return to work (depending on what they do) 1-2 weeks
    • Diet recommendations:
    • •Low fat
    • •Smaller, evenly spaced meals tolerated better
    • •Gradually increase fiber in diet
    • •Monitor for s/s infection at incision sites
  49. Post Cholecystectomy Problem/Interventions:
    • Diarrhea
    • •With no gallbladder to store bile, bile is less regulated
    • •Meal (esp. fatty) can trigger release of bile directly to GI tract --> stimulates colon
    • •Frequent watery diarrhea esp. immediately after meals
    • •Can be embarrassing and troubling to patients
    • •bile sequestrants
    • •Cholestyramine (Questran, etc.)
    •     Taken after meal –powder mixed in water
    • •Recommend food diary might be helpful
    • •Can identify offending foods
  50. Causes of Acute Pancreatitis
    • •Alcohol – most common cause
    • •Onset may follow binge drinking
    • •Always inquire about ETOH use in history
    • Other causes:
    • •Very high triglyceride level > 1000
    • •Stone lodged in pancreatic duct
  51. Clinical Manifestations of Acute Pancreatitis
    • •Epigastric pain – mild to severe
    • •May radiate to back or flank
    • •Pain worse when supine, better when sitting
    • •May have fever, tachycardia, jaundice

    • Labs:
    • •Amylase: elevated, peaks by 3 days, resolves 1 week
    • •Lipase: elevated, peaks by 24 hrs, resolves by 2 weeks
    • •Nausea/vomiting
    • •Hypocalcemia
    • •BUN may be elevated or high normal r/t dehydration
  52. Acute Pancreatitis Complications

    •Pleural effusion




    • •Hemorrhage into peritoneum
    • •Cullen’s sign – bruising around umbilicus
    • •Grey Turner’s sign – bruising at flank
    • •Tetany (caused by hypocalcemia)

    • •Can progress to
    •    Pseudocyst formation
    •    Necrosis
    •    Multiorgan System Failure
  53. Management of Acute Pancreatitis
    • •Pancreatic rest → decreasing enzyme production
    •    -NPO
    •    -May have NG tube ordered  (Newer research and trends discourage NG tube/suction unless nausea/vomiting severe)
    •    -Diet advanced SLOWLY

    •Low fat diet essential, high protein

    • •Pain Management
    •   -DO NOT use Morphine!
    •   -Morphine can cause spasm of Sphincter of Oddi 

    •Fluid Replacement

    •Antibiotic therapy may be ordered

    •Pain assessment and control

    •Medicate for nausea/vomiting if necessary

    •Management of NG tube (check to see if in place)

    •Strict I & O

    •Monitor for signs of hypocalcemia

    •Lung sounds, pulse oximetry

    • •Monitor lab values:
    •    -Amylase, lipase
    •    -Liver function tests
    •    -WBC
    •    -BUN
    •    -Electrolyte levels
  54. Chronic Pancreatitis
    •May follow acute pancreatitis

    •May occur without history of an acute condition

    • •Two major types
    •    -Chronic obstructive pancreatitis
    •    -Chronic nonobstructive pancreatitis
  55. Chronic Obstructive Pancreatitis CAUSES
    • •Associated with biliary disease
    • Most common cause of this type:
    • Inflammation of the sphincter of Oddi associated with cholelithiasis

    • •Other causes include
    •    -Cancer of ampulla of Vater, duodenum, or
    • pancreas
  56. Clinical Manifestations of Chronic Pancreatitis
    • •Abdominal pain located in the same areas as in acute pancreatitis
    • •Heavy, gnawing feeling; burning and cramplike
    • •Abdominal tenderness
    • •Malabsorption with weight loss
    • •Mild jaundice with dark urine
    • •Steatorrhea
    • •Weight loss
    •    -Due to malabsorption
    •    -Eating may exacerbate symptoms
    • •Frothy urine/stool
    • •Diabetes mellitus
    • (Inability of diseased pancreas to secrete enough insulin)
  57. Chronic Pancreatitis Management
    • •Pain management
    • •Supplemental pancreatic enzymes (pancrelipase)
    • •To combat malabsorption
    • •Low-fat diet
    • •Avoid alcohol
    • •Management of diabetes if present
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