Hepatobilliary

• •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.

Liver Inflammation

• 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

• Infectious Hepatitis
•    •Viral – A, B, C, D, E, G
•    •Less common infections
•      -Bacterial, protozoal, fungal, mycoplasmal

• Noninfectious Hepatitis
•    •Autoimmune
•    •Drug-induced

• •Jaundice 
• •Dark Urine
• •Fatigue/malaise
• •Light Stools
• •Abdominal Pain 
• •Joint pain
• •hepatomegaly
• •Anorexia
• •Nausea
• •Vomiting
• •Diarrhea
• •Pruritis

Acute (icteric stage: jaundice)

Convalescent Hepatitis

• CHRONIC hepatitis
• •With B, C
• •Detectable RNA levels can fluctuate
• •In hepatitis B, the HbSAb is not seen

• •Fecal/Oral transmission
• •Anti-HAV antibodies
•    IgM , IgG
• •Vaccine x 2 doses, 6 mos apart

• •Uncommon in US
• •endemic to SE Asia
• Transmission: drinking contaminated water

• •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

current acute or chronic infection

Successful vaccination OR prior resolved infection

• hepatitis B core antibody
• Intracellular, signifies current or past infection

Signifies presence of active virus

• •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

• •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

Self Limiting: Manage symptoms

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)

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)

Jaundice

• •Hemolytic
• •Hepatocelluar
• •Obstructive

• •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.

• •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.

• •Autoimmune hepatitis
• •Wilson’s disease
• •Hemochromatosis
• •Primary biliary cirrhosis
• •Nonalcoholic fatty liver disease and nonalcoholic steatohepatitis (NASH)

• •May be acute or chronic
• •Parenchymal necrosis from heavy alcohol ingestion.
• •Most frequent cause of 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.

• •Excessive alcohol ingestion.
• •Viral Hepatitis for postnecrotic.
• •Use of drugs
• •Acetaminophen
• •Methotrexate
• •Isoniazid
• •Hepatic Congestion-- via biliary blockage or invasion by fatty tissue

• •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

• •Monitor for complications
• •Maximize Liver function
• •Treat the underlying cause
• •Prevent Infection

• 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.

• 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.

• Sclerotherapy
• Transjugular
• Intrahepatic
• Portosystemic shunt   
• Vasopressin IV   
• Beta-Adrenergic 
• Blocking Agents   
• Balloon Tamponade

• Ascites
• Caused by:
• •Portal hypertension
• •Lowered plasma colloidal osmotic pressure
• •Sodium retention

• 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

• •Spironolactone (Aldactone)
• •Chlorothiazide (Diuril)
• •Furosemide (Lasix)

• Hepatic Encephalopathy
• Causes:
• •Liver’s inability to metabolize ammonia to form urea so it can be excreted.
• •Ammonia is a CNS depressant

• •Manifestations are neurologic-range from mild mental confusion to deep coma
• •Mortality is high among clients who progress into coma with hepatic failure

Neomycin

• •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

• •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

• •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

• •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.

Most common

• Risk factors:
• •Female
• •Obesity
• •Diabetes
• •High Cholesterol
• •OCP/hormone replacement
• •Pregnancy
• •“fair, fat, and forty”

• •Less common
• •Typically from hemolysis
• •Sickle cell anemia
• •E. coli infection

• •Due to spasms
• •Gallstone blocks the cystic duct
• •RUQ pain after eating high fat meal

•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

•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

• TEACHING:
• •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

• 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

• •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

• •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

•Pulmonary

•Pleural effusion

•ARDS

•Cardiovascular

•Hypotension

• •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

• •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

•May follow acute pancreatitis

•May occur without history of an acute condition

• •Two major types
•    -Chronic obstructive pancreatitis
•    -Chronic nonobstructive pancreatitis

• •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

• •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)

• •Pain management
• •Supplemental pancreatic enzymes (pancrelipase)
• •To combat malabsorption
• •Low-fat diet
• •Avoid alcohol
• •Management of diabetes if present