hepatobiliary Flashcards
hepatobiliary disorders
cholecystitis, cholelithiasis, jaundice, portal HTN, ascites, hepatic encephalopathy, esophageal varices, cirrhosis, hepatitis
cholecystitis
inflammation of the gallbladder; acute or chronic; majority of acute cases are calculous cholecystitis
acalculous cholecystitis
inflammation without obstruction by gallstones
cholecystitis manifestations
pain, tenderness, rigidity of RUQ; may radiate to midsternal area or right shoulder; accompanied by N/V if acute
cholelithiasis
aka gallstones; calculi which are conatituenta of bile (75% of cases are made of cholesterol); more prevalent with increasing age; 2-3x more common in woment
risk factors for developing cholelithiasis
CF, DM, frequent weight changes, estrogen therapy, obesity, rapid weight loss
clinical manifestations of cholelithiasis
may or may not be present; epigastric distress, abdominal distention, biliary colic, jaundice, dark urine, gray stool, vitamin deficiency (ADEK), vague RUQ/abdominal pain, pain may follow high fat meal
detecting cholelithiasis done via…
magnetic resonance cholangiopancreatography (MRCP) that can detect biliary tract obstruction
managing cholelithiasis
supportive care consists of rest, IV fluids, NG suction, analgesics, low fat diet (initially low fat liquid only); nonsurgical/surgical- lithotripsy is temporary solution infrequently used; laparoscopic cholecystectomy once s/s resolve; pharmacological agents to dissolve stones over months are rarely effective and recurrence is high
interventions for cholelithiasis
post op- low fowlers, IV fluids, NG suction, clear fluids to soft dieat as bowel sounds return; pain relief, monitor resp. status, skin integrity and promotion of biliary drainage, nutritional status, monitor for complications such as infection or disruption in GI tract (anorexia, vomiting, fever, distension), educate pt on wound care diet resuming activity and pain management
hepatic dysfunction
can be acute or chronic; chronic is the 12 leading cause of death in young-middle aged adults (40% d/t alcohol abuse); caused by infection, cirrhosis, liver failure d/t alcohol, fatty liver disease (nonalcoholic fatty liver disease or nonalcoholic steatohepatitis)
clinical manifestations of hepatic dysfunction
jaundice, ascites, edema, N/V, loss of appetite, weight loss, encephalopathy, hand tremor (asterixis), easy bruising/spider angioma, HLD
hepatic dysfunction risk factors
excessive/prolonged alcohol intake, obesity 9excessive fat deposition), viral hepatitis, certain meds (NSAIDs), comorbidities like DM HTN autoimmune hepatitis; toxin exposure, old ager/genetic predisposition, unhealthy diet/sedentary lifestyle
jaundice types
pre-hepatic- excessive breakdown of RBC overwhelms liver ability to process bilirubin; hepatic- livers impaired ability to process bilirubin, occurs in hepatitis cirrhosis and drug induced liver injury; post-hepatic- obstructive, blocked bile flow from liver to intestine that commonly occurs with gallstones tumors and bile duct disorders
s/s of jaundice
yellowing of skin/eyes, dark urine d/t excess bilirubin excretion, pale/clay colored stool d/t lack of bilirubin in GI tract, pruritis; may include symptoms of hepatomegaly, splenomegaly, abd pain, fatigue/weakness, cognitive changes, and bleeding
portal HTN
increased BP within portal venous system which carries blood from digestive organs to live for detoxification, caused by cirrhosis, thrombosis, hepatitis, fatty liver disease, splenomegaly; diagnosed with imaging (US, CT, MRI), endoscopy for detecting varices, labs to assess liver function
complications of portal HTN
varices- vessels developed in esophagus and stomach from increased pressure that can rupture and cause severe bleeding; ascites- increased pressure leads to fluid leakage from blood vessels into abdominal cavity; hepatic encephalopathy- elevated toxins bypassing liver can affect brain function
managing portal HTN
treat the underlying liver disease, medication to reduce pressure, endoscopic procedures to address varices, severe cases require liver transplant
portal HTN interventions
monitor VS and fluid balance, assess/manage variceal bleeding via vasoconstrictors, maintain airway and prevent asp., monitor neuro status (admin lactulose), manage ascites with diuretics and sodium restriction, nutritional support, psychosocial support, pt/fam education
ascites clinical manifestations
increased abdominal girth, rapid weight gain, shortness of breath
ascites nursing interventions
negative sodium balance to reduce fluid retention (2g), administration of diuretics and monitoring fluid/electrolyte balance, prepare for paracentesis (up to 5-6L removed)
transjugular intrahepatic portosystemic shunt
cannula threaded through portal vein by transjugular route and placed between portal circulation and hepatic vein; decreases sodium retention and prevents recurrence of fluid accumulation that would result in ascites
esophageal varices
varicosities developed from elevated pressure in veins that drain into portal system; prone to rupture and often cause massive hemorrhage; first hemorrhage has mortality rate of 10-30% and is one of the leading causes of death in pt with cirrhosis
manifestations of esophageal varices
asymptomatic unless bleeding; otherwise hematemesis, melena, gen. deterioration in mental/physical status, HX of alcohol abuse, s/s of shock, endoscopy used to find site of bleeding
managing esophageal varices
monitor for bleeding, admin of beta blockers to prevent first bleed by decreasing portal tension, admin of vasoactive drugs before endoscopy if bleeding, endoscopic sclerotherapy
hepatic encephalopathy
accumulation of ammonia and other toxic metabolites in blood d/t hepatic insufficiency and portosystemic shunting; early signs are mental changes and motor disturbances; late signs are constructional ataxia, asterixis and fetor hepaticus
assessment of hepatic encephalopathy
EEG, changes in LOC, potential seizures, fetor hepaticus, monitor fluid electrolyte and ammonia levels
4 stages of hepatic encephalopathy
- normal level of consciousness with periods of lethargy and euphoria, reversal of day night sleep patterns; 2. increased drowsiness disorientation, inappropriate behavior, mood swings, and agitation; 3. stuporous, difficult to rouse, sleeps most of time, marked confusion, incoherent speech; 4. comatose, may not respond to painful stimuli
managing hepatic encephalopathy
eliminate precipitating cause, lactulose to reduce serum ammonia, IV glucose to minimize protein catabolism, protein restriction, reduction of ammonia from GI tract via suction enema and oral antibx, discontinue sedatives analgesics and tranquilizers, monitor or treat complications/infections
hepatic encephalopathy interventions
assess LOC changes, IOs, bodyweight, VS q4, serial daily ammonia levels and electrolytes, restricted dietary protein, GI tract suctioning, administer lactulose, monitor therapeutic response, monitor resp. status
esophageal varices interventions
safe environment, prevent injury, prevent bleeding and infection, admin prescribed treatments, monitor for complications, encourage deep breathing and position changes, educate pt and fam
treatment of bleeding varices
treat for shock, admin O2, IV fluids, electrolytes, volume expanders, blood and blood product, vasopressin, somatostatin, octreotide (decrease bleeding), nitroglycerin and vasopressin combo to reduce coronary vasoconstriction, propanolol and nadolol to decrease portal pressure, balloon tamponade
hepatic cirrhosis
alcoholic: scar tissue characteristically surrounds portal areas; post-necrotic: broad bands of scar tissue; biliary: scarring occurs in the liver around bile ducts; hemochromatosis related; NAFLD/NASH related
manifestations of compensated cirrhosis
ankle edema, firm and enlarged liver, intermittent mild fever, palmar erythema, splenomegaly, vascular spiders, vague morning indigestion
uncompensated cirrhosis manifestations
ascites, clubbing of fingers, continuous fever, epistaxis, hypotension, jaundice, muscle wasting, purpura
cirrhosis interventions
promote rest, improve nutrition, provide skin care, reduce risk of injury, monitor/manage potential complications
cirrhosis complications
bleeding/hemorrhage, hepatic encephalopathy, fluid volume excess
liver transplant interventions
preop- support, educate, encourage (psychologically); postop- monitor for infection, vascular complications, respiratory and liver dysfunction, monitor closely; caregiver support
hepaptitis
viral- systemic viral infection causing necrosis and inflammation of liver cells with characteristic symptoms and cellular/biochemical changes; A/E: fecal-oral route; B/C: bloodborne; D: only people with B are at risk; nonviral- d/t drugs and medications
hepatitis A
spread via poor hand hygiene; oral-fecal route; incubates in 2-6 weeks; ill ness last 4-8 weeks; acute only, doe not progress to chronic disease
s/s of hepatitis A
asymptomatic, GI s/s, jaundice, dark urine, joint pain, fever, fatigue
managing hepatitis A
prevention via handwashing, vaccine, immunoglobulin for contacts to provide passive immunity; bed rest during acute, nutritional support
hepatitis B
transmitted via blood, saliva, vaginal secretions; is sexually transmitted; transmitted to infant at time of birth; acute and chronic result in cirrhosis and liver cancer; incubation is 1-6 months; risk factors are healthcare workers, birth, tattoo, IV drug use
s/s Hepatitis B
flu like symptoms, arthralgias, jaundice, dark urine
Hepatitis B diagnostic
+HBsAg/ anti-HBs
managing hepatitis B
chronic meds: alpha interferon (subq) and antiviral agents (oral entecavir ETV + tenofovir TDF), bed rest, nutritional support, hand hygiene, vaccine of those at high risk, vaccination of infants; passive immunity for those exposed, standard precautions and infection control measures, screening of blood/blood products
hepatitis C
transmitted via IV drug use, sex, and blood transfusions prior to 1992; most common bloodborne infection; 1/3 cause liver cancer (need transplant), incubates in 15-160 days, can be acute or chronic, risk factors are healthcare workers IV drug users and multiple sexual partners
diagnostic for hepatitis C
anti-HCV (chronic)
s/s of hepatitis C
flu like symptoms, jaundice, dark urine
managing hepatitis C
antiviral meds like DAA, avoid alcohol, prevention via public health programs to decrease needle sharing, screening blood supply, safety needles for healthcare workers
hepatitis D
only occurs with hep B; transmitted via blood, sex, IV drug use; HD/blood transfusions; can be acute or chronic;
diagnostic for hepatitis D
anti HDV, HDsAg
treatment for hepatitis D
interferon alfa
hepatitis E
fecal- oral route, contaminated water; incubates in 15-65 days; resembles hepatitis A; self-limiting, abrupt onset, not chronic; prevention via good hygiene and handwashing
other liver disorders are…
nonviral- toxic hepatitis and drug-induced hepatitis; fulminant hepatic failure can be caused by hepatitis
liver transplant education
educate on long-term measures to promote health, adhere to therapeutic regimen, side effect of immunosuppressants; educate on s/s that indicate problems that require consult with transplant team; importance of follow up labs and appointment with transplant team
ascites
caused by portal HTN which increases capillary pressure and causes obstruction of venous blood flow; failure to metabolize aldosterone causing increasing fluid and sodium retention and intravascular fluid; decreased albumin synthesis causing decreased serum oncotic pressure; movement of albumin causes fluid shifts to peritoneal cavity; vasodilation of splanchnic circulation
