Liver Flashcards
Biliary System
_____ + ____ = _____ , empties into small intestine (helps digest fats after a meal)
Hepatic duct (liver) + cystic duct (GB)=common bile duct
Hepatic Blood Supply
Largest visceral organ~dual blood supply:
The liver can store up to ___ mL blood to use during shock and hypovolemia.
Where does portal HTN occur?
portal vein 80% and hepatic artery (20%).
450
Portal hypertension is high blood pressure in the portal vein
Metabolic functions of the liver
Able to regenerate, metabolizes drugs (first pass effect: oral meds absorbed from Gi tract, metabolized by liver, may need to be given different route or larger dose),
stores Vit ADEK, maintains blood glucose levels,
synthesizes plasma proteins (albumin),
degrades toxins converts ammonia to urea excreted in urine),
synthesis of fibrinogen and coagulation factors;
Makes bile 600-1200 ml/day
____: bile
_____: slowing or stoppage of bile
______: gallstones
_____: inflammation of gallbladder
_____: gallbladder removal
_____: endoscopic retrograde cholangiopancreatography
“chole”
Cholestasis
Cholelithiasis
Cholecystitis
Cholecystectomy
ERCP
Diagnostic Evaluation
Liver function tests (LFTs)
Alanine transaminase (ALT): enzyme, an increase indicates liver damage.
Aspartate transaminase (AST): enzyme, an increase indicates liver or muscle damage/disease.
Alkaline phosphatase (ALP): an enzyme in liver, bile ducts, and bone; an increase indicates liver damage or blocked bile duct, or bone disease.
Liver function tests
These enzymes help metabolize ____
Liver function tests may look normal with _____
proteins
cirrhosis
Other labs
____: protein, made in the liver; _____ levels with liver damage or disease.
______: protein made by the liver; ____ in liver damage/dz ; monitor ____
______: a substance produced during the normal breakdown of red blood cells. ____ in liver damage/dz and certain anemias.
____: (NH3), a byproduct of amino acid catabolism. _____ with hepatic encephalopathy.
Albumin
decreased
Prothrombin time (PT)
prolonged
INR
Bilirubin (Tbili)
Increased
Ammonia
Increased
_____ helps keep your fluid in your bloodstream and binds with hormones and fatty acids
Need ____ for synthesis of PT/Internationalized Normalized Ratio (INR), calculated based on the PT test result, for people who are receiving the anticoagulant warfarin.
Prothrombin time (PT)
is a test that helps evaluate your ability to appropriately form blood clots. When the PT is ____, it takes longer for the blood to clot~
____ risk (TX with blood components: ________).
What is treatment for Coumadin overdose?
Albumin
Vit. K
high
hemorrhagic
clotting factors, platelets, plasma. Vit K
Vit. K
Labs help with identifying disease process & stagesFor example…
48 y.o. client with acute hepatitis B: elevated ALT, AST, bilirubin,& HBsAG
10 y.o. client with bone disease: elevated ALP, no liver disease
62 y.o. with end-stage cirrhosis, hepatorenal failure, and encephalopathy: normal ALT*, elevated BUN, creat, elevated ammonia, decreased albumin, prolonged PT
*ALT and AST return to normal when liver cells are no longer able to create an inflammatory response
Diagnostic Evaluation continued
Liver biopsy
US
CT
MRI
Endoscopy
Laparoscopy
Liver bx: ____ or ____
US guided helpful to diagnose If lab tests nondiagnostic.
______ complication
Health hx impt:
percutaneously or laprascopic.
Peritonitis
med hx, OTC, herbal, hx etoh and drug use (IV), occupational, recreational, travel hx, any exposure to hepatotoxic substances or infectious agents.
Manifestations of Hepatic Dysfunction
Jaundice
Portal HTN
Hepatic encephalopathy & coma
Manifestations of Hepatic Dysfunction 1. Jaundice
High levels of ____ in the blood
Jaundice: serum bilirubin levels > ____ mg/dL
Different causes
Can cause :
bilirubin in the blood (hyperbilirubinemia)
2-2.5
pruritus, urine bilirubin, and elevated liver function tests
Bilirubin is a substance produced during the normal breakdown of RBC.
It’s a waste product and that’s what causes the color.
Sometimes first sign; affinity for elastic tissues:
Causes:
sclera,mucous membranes.
prehepatic (hemolytic anemia)
intrahepatic (hepatitis, cirrhosis), posthepatic ( gallstones)
Types of jaundice:
Physiologic (newborn): immature gut, put under light, light absorbed by the skin and changes bilirubin into products which can pass thru urine
hepatocellular urine urobilogen, bilirubin excreted in urine
obstructive jaundice (gall stones : cholelithiasis)
Manifestations of Hepatic Dysfunction
2. Portal HTN
____ blocks the flow of blood through the liver and slows its processing functions portal HTN
Consequences:
Scar tissue
Ascites
Esophageal varices
Ascites treatment
Low Na diet
Diuretics (spironolactone)
Albumin
May require paracentesis
Nursing management
What kind of diuretic is spironolactone? first line therapy Potassium sparing, antagonizes aldosterone – reduces sodium retention
Why albumin? Increases intravascular fluid
Paracentesis complications? depending on cause…fill right back up, need paracentesis monthly, then weekly…
What is SBP? Spontaneous bacterial peritonitis- infection
Hyperaldosteronism –
Paracentesis- may need ultrasound, have the urinate prior to, may just fill back up
Nursing mgmt.- monitor vital signs (BP may drop), I&O, daily weights, resp. status,
Bedrest helps
Ascites is a result of portal hypertension
Esophageal & gastricvarices
treatment
Band ligation (next slide)
Administration of FFP, PRBC, PPI, Vitamin K, lactulose, antibiotics, meds to stop bleeding
Sclerotherapy
Balloon tamponade
Shunting procedures (TIPS)
Bleeding esophageal varices life-threatening!!
Observe for any signs of bleeding from varices, such as:
hematemesis & melena, s/symptoms of hypovolmic shock
Endoscopicvariceal ligation (EVL)
Manifestations of Hepatic Dysfunction
3. Hepatic encephalopathy & coma
Accumulation of ____
Liver unable to convert ______ to be excreted, crosses the blood-brain barrier
Changes in:
Treat with:
Stages of hepatic encephalopathy table 43-3.
neurotoxins
ammonia to urea
Ammonia toxic! Lactulose traps and expels ammonia
neurologic and mental responsiveness, asterixis (flapping tremors) and fetor hepaticus
lactulose (orally, rectally as an enema, or NGT)
Lactulose- lowers ammonia levels. Makes them deficate
Other Manifestations of Hepatic Dysfunction
Edema and bleeding
Vitamin deficiency
Metabolic abnormalities
Pruritus and other skin changes
Hepatitis
An acute or chronic inflammation of the liver resulting in lysis of ______
Causes:
infected hepatocytes
Viral (A, B, C, D, E, G and mononucleosis, cytomegalovirus, and rubella)
Autoimmune
Nonviral: toxic and drug-induced hepatitis
Clinical manifestations of hepatitis
Acute phase (1-4 mos)
Convalescent phase (2-4 mos)
Maybe asymptomatic but period of maximal infectivity!!!!!!!!!!
Malaise, fatigue, anorexia, weight loss, nausea/vomiting, RUQ abdominal pain, taste and smell alterations
headache, low-grade fever, arthralgias, skin rashes
Icteric (jaundice) or anicteric
May have dark urine and/or light or clay-colored stools
Pruritus
Hepatomegaly, lymphadenopathy, and sometime splenomegaly
Convalescent phase (2-4 mos)
Malaise and fatigue
Hepatomegaly
Hepatitis A Virus (HAV)
Mode of transmission
S&S
Person at risk
Chronic infection?
Vaccine?
HAV is found in the stool and blood of people who are infected. WASH HANDS!
NOT CHRONIC - clears on its own
YES VACCINE
Hepatitis B Virus (HBV)
Hepatitis B is spread when blood, semen, or other body fluids from a person infected with the virus enters the body of someone who is not infected. This can happen through sexual contact; sharing needles, syringes, or other drug-injection equipment; or from mother to baby at birth.
Mainly blood!
Can be chronic
Treat with antiviral meds
Yes Vaccine
Hepatitis C Virus (HCV)
causes
treatment
CDC recommendation: all adults born during 1945-1965 receive one-time testing for Hepatitis C Virus (HCV)
blood transfusions
sharing needles & other drug taking equipment
mother to baby transmission
body piercing
tattooing
unprotected sex with multiple partners
Yes chronic
Yes treatment, but expensive
NO VACCINE
Diagnostic Testing for Hepatitis
Test for specific antigen or antibody to determine form of hepatitis (for example, Anti-HAV IgM is specific for acute infection of HAV)
Viral genotype testing done in patients undergoing drug therapy for HBV and HCV
Liver function tests
All hepitits can become cirrhosis and liver failure
Collaborative Care for Acute Hepatitis
Rest
Adequate nutrition
Avoid alcohol
Notification of possible contacts
Pharmacologic Therapy for Chronic Hepatitis
Goal:
Monitor:
Goal: suppress viral replication and prevent complications
Monitor for anemia, leukopenia, and depression with drugs
Complications of Hepatitis
Most patients with acute viral hepatitis recover completely
Complications that can occur:
Acute liver failure
Chronic hepatitis (some HBV and majority of HCV)
Cirrhosis of the liver
Hepatocellular carcinoma
Autoimmune, Genetic, Metabolic Diseases of the Liver
Autoimmune hepatitis
Wilson’s
Hemochromatosis
NAFLD (nonalcoholic fatty liver disease) and NASH (nonalcoholic steatohepatitis)
NASH Increasing with obesity epidemic.
Nonviral Hepatitis
Toxic Hepatitis
Chemicals
Early treatment and removal of causative agent
No effective antidotes!!!!
Signs/symptoms: early (resembles viral hepatitis) to toxic (fulminant hepatic failure)
When hepatitis is caused by an autoimmune disorder or drug, it cannot be spread person to person
Nonviral HepatitisDrug-induced
alcohol
anabolic steroids
tylenol
Other meds: isoniazid, halothane, methyldopa, certain antibiotics, antimetabolites, & anesthetic agents; polypharmacy with older adults
What is the recommended maximum dosage of acetaminophen recommended in 24 hours? And for patients with known liver disease?
4 g in 25 hr
If you have liver issues, no more than 3 g
Cirrhosis
-
Progressive disease
In clinical notes you will read about “compensated versus decompensated.” How do you interpret that?
Cells attempt to regenerate but are disorganized
Diffuse fibrosis forms constrictive bands
Formation of nodules and scarring
Compensated: When you don’t have any symptoms of the disease, you’re considered to have compensated cirrhosis.
Decompensated: When your cirrhosis has progressed to the point that the liver is having trouble functioning and you start having symptoms of the disease, you’re considered to have decompensated cirrhosis
Cirrhosis Risk Factors
alcohol
malnutrition
viral hepatitis
biliary obstruction
obesity
right-sided heart failure
CirrhosisSigns and symptoms
early
late
Early manifestations:
Often no signs until disease is far advanced
Fatigue
Later manifestations:
Jaundice
Spider angiomas and palmar erythema
Thrombocytopenia, leukopenia, anemia
Coagulation disorders (bleeding tendencies)
Endocrine problems
Peripheral neuropathy
So remember all those functions of the liver, these are the s/sx you’ll see as it progresses. 70% of liver could be damaged before you show signs,
What lab is elevated with jaundice?
Endocrine problems- sex hormones- estrogen or testosterone increases
What causes spider angiomas and palmar erythema with cirrhosis?
You see how bulging and torturous those vessels are…imagine the esophagus with esophageal varices, hemorrhoids…
Circulating estrogen
Cirrhosis Diagnostic Studies
Liver function studies*
Liver ultrasound
Liver biopsy
*ALT and AST return to normal when liver cells are no longer able to create an inflammatory response
Cirrhosis Complication
Portal hypertension
varices (esophageal, gastric, hemorrhoids, superficial abd. veins)
ascites and edema
splenomegaly
hepatic encephalopathy
hepatorenal syndrome
Hepatorenal syndrome: Progressive azotemia-increased serum creatinine-oliguria; renal failure can be reversed by ___________
liver transplantation
Collaborative Carefor Cirrhosis
Goal: slow the progress of cirrhosis, prevent and treat any complications
Management of ascites
Prevent bleeding and hemorrhage from esophageal and gastric varices
Reduction of ammonia formation with hepatic encephalopathy
Diet high in calories, high CHO, moderate to low levels of fat; pt with ascites-low-sodium diet; protein restriction rare
Initiate appropriate referrals
Nursing Care for Patients with Cirrhosis
Dyspnea
Fatigue
Anorexia, n/v
Jaundice, pruritus
Edema, ascites
Monitor electrolytes (diuretics)
Bleeding tendencies
Hepatic encephalopathy
Fatigue- cluster care
Anorexia- food preferences
Edema, ascites- heart sounds, daily wights, electrolytes
Hepatic encephalopathy- safety
Acute Liver Failurefulminant hepatic failure
causes:
s&s
complications
treatment
Causes: drugs (acetaminophen), HBV
S/sx: change in mentation, jaundice, coagulation abnormalities, encephalopathy
Complications: renal failure, cerebral edema, sepsis
Treatment
People with acute liver failure are often treated in the intensive care unit of a hospital in a facility that can perform a liver transplant, if necessary. Your provider may try to treat the liver damage itself, but in many cases, treatment involves controlling complications and giving your liver time to heal
Liver Cancerhepatocellular cancer
___________ most common cause
_____ carcinoma is more common than ______ carcinoma
Manifestations often _____
Tx: hepatic resection of the tumor, different types of ablation, chemotherapy, or transplantation
Cirrhosis caused by chronic hepatitis C
Metastatic
primary
insidious
Liver Transplantation
Rigorous pre-surgery screening
Performed using both deceased and live donor livers
Split liver transplant (peds*)
Postop complications
Immunosuppressive therapy
Monitor for acute graft rejection (usually between 4 and 10 days after surgery).
*Pediatric patients receive partial liver transplant due to size; generally very sick, stay intubated for awhile, may have to go back to surgery to close belly to achieve better approximation of edges.
