Week 10: Hepatic Fxn and Transplant Flashcards
Liver
largest GLAND in the boyd at 3-4 pounds
highly vascular wiht 4 different lobes
Where is the liver located
beneath the diaphragm and right upper quadrant
this is important since it is close to the GI tract where it gets nutrients and plays a key role in whether these are stored or not
About how much blood circulates in the liver and how much is stored in the liver
1.5 L circulate within the liver with 200-400 mL of blood being stored by it
Portal Vein
75% of blood to the liver goes through the portal vein which is NUTRIENT RICH OXYGEN POOR blood from the spleen, intestines, etc
Hepatic Artery
25% of blood to the liver is goes through the hepatic artery from the heart and is NUTRIENT POOR OXYGEN RICH
What happens to the blood entering the liver lobules from the portal vein and hepatic artery
The blood mixes in the liver lobules –> through the hepatic veins –> inferior vena cava –> heart
Functions of the Liver
- Glucose Metabolism
- Ammonia Conversion
- Protein Metabolism
- Fat Metabolism
- Vitamin and Iron Storage
- Bile Formation
- Bilirubin Excretion
- Drug Metabolism
How does the liver do glucose metabolism
it helps maintain a stable blood glucose by storing glucose as glycogen and then converting it to glucose when needed
What is the ammonia conversion function of the liver
ammonia is what is left over after protein breakdown
liver takes ammonia and converts it to urea for excretion
Why are ammonia levels super important
ammonia can be toxic so levels are important to look at with hepatic disorders
What is the protein metabolism of the liver like
the liver makes proteins needed for clotting (so liver issues can lead to bleeding issues)
This means Vitamin K intake is important as it is needed to make factors in the liver
What does the liver do to fat
it stores fat and breaks it down to be used as energy, but too much can cause a fatty liver
What sort of vitamins adn minerals are stored in the liver
Vitamin A, B, D, Iron and Copper
Vitamin K is used a lot to make clotting factors here as well
Bile
a substance made and released in the liver to the gallbladder (storage)
when needing to digest fats the bile can emulsify them to help move them out of the body
Bilirubin
what is left once RBCs die and break down
it is carried into intestines and excreted in stool to cause the brown coloring
can be excreted in urine but the liver is working to get rid of the RBCs as they die and dispose of it in a timely manner
The liver is basically a ___ of the body
gatekeeper (think first pass)
More than ___% of the liver can be damaged before changes become abnormal
70
What sort of Liver Lab studies are done and seen with abnormal livers
CEA - presence can indicate cancer
PT increase - prolonged clotting = more bleeding
Protein Studies - Low levels means liver isnt making them
ALT, AST = Liver damage and enzymes release into blood
Bilirubin, Cholesterol (decreased in liver disease), and Ammonia (damage means higher as it usually becomes urea)
Liver Biopsy
Needle aspiration through the abdominal wall for analysis
A transvenous version can be done with fluoroscopy for real time rays guiding through the hepatic vein to the liver
Complications of a Liver Biopsy
bleeding
potential for bile peritonitis if gall bladder damaged
What needs to be done prior to a liver biopsy
coagulation studies since risk for bleeding is so high
we may even want to wait until pt is clear with meds to prevent bleeding
Blind Needle Aspiration
a version of liver biopsy where they are ultrasound guided or done laproscopically
used with severe ascites or abnormal anticoagulation studies
What needs to be done after a liver biopsy
Pt lay on right side for several hours to push liver against the costal margin for compression (can use a pillow)
2-3 hours of this
avoid coughing or straining
How often should you check VS after a liver biopsy
every 10-15 min for the first hour then every 30 minutes for the next 1-2 hours
Things neede after a liver biopsy
right side, pillow, dressing, 2-3 hours
avoid coughing and straining
VS protocol
avoid heavy lifting for a week
General CAUSES of Liver Dysfunction
Acetaminophen Overdose / Prescription Meds like NSAIDS, antibiotics, anticonvulsants
Herbal supplements (Skull cap, penny roal)
Hepatitis and other viruses like CMV, Herpes, and Epstein Barr
ETOH and Toxins
Autoimmune Diseases
Diseases of the veins in the liver
Metabolic Disease
Cancer
What are some general s/s of liver dysfunction
pallor
jaundice
muscle atrophy
edema
vitamin deficiencies
skin excoriation r/t itching
petechiae
ecchymotic areas
spider angiomas
palmar erythema
neuro changes
male specific changes
unstable blood glucose
What causes jaundice?
When the body cannot excrete bilirubin it will leek into the dermal layers causing the coloring
Also since it seeps onto the peripheral nerves it causes scratching and itching
Why does liver dysfunction cause muscle atrophy
because there is decreased ability to make protein
Why does edema occur from liver dysfunction
because of low protiein levels
proteins hold water in the bloodstream and prevent it from leaking out, but if these levels are low then water will begin third spacing
Why does petechiae occur with liver disease
broken capillaries
its because there is a low platelet count associated with it
What causes the ecchymosis seen with liver dysfunction
the increased clotting time since the lvier cannot make the clotting factors
Spider Angiomas
abnormal collection of blood vessels near the surface of the skin
the liver cannot metabolize the circulating estrogen causing dilation of the vessels and causing this to form
What about liver dysfunction causes the palmar erythema
red itchy hands
due to estrogen which is dilating the vessels
What sort of changes occur in males as a result of liver dysfunction
gynecomastia
testicular hypertrophy
(all due to hormone metabolism being improper)
What sort of neuro changes occur with liver dysfunction and why?
cognition issues, tremors, asterixis, weakness, slurred speech
It occurs because large amounts of ammonia build up and seep into the neuro system
Asterixis
s/s of hepatic encephalopathy/cirrhosis
the patient will hold the hand out and dorsiflex for a few seconds. If the patients hand begins flopping down and up it is a sign
“flapping tremor”
Child-pugh Classification
scale used to predict the outcomes of patients with liver disease
What is the total child-pugh score based on
5 Parameters:
Ascites
Bilirubin
Albumin
PT
Encephalopathy Stage
The ____ the child-pugh score the ___ the prognosis
higher; poorer
What are the points like in the child-pugh classification
Grade A = score of 1-6
Grade B = Score of 7-9
Grade C = Score of 10-15
Each category is 1,2, or 3 points from absent, slight to moderate
The higher the score the worse
What is the most common type of jaundice with liver disease
hepatocellular/ OBSTRUCTIVE jaundice
4 types of Jaundice
Hemolytic
Hepatocellular
Obstructive
hereditary
Hemolytic Jaundice
Increased destruction of RBCs - maybe liver is fxning but bilirubin isnt secreted as fast as breakdown is
could be from a hemolytic transfusion rxn with a high level fo free/unconjugated bilirubin
At what level of bilirubin is the CNS beginning to have effects on it
20-25 mg/dL
Hepatocellular Jaundice
Liver cells are damaged so bilirubin cannot be cleared
Can occur with cirrhosis, hepatitis, and other dx of damaged liver
underlying pathology - so there may be anorexia, fatigue, malaise, weakness, weight loss
Hereditary Jaundice
Result of several inherited disorders characterized by an increase in unconjugated bilirubin
hereditary in nature
Obstructive Jaundice
bile duct occlusion from gall stones, tumors, or inflammation
bile backs up in intestines
intolerance to fatt foods, voiding orange foamy urine and clay colored stool
What are some interventions for Jaundice
soothing baths for itchiness
keeping naisl as short as possible
other ways of providing good skin care to the patient
Signs/Symptoms of Hepatocellular Jaundice
mild or severely ill
lack of appetite, NV, weight loss
malaise, fatigue, weakness
HA, chills, fever, infection
S/S of Obstructive Jaundice
dark orange brown urine
clay colored stools
dyspepsia and intolerance of fatsand impaired digestion
pruritis
General Consequences of Liver Dysfunction
ascites
esophageal varices
hepatic encephalopathy
hepatic coma
Portal HTN
associated with cirrhosis
increased pressure in the portal venous system from obstruction of blood flow into and through the damaged liver
Major consequences of portal HTN are __ and __
ascites and varices
Why can splenomegaly and thrombocytopenia occur with portal HTN
blood back up increases platelet pooling in the spleen increasing the size
this pooling also accounts for the worsening thrombocytopenia
Ascites
Shifting of fluid into the peritoneal cavity
manifests as distention and pressure can lead to an umbilical hernia
Why does ascites occur
combination of portal HTN and obstruction of blood flow through the damaged liver cells which causes SODIUM and WATER RETENTION leading to hypovolemia
Basically, if liver not working no proteins are broken down –> albumin synthesis and osmotic pressure decreases –> fluid shifts into peritoneal cavity
Diagnostic Findings for Ascites
SHIFTING DULLNESS - on percussion
Flank Edema
Fluid Wave
Shifting Dullness
percussion sound of ascites
the area of dullness changes moving supine to side lying
Abdominal Fluid Wave
a way to assess for ascites
place hands on the sides of the patients flank and strike one side of the flank
this will detect a wave with the other hand on the opposite side
What is the major complication of ascites
spontaneous bacterial peritonitis (SBP)
Spontaneous Bacterial Peritonitis
ascites fluid in the peritoneal cavity gets infected
there may be no clinical signs of this but if they do show it is worsening liver fnx, malaise, and fever
What is needed to diagnose spontaneous bacterial peritonitis
a pericentesis
What is the treatment for SBP
antibiotics and prophylactic antibiotics to prevent recurrence
Hepatorenal syndrome
a potential complication coming from SBP
if the SBP is untreated or v aggressive this syndrome can occur which is renal failure without any pathological changes to the kidney
Medical management of Ascites
- Low Sodium Diet
- Diuretics
- Bed Rest (Lay Down)
- Paracentesis
- TIPS
What is the salt limitation maximum with ascites
500 mg-2 G a day
What is important to teach about the low salt diet with ascites the patient may not realize
to avoid salt substitutes because they can have ammonia in them and if the liver is damaged it cannot get rid of them
Paracentesis
removal of fluid from the peritoneal cavity via a puncture or small incision to the abdominal wall under sterile conditions
no longer routine tx, but just dx and examination of fluid or for large ascites
done via ultrasound
What position should a patient be in during paracentesis
Upright to keep the fluid near the abdominal wall and promote easier puncture and removal of peritoneal fluid
Risk of paracentesis
risk of infection
risk for bleeding (esp with a compromised liver)
Pre-Op Paracentesis
Check Consent
Have Patient Void (comfort and prevent injury)
Monitor VS
Obtain weight and abdominal girth
Intra-Op Paracentesis
position as upright as possible
monitor VS
monitor for s/s of hypovolemia (pallor, tachycardia, hypotension)
Post-Op Paracentesis
Monitor for s/s of hypovolemia
obtain weight and abdominal firth
measure, describe, document fluid collected
assess puncture site for drainage (pressure dressing may be applied)
check and monitor neuro status
limit activity
fluid/lyte replacement (albumin) (to correct ineffective blood volume that can lead to sodium retention)
TIPS stands for
Transjugular Intrahepatic Portosystemic Shunt (Procedure)
Purpose of TIPS
decrease portal HTN which can contribute to ascites
done for refractory ascites (ascites not responsive to Na restriction or diuretics) and after several rounds of paracentesis
Big Risk of TIPS
considerable risk for encephalopathy
What happens during TIPS
cannula goes into a portal vein and an expandable stent is placed to serve as a shunt between portal circulation and the hepatic vein
this decreases sodium retention and improves renal response to diuretic therapy as a result
What are some of the procedures to treat ascites
Paracentesis
Diet and Diuretic
TIPS
Peritoneovenous Shunts (Denver, LeVeen)
Peritoneovenous Shunts
Drains or catheters permanently placed if patients have frequent ascites hx and dont need to keep getting paracentesis
prevents incisions and constant procedures needed
can also drain lung fluid
shunts fluid from the peritoneal cavity into systemic circulation (through the internal jugular vein or superior vena cava)
What is the issue with peritoneovenous shunts
they are hard to maintain long term
a liver transplant may ultimately be considered
Education for those with Ascites
defintion of ascites
rationale for low sodium diet, bed rest
medications (diuretics)
major complication (spontaneous bacterial peritonitis
paracentesis and TIPS
Things to monitor with ascites
abdominal girth q shift
daily weight
strict I&Os
fluid and electrolyte balances
respiratory status
s/s of encephalopathy
Most common cause of Ascites
cirrhosis
Main contributor to why ascites occurs
portal HTN
exact patho is unknown but sodium retention related to portal HTN is the key
What is the pathway of treatment for ascites
1st line: Sodium restriction diet and aldactone K sparing diuretic
2nd: may add loop diuretic like lasix
3rd - paracentesis
4th - TIPS / P Shunt
5 - liver transplantation
Varices
Another complication from liver disorders
Portal HTN occurs so the veins drain into the portal system and are subject to high pressure from the liver
this makes the veins distended, tortuous, and varicosities develop
can occur in the esophagus and stomach
More than 50% of ___ patients will develop varcies
cirrhosis
Why is a varicosity rupture a medical emergency
the patient can bleed out fast
plus with liver issues theres coagulation issues so its even faster than normal
What sort of things can cause a varices rupture/bleeding
heavy lifting
sneezing
coughing
vomtiting
reflux
straining
ASA
What are some of the manifestations of varices
hematemesis
melena
general deterioration of physical and mental status
s/s of shock - develop fast
What can happen if the s/s of shock from varices does not occur
then renal perfusion may be decreasing leading to ammonia levels rising high and leaving them at risk for encephalopathy
What diagnosis presence of varices bleeding
ENDOSCOPY
Also: CT, Barium Swallow, Angiography
What are some of the interventions for bleeding varices
ICU admission and transfer:
Balloon tamponade
vasopressin
sclerotherapy
banding
TIPS
How does a balloon tamponade help bleeding varices
a gastric balloon entered through the nsoe will inflate and sit in the stomach to compress varices in the esophagus
but it will need frequent suctioning
Why should there always be scissors bedside with a balloon tamponade
in case the tube slips or move you need to be able to cut the tube fast to prevent asphyxiation
Why is cardiac monitoring important with a balloon tamponade
the placement of the tube can stimulate the vagal nerve so it could cause bradycardia and we need to monitor for thatq
What is used to minimize ballooon tamponade displacement
traction
Why use vasopressin for bleeding varices
Causes vaso constriction to decrease portal pressure
BUT contraindicated for those with CAD (can cause MI)
Caution: has diuretic effect so monitor lytes, Na, and K levels
Why use beta blockers for bleeding varices
decrease portal pressure and can be used as prophylaxis for bleeding
Sclerotherapy
endoscope
sclerosing agent injected into a varices to shrink it
you then monitor for esophagus perforation, aspiration pneumonia, and strictures
Varices Banding
using an endoscope, a tube with rubber bands goes in and suctions and then bands a bleeding varices until it necroses and falls off
Hepatic Encephalopathy
(Portosystemic Encephalopathy (PSE))
The FINAL consequence of hepatic dysfunction
Life Threatening
Profound liver failure causing neuropsychiatric (not physical) manifestations
How fast is the presence or onset of hepatic encephalopathy
can be gradual OR sudden
What are some s/s of Hepatic Encephalopathy
sleep and behavioral changes
patient is confused and unkempt
alterations in mood or sleep patterns
What are the 2 explanations for Hepatic Encephalopathy
- Ammonia
2. Portosystemic Shunting
Ammonia explanation of hepatic encephalopathy
The liver is unable to detoxify these ammonia byproducts, so levels build up to neuropsych conditions by saturating the CNS
Portosystemic Shunting explanation of hepatic encephalopathy
Since the liver is not working, the blood if shunted through with toxic substances to collateral vessels
These substances end up in systemic circulaton causing the neuropsych symptoms
What are some things that can precipitate encephalopathy when there is liver dysfunction
things increasing ammonia levels!!!:
GI bleeding (HgB breakdown stimulating ammonia increase)
high protein diets
bacterial infections
hypercatabolic state (excessive breakdown of body tissue or substances)
renal failure leading to inability to clear ammonia
How many stages of hepatic encephalopathy are there
4 stages
Stages of Hepatic Encephalopathy S/S
1: LOC nL, lethargy, euphroai, up at night sleep during day, normal EEG, inability to draw line figures, asterixis
2: drowsy, disoriented, mood swings, abnormal EEG
3: Stupour, hard to rouse, sleeps a lot, confusion, increased DTRs, rigid extremities
4: Comatose, absence of DTR and asterixis, flaccid extremities, seizures
Nursing Dx for Hepatic Encephalopathy
1: Activity intolerance, self care deficit
2: impaired social interaction, ineffective role performance, risk for injury, confusion
3: Imbalanced nutrition, impaired mobility, impaired verbal communication
4: risk for aspiration, impaired gas exchange, impaired tissue integrity
Constructional Apraxia
a symptom of hepatic encephalopathy
graphic evidence of hep. enceph.
Progresses from not being able to produce a simple figure in 2 or 3 dimensions and gets worse
Medical Management of Hepatic Encephalopathy focuses on what
eliminating precipitating factors
What are some of the nursing care ways for patients with hepatic encephalopathy
ammonia lowering therapy - medicine, fruit juice po, NG or enema
IV glc - record I&O, monitor sugar, explain meds
Vit/Lyte - explain reason and monitor
antibiotic - explain and report s/s infection
prevent worsening and consider liver transplant - VS q 4 hours, neuro check, daily weight, etc
home care teaching like diet
Why is lactulose given to hepatic encephalopathy patients
it works to remove ammonia by trapping it and allowing for it to be expelled in feces
Why is IV glucose given to someone with hepatic encephalopathy
to minimize protein breakdown and reduce the amount of free ammonia floating around in the body
When is a protein restricted diet used for hepatic encephalopathy
only if lactulose does not work
it only is used short term because longer restrictions do more damage than good
vegetable proteins are tolerated better and high protein diet is contraindicated because of ammonia production
Viral Hepatitis
systemic infection that can cause necrosis of liver cells
this can then produce a cluster of physical, chemical, and biochemical changes
Hepatitis A
A viral hepatitis spread by poor hand hygiene
liver infection
How is Hep A Spread
fecal-oral
Hep A mostly infects what population
younger children - esp those in daycare
Incubation of Hep A
2-6 weeks
How long does Hep A last
4-8 weeks
What is the mortality rate of Hep A
0.5% for those younger than 40 and 1-2% for those over 40 years old
Manifestations of Hep A
2 Phases:
- Mild flu like symptoms, low grade fever, anorexia
- Jaundice, dark urine, indigestion, epigastric distress, enlargement of spleen and liver
What is management of Hep A like
PREVENTION
Bed rest during the acute phase
Nutritional Support
What are some ways to prevent Hep A
good handwashing, safe water, proper sewage disposal
vaccination
immunoglobulins for passive immunity
When must immunoglobulins be given to prevent Hep A
must be administered with 2 weeks of having symptoms, but past that there is less effectiveness
Hepatitis B
viral liver infection transmitted through blood, saliva, semen, and vaginal secretions
How is Hep B transferred
sexual transmission
Needle drug use
to infants at time of birth
(blood semen saliva vaginal secretions)
Hepatitis ___ is a major worldwide cause of cirrhosis and liver cancer
B
How long is the incubation period of HepB
1-6 months
S/S of Hepatitis B
Variable and Insidious
Similar s/s to A: loss of appetitive, dyspepsia, abdominal pain, generalized aching, malaise, weakness
Jaundice may or may not be evident unlike in HepA
Medications for Chronic Hepatitis Type B
alpha interferon and antiviral agents: entecavir (ETV) and tenofovir (TDF)
Treatment for Hepatitis B
Medications
Bed rest and nutritional support
vaccinations
What is vaccination like for Hep B
for person at high risk
routine vaccination of infants
passive immunization for those exposed
standard precautions and infection control measures
screening of blood and blood products
Hepatitis C
virla liver infection transmitted by blood and sexual contact including needle sticks and sharing of needles
s/s usually mild
Hep _ is the most common bloodborne infection
C
Hep _ is a cause of one third of cases of liver cancer and most common reason for liver transplant
C
Incubation period of Hep C
variable - 15 to 160 days
wide incubation period
What frequently occurs with Hep C
chronic carrier state
Management Methods of Hep C
antiviral meds
avoid alcohol which potentiates the disease and medicines impacting the liver
prevention (programs to decrease needle sharing in drug users)
screening of blood supply
safety needles for healthcare workers
Hepatitis D
blood and sexual contact transmission viral liver infection
Hepatitis D can only occur…
in persons with Hepatitis B
What are some examples of ways to get Hep D
use of IV or injection drugs
patients undergoing hemodialysis
recipients of multiple blood transfusions
What is likely to develop because of Hep D
fulminant liver failure or chronic active hepatisis and cirrhosis
Incubation period of Hep D
30-150 days
What is the only licensed drug available for Hep D infection
interferon alfa
Hepatitis E
transmitted fecal-oral route through contaminated water
viral liver infection
Incubation period of Hep E
15-65 days
How does Hep E present
similar to Hep A
self limiting
abrupt onset
not chronic
How to prevent Hep E
handwashing
clean water
good hygiene
Non-Viral Hepatitis
inflammation of the liver r/t hepatotoxins rather than a virus
Can be Toxic Hepatitis or Drug Induced Hepatitis - both are acute events with chronic implications
things like carbon tetrachlorides and meds like acetaminophen cause it
Toxic Hepatitis
non viral hepatitis but resembles viral hepatitis
ingestion of hepatotoxic chemicals causes this
S/S of Toxic Hepatitis
fever
extreme physical weakness
hematemesis
vascular collapse
delirium
seizure
coma
Drug Induced Hepatitis
non viral hepatitis
comes from ingestion of hepatotoxic chemicals in medications
S/S of Drug Induced Hepatitis
abrupt onset of:
chills, fever, rash
pruritis, arthralgia, anorexia, nausea
jaundice, dark urine, enlarged and tender liver
WHy are tx options limited for non viral hepatitis
because antidotes are limited
What may have to happen if non viral hepatitis is not caught early enough and gets severe
liver transplantation will have to be considered
`in the interim fluid and electrolyte balance, blood replacement, and comfort/support measures are the treatment options
Fulminant Hepatic Failure
a clinical syndrome of sudden and severely impaired liver function
Normally appears in a previously health person - and the patient has gone from being well to jaundice which progresses to encephalopathy quicky within 72 days
Most common cause of fulminant hepatic failure
viral hepatitis
but it can be caused by drug and toxic hepatitis, and hereditary issues
Assessment Findings of Fulminant Hepatic Failure
jaundice
profound anorexia
coagulation defects
renal failure
lyte disturbances
cardiovascular abnormalities
infection
hypoglycemia
encephalopathy
cerebral edema
Tx of Fulminant Hepatic Failure
liver transplant
however plasma exchange and prostaglandin therapy can be used to treat with less favorable results
What is Plasma Exchange therapy for hepatic failure
A correction of coagulation defects where pt blood is separated from plasma and returned with the plasma of a donor
not great results and usualyl they still will need a liver transplant anyways
Interventions for Fulminant Hepatic Failure
ID root cause
ICU admission and transfer
Antidote
plasma exchanges
prostaglandin therapy
intracranial monitoring
mannitol (cerebral edema)
liver transplant
The liver is able to regenerate itself, but what is the point where there is total hepatocyte damage that is irreversible
if more than 70% of liver fxn declines
Cirrhosis
when liver fxn declines more than 70% and hepatocyte cells that are damaged are replaced by scar tissue causing nodules, bumpy appearance of the lvier, and interfere with normal vascular pathways
“Irreversible scarring that disrupts normal function and structure of the liver”
Alcoholic Cirrhosis
most common cirrhosis
Cirrhosis due to alcoholism, chronic
Postnecrotic Cirrhosis
second most common cirrhosis type
Cirrhosis commonly caused by viral hepatitis
appears as broad bands of scar tissues
Biliary Cirrhosis
Least common type of cirrhosis
scarring occurring on bile ducts causing biliart obstruction and infection itself
How do we learn of diagnosis and severity of cirrhosis
CT
Liver Biopsy
MRI
Radioisotope Liver Scan
The two phases of liver cirrhosis are ___ and ___
compensated ; decompensated
Compensated Cirrhosis
first stage of cirrhosis with vague symptoms of the body trying to compensate but can only do so for so long
S/S of Compensated Cirrhosis
intermittent mild fever
spider hemangiomas
palmar erythema
unexplained nosebleed
ankle edema
vague morning indigestion
flatulent dyspepsia r/t malabsorption
abdominal pain
firm and enlarged liver
splenomegaly
Decompensated Cirrhosis
second stage of cirrhosis
body cannot compensate anymore and signs get much worse and severe
S/S of Decompensated Cirrhosis
ascited
jaundice
weakness
muscle wasting
weight loss
continuous mild fever
clubbing of fingers r/t hepatopulmonary syndrome
purpura r/t thrombocytopenia
spontaneous bruising
nosebleeds r/t low plts and portal HTN
hypotension
sparse body hair (blood flow drops and albumin level)
white nails
gonadal atrophy
What are the 2 main complications from Cirrhosis
Hepatorenal Syndrome
Hepatopulmonary Syndrome
Hepatorenal Syndrome
decrease in renal function related to liver disease/cirrhosis
the kidneys are fine and functionally fine but the blood flow is compromised due to portal HTN causing the renal system to fail
Hepatopulmonary Syndrome
decrease in lung function related to liver disease/cirrhosis
the lungs are fine and functionally fine but increased portal HTN leads to backflow in the pulmonary system
this can then stress out the heart because it increases CO and decreases peripheral resistance as well
Most liver cancer comes form what?
Few cancers actually originate in the liver, mostly cancer metastasizes there and the liver is a frequent site of metastatic cancer
If cancer does originate in the liver, what is it related to
usually associated with hepatitis B and C (hepatocellular carcinoma - HCC)
Manifestations of Liver Cancer
Dull persistent pain in the RUG, back, or epigastrum
Weight loss, anemia, anorexia, weakness
Jaundice, bile ducts occluded, ascites, or obstructed portal veins
What are some early signs and diagnostic findings of liver cancer
early signs - liver pain (RUQ, epigastric, back)
weight loss, anorexia, and anemia
enlarged liver (jaundice and ascites)
if cancer is big enough to block portal veins it causes ascites
Labs indicative of Liver Cancer
Increased serum bilirubin
Increased serum alkaline phosphatase
Increased AST, GGT, Lactic Dehydrogenase
Leukocytosis, erythrocytosis, hypercalcemia, hypoglycemia, hypercholesterolemia
Serum Alpha Fetoprotein (AFP)
tumor marker elevated in 30-40% of primary liver cancer patients
Carcinoembryonic Antigen (CEA)
marker of advanced cancer
What are some ways to diagnose Liver Cancer
AFP
CEA
Imaging - X Ray, MRI, CT, Liver Scan, ultrasound, Arteriography, Laproscopy, PET
Liver Biopsy
Medical Management of Liver Cancer
Radiation
Chemotherapy
Percutaneous Biliary Drainage
Surgical Management: Lobectomy, Local Ablation, Liver Transplant
Percutaneous Biliary Drainage
PALLIATIVE NOT CURATIVE
For liver cancer
Catheter is inserted under fluoroscopy to bypass obstructed biliary ducts
Liver Transplant
total removal of liver and a replacement with a health donor from cadaver, donor, or partial lobe from live donor in same anatomical position is placed
When is liver transplant usually used
for life threatening and end stage liver disease with no other treatment available
Model of End Stage Liver Disease (MELD) Score
A score that helps caculate the degree of need for a liver transplant based on bilirubin levels, PT time, INR, creatine, and cause of liver disease
there are some ethicaly questions sometimes for this in regard to alcohol dependent patients
Liver Transplant Preoperative Nursing INterventions
support, education, and encouragement aare provided to help prepare psychologically for the surgery
Liver transplant postoperative nursing interventions
monitor for infection, vascular complications, respiratory and liver dysfunction
close constant monitoring
Other than the patient what are 2 other concerns for liver transplants
caregiver stress
ethical dillemmas
Liver transplant success depends on ___
immunosuppression
What do patients need to understand after a liver transplant
they need lifelong immunosuppressant medications
Patient Education for LIver Transplants include…
education about lifelong measures to promote health
adhere close to therapeutic regimen with emphasis on immunosuppressive agents
education on s/s that indicate problems needing consultation with team
emphasize importance of follow up lab tests and apptments with the team
