Week 1 Liver Flashcards
What is cirrhosis?
extensive scarring of the liver
Most common causes for cirrhosis in the US
hepatitis C, alcoholism, and biliary obstruction
Basic functions of the liver
digestion, nutrition metabolism, protein synthesis, detoxify blood, produce bile, converts glucose to glycogen, converts ammonia, regulates platelets, produces heme
What happens when there is a lack of albumin (a protein created by the liver)?
Because of the large molecule keeping pressure in the vascular system, patients will start third spacing huge volumes of fluid in their gut and lower extremities
What is the tx for tylenol overdose?
Mucomyst
What medications cause the most liver problems?`
Tylenol, “glitazone” diabetic drugs and anti-TB drugs
What happens when someone doesn’t make bile?
They can’t emulsify fat and develop steatorrhea and fat leave through the stool. Also can not get fat soluble vitamins (AEDK)
Function of vitamin K in liver patients
responsible for much of the blood clotting cascade
Why give FFP over FP to a liver PT?
FFP has more clotting factors (7&9) that the PT lacks
Will the PT with ESLD by hypo or hyper glycemic?
Hypoglycemic because the liver can not convert glucose to glycogen for storage
Ammonia and ESLD
the liver is unable to convert ammonia which is a bi-product of protein and excrete it so it builds up in the body
Anemia and ESLD
the liver processes heme so you will be anemic in ESLD
What medication is used to remove ammonia?
Lactulose
Which antibiotic is commonly used in liver disease?
Rifaximin according to Rita
Function of antibiotic use in liver disease
Helps prevent episodes of HE and keeps PTs out of the hospital
Kupffer cells
found in the liver and involved in the immune system and infection response. They decrease as your liver function decreases and you are less able to fight infections
AST/ALT levels in liver disease
Both will be elevated, ALT is more specific to liver cells
Bilirubin levels in liver disease
they will be very high because the body can’t excrete it. It will cause urine to be light to dark brown
Level of ammonia in liver disease
elevated
Level of albumin in liver disease
decreased
Level of Ca2+ in liver disease
decreased
Qty of platelets in liver disease
drastically decreased
Number of WBCs in liver disease
decreased
the immune system is inhibited
PT/INR levels in liver disease
prolonged
Function of EGD test
looking for esophageal varicies. If there are, you have portal HTN (over 5mmHg of pressure)
MARs procedure
Dialysis of the liver to purify their blood
Why give aldactone in liver disease?
It decreases aldosterone which regulates H2O and Na in the body
What type of diet should liver patients be on?
High calorie, high carb, low/moderate fat, high protein, LOW salt
6 meals/ day
What is hepatitis?
Inflammation of the hepatocytes in the liver
How is Hep A transmitted
fecal-oral route, contaminated H2O, food, more common in underdeveloped areas
Hep A vaccine?
Yes
Hep B vaccine?
Yes but people who are overweight should have their titers checked because the vaccine may not remain as effective
Hep B infection series of events
May not know infection has occurred, most recover and develop immunity, a small # become carriers and need lifelong tx
Tx for chronic Hep B infection
lifelong Ribavirin and pegylated interferon only if you become a chronic carrier, otherwise, you won’t need these meds
Hep C Sx
Most people a asymptomatic which delays tx and can lead to ESLD
Hep C transmission
Parenteral
Hep C vaccine?
No
Hep D incidence
rare, must have coexisting Hep B to be infected
Hep D vaccine?
No but getting the Hep B vaccine will likely keep you from getting Hep D
Hep E transmission
fecal-oral route
Mostly seen in Asia and Africa
fulminant hepatitis
A severe, acute and often fatal form of hepatitis
Liver cells fail to regenerate and necrosis takes over
When is hepatitis considered chronic?
when liver inflammation lasts longer than 6 months
Cause of chronic hepatitis
Hep B, C or B superimposed with hep D
Complications of chronic hepatitis
cirrhosis and liver cancer
infections, especially the combination of HBV with HCV, HDV, or HIV infections.
Measures to prevent HAV infection include
handwashing especially after handling shellfish
Receiving immunoglobulin within 14 days of virus exposure
Being vaccinated
Clinical manifestations of hepatitis to look for on assessment
- Abdominal pain
- Changes in skin or sclera (icterus)
- Arthralgia (joint pain) or myalgia (muscle pain)
- Diarrhea/constipation
- Changes in color of urine or stool
- Fever
- Lethargy
- Nausea/vomiting
- Pruritus (itching)
Confirmatory test for HAV, HBV and HCV
acute elevations of liver enzymes indicating liver damage
. Serum total bilirubin levels in hepatitis
elevated and are consistent with the clinical appearance of jaundice
Elevated levels are also seen in urine
When is the presence of hepatitis A established
when hepatitis A virus (HAV) antibodies (anti-HAV) are found in the blood
When is the presence of the hepatitis B virus (HBV) established
in the presence of hepatitis B antigen-antibody systems in the blood and a detectable viral count
How long is the Hep B PT contagious?
as long as HBsAg (hepatitis B surface antigen) is present in the blood, presence after 6 months indicates a carrier state or chronic hepatitis. People who have been vaccinated against HBV have a positive HBsAb because they have immunity
Liver biopsy
biopsy may be used to confirm the diagnosis of hepatitis and to establish the stage and grade of liver damage
Interventions during the acute stage of viral hepatitis
aimed at resting the inflamed liver to promote hepatic cell regeneration
Hepatitis nutrition
high in carbohydrates and calories with moderate amounts of fat and protein, small frequent meals, supplement vitamins
STEATOSIS
Fatty liver
Cause of fatty liver
accumulation of fats in and around the hepatic cells, may be caused by alcohol abuse or other factors
Causes of Nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH)
- Diabetes mellitus
- Obesity
- Elevated lipid profile
Common findings in fatty liver disease
asymptomatic
elevated ALT and AST or normal ALT and elevated AST
Tx for fatty liver
Weight loss, glucose control, and aggressive treatment using lipid-lowering agents
Biproducts of protein breakdown
Ammonia and bacteria
Levels of AST/ALT, bilirubin and alkaline phosphatase through liver disease
They will all go up until the end stage and then they will go down
Critically low platelet value
40,000
Sx of portal HTN
anorexia
excess fluid/3rd spacing
HF
Teaching plan for liver disease PTs
No alcohol Watch OTC (tylenol/NSADIS) Take rest periods Low salt diet Need bleeding precautions Daily WT
When to get liver dialysis (MARs procedure)
increased weakness, tremulous, change in mental status
What to teach about meds for liver
Teach why they use each med
Lactulose, they dont like the diarrhea
Diuretics, Lasix, aldactone, not HCTZ (too weak)
Why do we give aldactone?
decreases aldosterone levels
Phases of hepatitis
Pre-icteric
Icteric
Convalescent
Pre-Icteric phase of hepatitis
No jaundice but you won’t feel well
Sx: anorexia, N/V, fatigue, rash, possible RUQ pain
Icteric phase of hepatitis sx
Jaundice (first seen in the sclera), itching, dark urine due to bilirubin excretion, clay colored stool, fatigue, wt loss
Convalescent phase of hepatitis
PTs will feel better but they need more rest, appetite returns, no jaundice
NAFLD is correlated with what disease?
Diabetes and being obese
Stages of liver damage
steatosis
steatohepatitis
Cirrhosis
Steatosis in NAFLD
deposits of fat cause liver enlargement
steatohepatitis in NAFLD
scar tissue begins to form
S/Sx of NAFLD
Asymptomatic RUQ discomfort (possibly) Fatigue Belly fat (very common Diabetes HTN Hyperlipidemia Hepatomegaly (especially when they are in the inflammatory phase) Splenomegaly Acanthosis nigricans
Tx for NAFLD
No FDA approved treatment
TZD possibly statins
TLC = therapeutic lifestyle changes (lose 10% of body wt)
Complications of cirrhosis
Portal hypertension Ascites Bleeding esophageal varices Coagulation defects Jaundice Portal systemic encephalopathy (Hepatic Encephalopathy) Hepatorenal syndrome Spontaneous bacterial peritonitis
Tx for portal HTN
TIPS procedure (trans-jugular intrahepatic portal shunt.)
Portal HTN
caused by obstruction of blood through the portal vein
Can result in ascites, esophageal varices, anorexia
Over years, it can result in HF
Issues with albumin and ascites
Free fluid in peritoneum pulls albumin with it.
Need to give albumin post paracentesis
If liver unable to make albumin then have oncotic pressure issues in the blood vessels
Sx and Tx of bleeding esophargeal varicies
Sx: hematemesis, melana
Tx: Endoscopy to stop bleeding, Banding, Sclerosing
Portal Systemic Encephalopathy (Hepatic Encephalopathy) cause
Unknown cause, possibly due to toxins, not due to ammonia
Portal Systemic Encephalopathy (Hepatic Encephalopathy)
causes changes in LOC and personality
There are 4 stages of severity
Sx seen in early stage of Portal Systemic Encephalopathy (Hepatic Encephalopathy)
asterixis (flapping) of the hands when hands are put up
Hepatorenal Syndrome
As liver fails the kidneys fail
Prognosis is poor
Hepatorenal Syndrome sx
Sudden decrease in urine output
↑ BUN/Cr, urine osmolarity
↓ urine sodium
GFR declines
Spontaneous Bacterial Peritonitis
Seen in ESLD
Translocation of bacteria from intestines into peritoneal fluid
Spontaneous Bacterial Peritonitis sx
ascites, rigid abdomen, belly button may be popping out, caput medusa, Gynecomastia, palmar erythema, abnormal bruising, and spider angiomas.
Spontaneous Bacterial Peritonitistx
Low Na, fluid restriction, vitamin/nutrition supplements, diuretics, Rifaximin, paracentesis
Spontaneous Bacterial Peritonitis labs
Increased: AST/ALT, Alkaline phosphatase, Bilirubin, Coags
Decreased: Albumin, Platelets, RBCs
TIPS procedure
creates a tunnel in the liver, connects the portal vein to a hepatic vein, stent is placed to keep open
Nursing interventions post TIPS procedure
Bedrest, assess for fluid leaking or abd distention, monitor urine, check VS
4 problems seen in ESLD patients
Decreased bile production
Anemia
Coagulation issues
Decrease in albumin and other proteins
S/Sx seen when bile production is decreased
Steatorrhea
Jaundice
Decrease in fat-soluble vitamins (that’s a biggie)
High cholesterol (because the bile doesn’t carry it out)
Why are ESLD Pts anemic?
liver bifurcates the heme from the globin and store it and produce it
Nursing interventions for decreased bile production
Modify diet: decreased fat, increase protein, supplement vitamins
Skin care: no hot soapy water, anti-itch cream
Interventions for anemia
if Hct is < 25%, administer blood, try to reduce liver toxins
Interventions for coagulation problems
FFP, Vitamin K, Bleeding precautions, administer platelets
Interventions for decreased albumin
small frequent high protein meals, give albumin, low salt, diuretics, beta blockers
Ways to promote appetite in liver disease
Paracentesis relieve pressure)
Dark chocolate will relieve portal HTN
Maintain clean environment
Administer anti-emetics cautiously (can be toxic to liver)
