Liver Problems Flashcards
major functions of the liver
–metabolism and/or storage of fat, CHO, proteins, vitamins, and minerals
–blood volume reservoir
–blood filter
–blood clotting factors
–drug metabolism and detox
blood volume reservoir
distends/compresses to alter circulating blood volume
blood clotting factors
prothrombin and fibrinogen
where is the liver located?
right epigastric region
liver cells
hepatocytes
portal circulatory system
brings blood to the liver from the stomach, intestines, spleen, and pancreas
how does portal circulation work?
–deoxygenated blood enters the liver through the portal vein
–absorbed products of digestion come directly to the liver and are sent to the lobules
–“first pass effect”
Liver Function Tests (LFTs)
–liver enymes (AST, ALT, Alk Phos)
–Bilirubin
–Serum Ammonia
–Serum protein
–Serum albumin
–Prothrombin Time
Liver enzymes with liver failure
> 150; not great indicator of severity
serum ammonia level with liver failure
increased
serum protein level with liver failure
decreased
serum albumin level with liver failure
decreased
prothrombin time with liver failure
increased
jaundice
–caused by increased levels of bilirubin in the bloodstream
–yellowish discoloration of skin and deep tissues
when is jaundice noticeable?
when bilirubin > 2-2.5 mg/dl
hemolytic jaundice
increased breakdown of RBCs
hepatocellular jaundice
liver unable to take up bilirubin from blood or unable to conjugate it
obstructive jaundice
decreased or obstructed flow of bile
example of cause of obstructive jaundice
gallstones
examples of hemolytic jaundice
bleeding, polycythemia, pathologic
direct jaundice
conjugated (30%)
indirect jaundice
unconjugated (70%)
elevations of indirect bilirubin
bilirubin overproduction OR impaired liver functioning
elevations of direct bilirubin
liver working, but can’t get the bilirubin out
examples of direct bilirubin
–bile duct obstruction
–gallstones
what is bilirubin?
byproduct of heme breakdown –> mainly hemoglobin
symptoms of jaundice
–darker urine
–elevated LFTs
–normal or clay colored stools
–pruritis
viral hepatitis
–inflammation of the liver
–hepatitis (not the infection) can occur from other causes (alcohol abuse, drugs, chemicals, and bacteria)
other viruses that cause hepatitis
–Epstein-Barr
–cytomegalovirus
pathogenesis of viral hepatitis
viral infection –> immune response from inflammatory mediators –> lysis of infected cells –> edema and swelling of tissue –> tissue hypoxia –> hepatocyte death
symptoms of viral hepatitis
–similar between all types
–asymptomatic
–abnormal elevated LFTs
when does the prodromal phase of viral hepatitis occur?
2 weeks after exposure
symptoms of prodromal phase of viral hepatitis
–fatigue
–anorexia
–malaise
–N/V
–HA
–hyperalgesia
–cough
–low-grade fever
hyperalgesia
increased pain response
when is viral hepatitis highly transmissible?
prodromal phase
what does the icteric phase of viral hepatitis begin with?
jaundice
symptoms of icteric phase of hepatitis
–jaundice
–dark urine
–clay colored stools
–enlarged liver potentially painful to palpation
–fatigue and abdominal pain
length of icteric phase of hepatitis
2-6 weeks
recovery phase of hepatitis
–resolution of jaundice
–6-8 weeks after exposure, symptoms diminish
–liver remains enlarged/tender
complications with viral hepatitis
–mostly recover completely with no complications
–low mortality rate
–chronic hepatitis
–liver cirrhosis
–liver cancer
–fulminant viral hepatitis
transmission of Hep A
fecal-oral, parental, sexual
specifics of Hep A
–acute onset with fever
–usually mild severity
–does NOT lead to chronic hepatitis
–usually affects children and adult
–food-borne illness
prevention of Hep A
–hand hygiene
–vaccine
routes of transmission of Hep B
–dirty needles (parental)
–unsafe sex (sexual)
Hep B specifics
–severe disease
–may be prolonged course or develop into chronic
–any age group affected
prevention of Hep B
–HBV vaccine
–safe sex
–hand hygiene
routes of transmission of Hep C
–IV drugs (parental)
–unsafe sex (sexual)
Hep C specifics
–insidious onset
–mild to severe symptoms
–can develop into chronic hepatitis (80%)
–any age is affected
prevention of Hep C
–screening blood
–hygiene
–NO vaccine
what can Hep C cause?
–hepatocellular carcinoma
–liver transplant
Hep A vaccine series
–2 doses, 6 months apart
–all children beginning at 12 months
–special “high risk” populations (traveling, HC, food handlers)
Hep B vaccine series
–3 doses at least 4 months apart
–all infants beginning as newborns
two classes of drugs used for chronic HBV
–interferons
–nucleoside analogs
treatment indications for HBV pharm
–increased AST levels
–hepatic inflammation
–advanced fibrosis
disadvantages of HBV pharm
–prolonged therapy
–costs and adverse effects
–high relapse
who is HCV treatment recommended for?
patients with chronic disease
HCV treatment regimen
direct-acting antiviral therapy and interferon-based
Tylenol and hepatitis
active hepatitis can only take <2g of Tylenol per day
examples of hepatitis meds
–entecavir
–tenofovir
cirrhosis
–irreversible
–inflammatory
–fibrotic
effect of fibrosis in liver
–leads to obstructive biliary channels and blood flow
what do obstructive biliary channels and blood flow lead to?
–jaundice
–portal HTN
effect of removal of toxin with cirrhosis
removal can slow progression, but won’t stop it
what is liver regeneration interrupted by with cirrhosis?
hypoxia, necrosis, atrophy, and liver failure
common cause of cirrhosis
–Hep B and C
–excessive alcohol intake
–idiopathic
–non-alcoholic fatty liver disease
alcoholic fatty liver
–mildest
–asymptomatic
–increased lipogenesis
–reversible if stop drinking
alcoholic steatohepatitis
–precursor to cirrhosis
–inflammation
–degeneration of hepatocytes
–becomes irreversible
alcoholic cirrhosis
–fibrosis and scarring alter liver structure
–irreversible
symptoms of alcoholic steatohepatitis
–jaundice
–anorexia
–edema
–nausea
how does alcoholism cause cirrhosis?
increased acetylhyde = altered hepatocyte function –> hepatic stellate cells
hepatic stellate cells
primary cell in liver fibrosis
patho of cirrhosis
liver cells destroyed –> cells try to regenerate –> disorganized process –> abnormal growth –> poor blood flow and scar tissue –> hypoxia –> liver failure
early manifestations of cirrhosis
–N/V
–anorexia
–flatulence
–change in bowel habits
–fever
–weight loss
–palpable liver
late manifestations of cirrhosis
–jaundice
–peripheral edema
–decreased albumin and PT
–ascites
–skin lesions
–hematologic problems
–endocrine problems
–esophageal and anorectal varices
–encephalopathy
portal hypertension
–resistant portal blood flow = varices and ascites
causes of portal hypertension
–systemic hypotension
–vascular underfilling
–stimulation of vasoactive systems
–plasma volume expansion
–increased CO
complications of portal HTN
–variceal hemorrhage
–ascites
–peritonitis
–hepatorenal syndrome
–cardiomyopathy
treatment of portal HTN
–prevent/treat complications
–no treatment except liver transplant
hepatic encephalopathy
–liver isn’t filtering out toxins
–increased toxins in brain
diagnosis of hepatic encephalopathy
LOC = primary driver of diagnosis
minimal severity hepatic encephalopathy
abnormal results on psychometric or neurophysiological testing without clinical manifestations
Grade I hepatic encephalopathy
changes in behavior, mild confusion, slurred speech, disordered sleep
Grade II hepatic encephalopathy
lethargy, moderate confusion
Grade III hepatic encephalopathy
marked confusion, incoherent speech, sleeping but arousable
Grade IV hepatic encephalopathy
coma, unresponsive to pain
labs and hepatic encephalopathy
–correlate with liver labs
–mainly ammonia = LOC changes
–ammonia crosses BBB
acute liver failure
separate liver failure not caused by cirrhosis or other types of liver disease
most common cause of acute liver failure
acetaminophen overdose
–treated with acetylcysteine
patho of acute liver failure
edematous hepatocytes and patchy areas of necrosis and inflammatory cell infiltrates and disrupts the liver tissue
timing of acute liver failure
can occur 6-8 weeks after a viral hepatitis or metabolic liver disease
symptoms of acute liver failure
similar to cirrhosis symptoms
treatment of acute liver failure
liver transplant
class of lactulose
hyperosmotic laxative
indication of lactulose
reduction of ammonia absorption in hepatic encephalopathy
where does lactulose work?
colon and large intestines
MOA of lactulose
reduces blood ammonia levels by converting ammonia to ammonium
route for lactulose
PO or enema/rectal
when is lactulose given?
–titrated by number of stools or by ammonia levels
–not just high ammonia levels…must have s/s of encephalopathy
nursing consideration for giving lactulose
make sure patient is not hypokalemic
when is rifaximin given?
second line of defense if lactulose isn’t working
MOA of rifaximin
inhibits bacterial RNA synthesis by binding to bacterial DNA
route of rifaximin
PO
side effects of rifaximin
–peripheral edema
–nausea
–ascites
–dizziness
–fatigue
–pruritis
–skin rash
–abdominal pain
–anemia
specifics of rifaximin
–can sometimes be given preventatively
–has been associated with increased risk of c. diff
