Liver lecture 2 Flashcards
what is hepatitis? what can it be due to?
acute or chronic inflammation of the liver due to virus, alcoholism, drug toxicities (Tylenol), and autoimmune
what elevated lab values signal the presence of hepatocyte damage?
LFTs (AST/ALT)
what are three lab tests of liver function?
albumin, bilirubin, PT/INR
what does disease of the biliary drainage system cause?
it obstructs the flow of bile and interferes with the elimination of bile salts and bilirubin (produces cholestatic liver damage bc of bile backup into liver)
what does disease of the hepatocytes cause?
disorders of carb, protein, fat metabolism; causes disorders of metabolism and removal of drugs, hormones, toxins. ammonia, and bili
what do elevations in bili and alk phos levels a sign of?
signal the presence of cholestatic liver damage
what is acute hepatitis? what viruses cause it?
disease duration of less than 6 months; all five virus forms can cause it
what is chronic hepatitis? what virus types can cause it?
disease duration greater than 6 months; only B C and D can cause chronic hep
what two things do hep viruses B, C, and D have the potential to cause? what is the main tx for these viruses?
cirrhosis and hepatocellular carcinoma; tx = liver transplant
is chronic hepatitis symptomatic?
not always (depends on the patient)
what are the three phases of acute symptomatic viral hepatitis?
1) . prodromal “pre-jaundice”
2) . icterus
3) . convalescent
what is the prodromal/pre-jaundice phase of acute viral hep characterized by?
abrupt to insidious onset
general malaise, myalgia, arthralgia, fatigue (overall vague symptoms, sounds like flu)
what is the icterus phase of acute viral hep characterized by?
follows phase #1 by 5-10 days; jaundice, pruritis (bile salts cause irritation), liver pain
what is the convalescent phase of acute viral hep characterized by?
increased sense of well being, return of appetite, jaundice resolves
what is the largest group of chronic HBV infected patients?
inactive carriers
what three hep viruses can have a carrier state?
HBV, HCV, and HDV (pt doesn’t have symptoms but can transmit the disease)
what % of inactive hep B carriers undergo spontaneous reactivation of Hep B?
20-30%
how is Hep A and E transmitted?
fecal-oral
how is hep b, c and d transmitted? (4)
blood transfusion, needle sticks, sexual, across the placenta
what disease can hep A cause? what are symptoms of that disease?
acute viral hepatitis: fever, jaundice, and painful enlarged liver
what are four clinical courses of hep B?
acute viral hep, fulminant hep, chronic hep (10%), coinfection/superinfection with hep delta virus
what is fulminant hepatitis?
severe acute hepatitis with rapid destruction of the liver
what are two main complications of hep B?
primary hepatocellular carcinoma and cirrhosis
what % of people with hep A will develop fulminant hepatitis?
1%
what two types of hepatitis are more likely found in a person who traveled to a less developed country?
A and E
what are some common risk factors for acquiring Hep c? (4)
sexual contact w infected person, recipients of blood products, IV drug users, infected needles (healthcare workers or tattoos/piercings)
what are some risk factors for acquiring Hep B & D? (6)
men having sex with other men, multiple partners, IV drug users, healthcare providers in contact w infected needles, blood product recipients, pts undergoing dialysis
what is incubation period for Hep A? what three places can the virus live? what age people may be asymptomatic and spread disease more?
4 weeks; seawater, freshwater, and soil; young children less than 6
presentation of Hep A? how long does it usually last?
fever, malaise, nausea, anorexia, abd pain, dark urine, jaundice; about 2 months
what are lab manifestations of Hep A? (3)
resembles hepatocellular inflammation; increased AST/ALT ratio (usually 1-1 ratio); if bilirubin is over 2 pt will have jaundice
what is hepatitis without jaundice called?
non-icteric hepatitis
how long does it take for Hep A to resolve?
2 months (0.1% fatality rate)
what is tx for Hep A?
supportive care
what is the vaccine series for Hep A? what age is it recommended to vaccine?
2 shots, 6 months apart; recommended for all children at 1 yr
what type of person has a sicker/more difficult course of Hep A?
pregnant women
what are the three most prevalent modes of Hep B spread?
IV drug use, people with multiple partners, and perinatal (infants born of HBV positive mothers)
what is the incubation period of hep b?
4-10 weeks
what is the first serology marker that appears for Hep B? what does this mean? what does it not distinguish?
Hep B surface antigen (HBsAg); patient is infectious and has active disease; doesn’t distinguish between acute vs chronic
what is HBeAg? what does it indicate?
pre core envelope antigen for Hep B; indicates active viral replication (VERY infected)
what is the first antibody to Hep B to show up on serology? what is IgM and IgG to anti-HBc mean?
anti-HBc (antibody to hep B core antigen); IgM to antiHBc is a marker of acute disease; IgG to HBc is marker of prior infection
what is anti-HBs a marker of?
antibody to hep B surface antigen is a marker of prior vaccination or resolution of the infection (no longer ACTIVE infection or infectious to others)
presence of what in the serum is the most reliable indicator of hep B infection ?
viral DNA (HBV DNA); even seen in chronic disease
what is the serologic gap or window period for Hep B?
HBsAg is no longer present, but anti-HBs is not present either. The patient is infectious. This period of time is detected by the presence of IgM anti-HBc (this antibody is a marker of acute disease, but does not confer immunity like anti-HBs).
What is tested in blood donors to prevent transfusion of infectious blood during the patient’s serologic window?
IgM antiHBc
what are the lab findings for Hep B? what if the pt is jaundiced?
inc ALT and AST; if jaundiced will have increased total bilirubin
what % of Hep b cases have acute fatality rate? what type of Hep can hep B lead to? what % of people develop this type of hepatitis?
1%; can lead to chronic hepatitis (2-10%), which then can lead to cirrhosis
cirrhosis secondary to HBV is a risk factor for what?
hepatocellular carcinoma
what % of infants born from HBV infected mothers develop Hep B if not treated with vaccine/immunoglobulin within 12 hrs of birth?
10-85% (variation due to misdiagnosis of mother or mother didn’t do tx)
Hep B prognosis is related to what 4 things?
albumin, PT/INR (unresponsive to vitamin K), bilirubin elevation (prognostic marker for severity of disease), physical findings of ascites and hepatic encephalopathy (liver cant convert ammonia to urea)
what is albumin a measure of?
synthetic function of the liver
what is Hep B tx for acute and chronic courses?
acute- supportive (rest & hydration)
chronic- interferons or antivirals (-vir drugs)
what are the two HBIg (hep b immuneglobulin) prevention guidelines?
within 12 hrs of infant birth if mother was HBV positive and for healthcare worker exposed to infected pts’s blood/bodily fluids within 24 hrs
what does the Hep B vaccine contain?
HBsAg (recombinant hep B surface antigen)
what hep virus is the most common cause of chronic hepatitis?
C
what is the incubation period of hep c? what is the major mode of transmission?
6-12 weeks; IV drug abuse (less frequent sexual transmission/perinatal)
what are some elevated lab findings of Hep C?
mildly elevated AST and ALT
what Hep C serology test is the most accurate for infection? what about marker of disease?
HCV RNA- infection
Anti-HCV antibody- marker for disease (not sign of immunity)
describe clinical course of Hep C: symptoms, infection type, has potential to develop what things?
nonspecific symptoms; typically becomes chronic in 75-80% of people; can develop cirrhosis, end stage liver disease, hepatocellular carcinoma
tx for Hep c
interferons, nucleotide analog (ribavirin), and/or DAAs (direct acting antiviral agents)
what are prevention methods for hep c?
no vaccine, immunoglobulin not helpful post exposure
what two things must a Hep D patient already have to be classified as having Hep D?
pt needs to already be infected with HBV and be positive for HbsAg
is serology helpful in diagnosing Hep D?
no because titers of IgM and IgG anti-HDV are present only sometimes
how does Hep D impact the severity of Hep B infection?
it increases Hep B severity and increases the risk of developing chronic hep from hep B infection
what is the tx for Hep D?
PEGylated interferon alpha is only effective drug
what is the prevention for Hep D?
vaccination for HBV
why is there a high mortality rate in pregnant pts for Hep E?
20% mortality rate is due to developing fulminant hepatitis (worse than Hep A)
what is autoimmune hepatitis? what two things can it be due to? what population is it most commonly found in? Is it symptomatic?
its immune mediated liver disease; due to genetics (HLA that encodes histocompatibility complexes) and/or environmental factors (drugs, prior viruses); most common in young women; may or may not be symptomatic
what are the two types of autoimmune hepatitis?
type 1 and type 2
what type of autoimmune hepatitis is most common? does it have high or low levels of antinuclear antibodies? how about anti-smooth muscle antibodies?
most common is type 1; high levels of both antibodies
what aged kids get type 2 autoimmune hepatitis? what two things do these kids have positive antibodies to?
2-14 yrs old; positive antibodies to liver/kidney microsomes and liver cytosol
what lab values do you look for in autoimmune hepatitis?
elevated ALT, AST, ALP; neg serology for viral hepatitis; look for positive antibodies specific to each type; hypergammaglobulinemia (inc immunoglobulin in blood serum)
what is the tx for autoimmune hepatitis?
PREDNISONE, immunosuppressants, transplant
what is a fibrotic liver?
continuous inflammation of liver caused by Hep B, which leads to fibrosis (formation of scar tissue within the liver)
what is a cirrhotic liver?
scar tissue replaces normal, healthy tissue & blocks blood flow through the liver & prevents the liver from working normally
what is acute fulminant hepatitis? what type of people does this occur in?
hepatic failure that progress from hepatitis to hepatic encephalopathy within 2-3 weeks; in persons who don’t have chronic liver disease(considered worst sequalae of acute liver injury)
what is the most common cause of acute fulminant hepatitis?
acetaminophen toxicity (45%)
what is tx for acute fulminant hep?
correct underlying issue, supportive tx, and liver transplant
what is the mortality rate for acute fulminant hep?
85% in people without transplant and 35% with one
what are presentation signs of acute fulminant hep?
GI symptoms, inflammatory response, hemorrhagic signs, may/may not jaundice, labs reveal hepatocellular damage, elevated NH3
what is primary biliary cirrhosis (cholangitis)? what population does it usually occur in? what does the immune system destroy?
its a immune mediated cholestatic liver disease; middle aged women; immune destruction of intrahepatic small bile ducts (inflammation and scar tissue is in ducts)
describe the progression of primary biliary cirrhosis? what are the three lab findings?
slow progression, symptoms of pruritus, fatigue which leads to cirrhosis and liver failure; elevated alk phos, inc cholesterol, and 90% positive for antimitochondrial antibodies
what is tx for primary biliary cirrhosis?
symptomatic, ursodiol (inc bile flow and dec toxicity of bile contents); transplant is definitive tx (& disease DOESNT recur after)
what is secondary biliary cirrhosis? what are the two most common causes? what is tx?
cirrhosis that results from prolonged obstruction of extrabiliary tree; cholelithiasis or tumor; surgery to relieve obstruction
what is primary sclerosing cholangitis? what population does it affect? what disease it is usually associated with?
disease of large bile ducts causing scars within the ducts, leads to liver damage; most often affects men; often associated with inflammatory bowel disease, UC
what is two lab values will be elevated in primary sclerosing cholangitis? what is most effective tx?
will present with obstructive labs (elevated direct bili and AP); transplant
what is the leading cause of acute liver failure in US?
drug induced liver disease (Tylenol)
what does drug induced liver disease cause?
hepatocyte injury or death OR injuring biliary drainage structures
what labs are elevated in drug induced liver dz? how is prognosis when jaundice is present? what is tx?
ALT, AST, bili mildly elevated alk phos; poor prognosis w jaundice; tx is remove offending agent from system (activated charcoal first and then mucomyst)
what is the max dose of acetaminophen per 24 hours?
4000 mg but recommended telling pts 3000 mg (usually takes about 10,000 mg to overdose)
what is the first enzyme to be elevated in alcoholic liver disease?
GGT
for alcohol induced liver disease, what are the three stages of progression?
fatty liver disease, alcoholic hepatitis, then alcoholic cirrhosis
what is fatty liver disease? describe reversibility
fat in the hepatocytes; reversible once ETOH is stopped
what two things occur during alcoholic hep? how is the AST/ALT ratio? how are liver enzymes impacted? what symptoms are present
hepatic inflammation and necrosis; 2-1 ratio; inc liver enzymes; jaundice, ascites, anorexia, fever
what is alcoholic cirrhosis?
nodules compress hepatic veins causing portal HTN, extrahepatic shunts, and cholestasis (can get bleeding esophageal varices here)
what is nonalcoholic fatty liver disease (NAFLD)? what is it often associated with? what are the three stages in the spectrum of dz?
spectrum of liver disease that resembles alcoholic liver disease but in people who don’t abuse alcohol; lipid accumulation in hepatocytes; fatty liver (steatosis), non-alcoholic steatohepatitis, cirrhosis
describe AST/ALT ratio in NAFLD.. what is prevention for it? tx is what?
normal 1:1 ratio; prevention is weight loss, exercise, and avoid ETOH; liver transplant if behavioral changes don’t improve
what does cirrhosis cause?
portal HTN, liver failure, inc bleeding risk, thrombocytopenia, gynecomastia, encephalopathy
what is Wilson’s disease?
recessive genetic disorder where copper accumulates in tissues (leads to neurological/psych symptoms and liver disease); need meds that reduce copper absorption or transplant
describe pH and H/H levels for cirrhosis
pH- decrease
H/H- decreased (leads to anemia)
what is portal HTN? what five things can it cause?
inc resistance to flow in portal venous system and inc pressure (>10mmg); ascites, caput medusae, congestive splenomegaly, encephalopathy, formation of shunts with bleeding from esophageal varices
what are prehepatic, intrahepatic, and posthepatic causes of portal HTN?
prehepatic- obstructive thrombosis, massive splenomegaly
intrahepatic- cirrhosis
posthepatic- right sided heart failure and hepatic vein outflow obstruction
what is tx for portal HTN?
BB’s, tx varices, Na+ restriction
what is ascites? what volume is it noticeable at? whats it most often caused by?
increased fluid in the peritoneal cavity (>25cc); noticeable at 500 ml; portal HTN
what is Tx for ascites?
Na+/water restriction, diuretic therapy, spironolactone, give K+ to prevent hypokalemia, paracentesis, consider TIPS for refractory ascites
what is TIPS?
tract created within the liver which connects the hepatic and portal veins (keeps it open with a stent)
what formula do you use to determine where the ascites is coming from?
SAAG (serum albumin ascites gradient) = albumin concentration of serum- albumin concentration of ascetic fluid
explain what a high SAAG result means? what about a low gradient?
high gradient (>1.1) means ascites is due to portal HTN w 97% accuracy; low is worse (can be caused by pancreatitis, kidney failure, bowel obstruction, malignancy)
what is budd chaiari syndrome? what is it a sign of?
blood clot occlusion of the hepatic veins that drain the liver; sign of portal HTN
what is spontaneous bacterial peritonitis? what % of cirrhotic pts w ascites does it occur in? hows the mortality rate?
bacterial infection of ascetic fluid without any intrabdominal source of infection; 10-20%; high mortality rate
what are some symptoms besides cirrhotic pt with ascites for SBP?
fever, abd pain, change in clinical status
what is dx for SBP?
paracentesis with >250 neutrophils and protein concentration 1 g/dl or less
what is tx for SBP?
based on peritoneal neutrophil count (NOT culture results); ABX: cefotaxime 2 g every 8 hrs
how do you get splenomegaly from portal HTN? what three things does this cause?
portal HTN shunts blood into the splenic vein; causes dec life span of blood elements (anemia, thrombocytopenia, leukopenia)
what is the primary prevention strategy of bleeding esophageal varices or secondary prevention of rebleeding? how about surgical tx?
nonselective BB (propranolol); cauterize varices
what is a significant cause of mortality in cirrhotic pts with portal HTN?
esophageal varices
what percent loss of liver function classifies liver failure? what is tx of failure?
80-90%; correct fluid/electrolyte imbalances, dec ammonia production by controlling protein intake, eliminate alcohol, provide nutrition, transplant
what is hepatic encephalopathy? what is often elevated in this disease?
CNS disturbance from liver failure; elevated serum ammonia due to inability to convert to urea
what is tx of hepatic encephalopathy?
protein restriction (protein breakdown leads to ammonia), lactulose which dec ammonia absorption, rifaximin (ABX that dec intestinal load of ammonia producing bacteria)
what is the MELD score?
reliable measure of mortality risk in pts with end stage liver disease; assesses disease severity to prioritize liver transplant allocation (higher the number, the higher the mortality)
what are the two types of liver cancer?
hepatocellular and cholangiocarcinoma
what two things confirm diagnosis of hepatocellular cancer?
biopsy and 90% increase in serum alpha-fetoprotein
where is hepatocellular cancer located? what disease is it usually associated with?
hepatocytes; associated with chronic liver disease (chronic viral hep B, C, D, alcoholism, or cirrhosis)
what is tx of hepatocellular cancer?
surgery (hepatectomy), chemo and radiation are palliative (7% 5 yr survival rate)
what is cholangiocarcinoma? what causes it? what is more common than primary liver carcinoma?
carcinoma of the bile ducts; its jaundice related to long standing inflammation and injury in bile duct epithelium; metastatic tumors to the liver from other cancers are most common
what is the earliest lab finding for cholangiocarcinoma? what is diagnostic confirmation?
inc AP; liver biopsy
what lab value is elevated in cholestasis?
alk phos
