Disorders of the Liver II - Exam 4 Flashcards
What are the different ways viral hepatitis A-D are transmitted?
A: fecal-oral route
B: Bloodborne, sexually transmitted
C: Bloodborne, sexually transmitted
D: Only associated with Hepatitis B co-infection
What type of virus is Hep A? Where is it commonly found?
RNA virus
fecal-oral route and commonly seen in crowded living areas with poor sanitation and RESTURANTS
What is the incubation period for Hep A? How long can it be fecally excreted? Is there a chronic carrier state?
Incubation period averages 30 days
Can be fecally excreted for up to 2 weeks before clinical illness and up to a week after clinical illness
no chronic carrier state
Is Hep A more severe in adults or children? What is a weirdly sorta unique finding with Hep A and B?
more severe in adults
distaste for smoking
Hep A jaundice usually occurs after _____ days. What will their stools look like?
jaundice occurs after 5-10 days
stools may be acholic (very pale stools)
________ levels will be elevated in a pt with Hep A. **How is the dx of hep A established?
Elevated serum aminotransferase levels
The diagnosis is established by detection of: serum IgM anti-HAV antibodies:
Antibody to Hepatitis A (anti-HAV)
_____ is the best lab indicator for active hep A infection. **_____ is the best indicator of previous exposure, non-infectivity and immunity
IgM: active infection
IgG: previous exposure, non-infectivity, and immunity
What will the liver labs be doing in an acute hep A infection? What additional labs will be elevate?
**Striking ALT/AST elevations
elevated levels of bilirubin, WBC normal to mildly elevated
What is the tx for Hep A? What is the prevention? What is the prognosis?
tx: symptomatic: rest and fluids
prevention: wash hands and vaccination!!
Clinical recovery typically complete within 3 months (relapses may occur)
the diagnosis of acute hep A infection depends on the detection of _____
IgM anti-HAV
the development of an __________, which occurs subsequent to the IgM response, is protective and provides lifelong immunity
immunoglobin G anti-HAV (IgG anti-HAV)
Hep B structure is ______. What are the 2 parts that make it up?
partially double stranded DNA
inner core protein and outer surface coat
**What are the 2 components of the Hep B inner core protein? _____ makes up the outer surface coat
Hepatitis B core antigen (HBcAg)
Secretes Hepatitis B e antigen (HBeAg)
HBcAg secretes HBeAg
______________
Hepatitis B surface antigen (HBsAg)
Who are the at risk populations for hep B? What is the prevention?
IV drug users
Prison inmates
Healthcare workers
vaccination!
_____ occurs in less than 1% of Hep B infections, but if occurs, has a mortality rate of up to 60%
Acute liver failure
What is the incubation period of Hep B? What is the average incubation period?
6 weeks to 6 months
12-14 weeks
**What does HBsAG stand for? What does it indicate?
Hepatitis B surface antigen
Active infection (acute or chronic)
**What does Anti-HBs (HBsAb) stand for? What does it indicate?
Hepatitis B surface antibody
Immunity (from recovery or vaccination)
**What does HBeAg stand for? What does it indicate?
Hepatitis B e antigen
High infectivity and active viral replication
**What does Anti-HBe (HBeAb) stand for? What does it indicate?
Hepatitis B e antibody
Lower infectivity, less active viral replication
**What does Anti-HBc (HBcAb) - Total stand for? What does it indicate?
Current or past infection (not from vaccination)
**What does anti-HBc IgM stand for? What does it indicate?
Hepatitis B core antibody (IgM)
Acute or recent infection
**What is the first HBV serologic markers to elevate/first sign of infection? If it persists beyond 6 months, what does it indicate?
Hepatitis B surface antigen (HBsAG)
first sign of infection
indicates chronic disease
Appearance of ____ and decline in ____ indicates recovery of acute infection and non-infectivity.
anti-HBs
HBsAG
What markers need to be present that would indicate previous vaccination with immunity?
Persistence of anti-HBs without elevated HBsAG
____ appears one month after HBsAg is detected. What does it indicate?
IgM anti-HBc
indicates a diagnosis of declining acute Hepatitis B
_____ also appears during acute hepatitis B, but persists ____. What will show in recovery? Chronic dz?
IgG anti-HBc
indefinitely
With recovery → IgG occurs with Anti-HBs
With chronic ds → IgG occurs with HBsAG
**______ Indicates viral replication and infectivity (when patient is most infectious). When does it appear? What follows it?
Hepatitis B envelope antigen (HBeAG)
Appears: shortly after HBsAG in the serum in the incubation period
followed by appearance of anti-HBe
presence of _____ indicates the hep B acute phase is over and the chance of infectivity is low
Hepatitis B e-antibody (HBeAb)
______ parallels the presence of HBeAg. ** What is important to note about it?
HBV DNA
precise marker of viral replication and infectivity
_______ and _____ makes the diagnosis of acute Hep B infection
IgM anti-HBc with combo of HBsAG
What is the tx for ACUTE hep B?
What is the prophylaxis Hep B tx after exposure? **What is the associated timeframe?
Hepatitis B immune globulin (HBIG) then initiation of the vaccine series
Must give within 7 days of exposure
What is the tx for an infant born to a Hep B positive mother?
Hepatitis B immune globulin (HBIG)
Indicated in newborns with HBV + mothers: HBIG and initiation of vaccine series within 12 hours of birth to infant
What is the prevention for Hep B?
universal precautions
safe sex education
do NOT share needles
VACCINATION
What lab values would make you think chronic Hep B? 40% of chronic hep B will develop _____
Elevated ALT/AST for > than 6 months and presence of HBsAg
cirrhosis
**What is the tx for CHRONIC hep B?
1st line: Nucleoside and nucleotide analog (first line)
Entecavir (Baraclude) or Tenofovir (Vemlidy)
2nd line: Interferon
________ MOA incorporates into viral DNA and inhibits reverse transcriptase = mutations of virus rendering ineffective
Nucleoside and nucleotide analog (first line)
Entecavir (Baraclude) or Tenofovir (Vemlidy)
____ MOA inhibits viral replication. What is the BBW?
interferon
BBW: for infections
What is the interpretation?
prior infection (inactive)
What is the interpretation?
immune due to Hep B vaccination
What is the interpretation?
acutely infected
What is the interpretation?
chronically infected
The diagnosis of Hep B relies on the presence of _____ in the serum
HBsAg
Which antibody shows immunity?
anti-HBs
What is the structure of Hep C? **50% of cases are transmitted via _____
single stranded RNA
IV drug use
What is the risk of Hep C maternal-neonate transmission?
Risk of maternal-neonatal and sexual transmission low in Hep C
higher transmission rate for Hep B
______ is the most common bloodborne infection in the United States, with an estimated 2.4 million people harboring an active infection. Approximately 21% of ____ pts also have Hep C
Hep C
HIV
What is the incubation period of Hep C? High incidence develop _____ (up to 85%)
Average 6-7 week incubation period
with waxing and waning jaundice
chronic hepatitis
**diagnosis of Hep C is based on ______. What does the presence of HCV RNA tell you?
HCV antibodies = presence of Anti-HCV
HCV RNA: Presence indicates current infection
**What does the presence of Anti-HCV without HCV RNA indicate?
prior Hep C exposure with recovery.
What hep has the highest incidence of becoming chronic? What does Hep C increase your risks for?
Hep C
Non-Hodgkin’s lymphoma
Glomerulonephritis
idiopathic pulmonary fibrosis
thyroiditis
What is the prevention for Hep C?
NO VACCINE!!!
NOT spread sexually or during childbirth
really just spread from dirty needles associated with IV drug use
What is the older tx method for Hep C?
Interferon x 6-24 weeks and can add Ribavirin if no improvement
**What is the newer tx options for Hep C?
A 6 week course of ledipasvir/sofosbuvir (Harvoni)
What are 3 risk factors that would add to the progression of chronic hep C to cirrhosis?
Increased risk in men
Those who drink more than 50g alcohol daily
Those who acquire HCV infection after age 40 years
_____, _____ and _______ promotes progression of Hep C to fibrosis. What can slow progression?
Tobacco
cannabis smoking
hepatic steatosis
coffee can slow progression
antiviral cure about _____ of hep C infections
95%
**What is Hep D associated with? What pt population? How is it dx? What is the tx?
Only associated with Hepatitis B - coinfection
mainly among IV drug users
detection of serum antibodies: anti-HDV
tx: self care, supportive and avoiding alcohol
Where is Hep E commonly found? What is the structure?
Central and Southeast Asia, the Middle East, and North Africa, where it is responsible for WATERBORNE hepatitis outbreaks
RNA virus
not common in the US, need to ask travel history
**What is the MC pt population associated with Hep E? In developed countries, how is it commonly spread?
pregnant women
swine, and consuming undercooked organ meats
What is the incubation period for Hep E? How is the dx made?
2-10 weeks
The diagnosis is made most readily by testing for IgM anti-HEV in serum
“flu-like symptoms” followed by “icteric phase” of frank jaundice
What am I?
What are some extrahepatic manifestations?
What labs will be elevated?
Hep E
arthritis; pancreatitis; thrombocytopenia; and a variety of neurologic complications, including Guillain-Barré syndrome and peripheral neuropathy
elevated aminotransaminase and bilirubin levels
What is the tx for Hep E? **What is the important take away regarding Hep E?
A 3-month course of treatment with oral ribavirin
can be very severe in preg women!! mortality rate can reach 15-25%
no vaccine approved in the US, but there is a promising one in China
What is hemochomatosis? How is it inherited? What is the associated gene?
Increased iron absorption from duodenum and stored in liver
autosomal recessive
HFE gene mutation
How is iron stored?
stored in the liver as hemosiderin
When does hemochromatosis typically present? What are some late findings?
usually around 50
symmetric arthropathy
hepatomegaly
hepatic dysfunction
bronze skin pigmentation (melanin deposition), cardiac enlargement (can progress to heart failure)
DM
What will the iron lab values show of a pt with hemochromatosis?
Elevated serum iron levels and serum ferritin
LOW TIBC: total iron binding capacity
____ can be used to confirm hemochromatosis dx and ____ to determine the extent of liver damage
genetic testing
liver bx
What is the tx for hemochromatosis? What are the chelating agents?
low iron diet
decrease alcohol
weekly phlebotomy until iron stores are depleted then PRN
Deferoxamine IV or Deferasirox po
What is Wilson Dz? How is it inherited?
genetic defect on chromosome 13 that affects the copper transporting enzyme and leads to excessive absorption of copper form intestines, and decreased excretion by the liver
rare autosomal recessive disorder
What does Wilson disease lead to ? When does it commonly present?
deposition of copper in liver and brain
childhood or young adult
What are the 2 organs systems affected the most by Wilson disease?
liver and brain: can present with parkinsonian like symptoms, ataxia, dysphagia, incoordination
elevated LFTs and cirrhosis
can also have psych features
**What is the pathognomic sign for Wilson disease?
Kayser-Fleischer ring
copper deposits in cornea
What are some common lab findings on a pt with Wilson disease?
Increased urinary copper excretion
Low serum ceruloplasmin levels
Liver biopsy to assess chronic hepatitis and cirrhosis
What is the tx for Wilson Disease?
restriction of dietary copper: shellfish, nuts, mushrooms, chocolate
**oral penicillamine: chelating agents with vit B6
oral zince to promote fecal excretion of copper
What is Gilbert syndrome? What enzyme?
Characterized by MILD unconjugated bilirubinemia
Reduced activity of glucuronyl transferase
What is the role of glucuronyl transferase?
Liver enzyme that gives glucuronic acid and changes bilirubin into a form that can be removed from body in bil
**Recurrent episodes of jaundice that are triggered dehydration, fasting, infection, menstruation, over-exertion, alcohol
What am I?
What lab finding?
What is the tx?
Gilbert Syndrome
Unconjugated hyperbilirubinemia ( < 3mg/dL)
and NORMAL everything else!
benign, no tx is necessary
What is Crigler Najjar Syndrome? What is it caused by?
Congenital nonhemolytic jaundice
Rapidly severe, High levels of unconjugated hyperbilirubinemia
Rare autosomal recessive disorder that is either a complete or partial Glucuronyl transferase deficiency
When does Crigler Najjar Syndrome present? What can it lead to?
Occur in infancy
High levels of bilirubin can lead to neurological damage.
“Kernicterus”
**What are the different levels of Crigler Najjar Syndrome?
Type I levels 20-50 mg/dL
Type II levels < 20mg/dL
High levels definitive for diagnosis
What is the tx for Crigler Najjar Syndrome? What is the tx for Type II?
Phototherapy!!
phenobarbital which will also induce the enzyme
Why does phototherapy work well for Crigler Najjar Syndrome? ______ is curative
Lowers bilirubin levels through photo-oxidation
Adds oxygen to the bilirubin so it easily dissolves
Body can excrete through urine/feces
liver transplant is curative
What is Dubin Johnson Syndrome? What is the key word here? What does it result in?
Genetic mutation affecting transport proteins of bilirubin
Elevations in Conjugated serum bilirubin
Intermittent Jaundice, fatigue
May see darkly pigmented liver on gross inspection
Conjugated hyperbilirubinemia in the absence of other abnormalities
What am I?
What is the tx?
What can exacerbate the condition?
Dubin Johnson Syndrome
benign condition: no tx needed
illness, OCP and pregnancy
What is the Rotor Syndrome? What are the 2 key words?
Rare genetic disorder
Hepatic defect in storage of conjugated bilirubin
Leaks back into bloodstream
How can you tell Rotor Syndrome apart from Dubin Johnson?
Can inject dye and do “transport study” to determine if Rotor or Dubin Johnson
liver bx: Rotor will have a norma looking liver and Dubin Johnson will have dark liver
What is the tx for Rotor Syndrome?
benign condition: no tx needed
What is Budd-Chiari Syndrome? What is the usually underlying cause?
Hepatic venous outflow obstruction
Hereditary and acquired hypercoagulable states can be defined in 75% of patients
tender, painful hepatic enlargement (RUQ pain)
Jaundice
Splenomegaly
Ascites
chronic: bleeding varices and hepatic encephalopathy may be evident
What am I?
**What is the imaging of choice? What will it show?
Budd-Chiari Syndrome
Doppler ultrasonography: occlusion/absence blood flow in hepatic veins/IVC
May see “spider web” pattern of occluded hepatic veins
In Budd-Chiari Syndrome, the doppler ultrasonography may show prominate _______ since its venous drainage may be occluded
caudate lobe: venous drainage may be occluded since it is supplied by L/R hepatic veins
_______ allows visualization of the obstructed veins and collateral vessels in _______
MRI with contrast
Budd-Chiari Syndrome
What is the tx for Budd-Chiari Syndrome?
Hepatocellular Carcinoma arise from liver _______ cells and 80% are due to ________
parenchymal cells
d/t Cirrhosis
What are the hepatocellular carcinoma risk factors for patients with cirrhosis?
Obesity
Male gender
Age > 55
Family History
DM
HCV or HBV infection
Alcohol
**What are the 2 lab findings associated with hepatocellular carcinoma?
Spike in ALP
Alpha fetoprotein in 70% of patients
**What are the first line imaging for hepatocellular carcinoma? What confirms?
CT and MRI are first line imaging to identify masses
liver bx confirms
**When can a liver bx be deferred in Hepatocellular Carcinoma?
Can be deferred if mass on CT and + alpha fetoprotein
What are the staging classifications for Hepatocellular Carcinoma?
What is the screening for hepatocellular carcinoma?
What is the tx for Hepatocellular Carcinoma? What MELD score?
